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This week I wanted to take a break from all the SARS-CoV2 research and look at a few other interesting new studies.
74 comments:
The article discussing the gene edits to mitochondrial DNA is interesting because now that we have made so much technological advances, we are now able to apply them to science to save lives and understand the basis of diseases and disorders that we were not able to do before. In this particular instance, technology such as the CRISPR-Cas9 genome editing system was unable to do the work that the scientists needed. A bacterial enzyme actually helped researchers with this discovery because it was able to detect the changes of the mitochondrial genomes through a process called base editing and could now allow researchers to create new ways of studying and also potentially allow the treatment of mutations in the mitochondria. This development is important because now researchers and scientists can potentially fix this disorder and people will be able to generate energy to their fullest extent. This will also prevent damage to the nervous system and heart which can be dangerous to people with the disease. Researchers are able to make models of organisms with the same mutations as the ones seen in humans and this is now the first step at change with this disorder. This development now allows for more doors to be opened in the science world and can hopefully lead to more discoveries in the future. The CRISPR-Cas9 allows scientists to use a strand of RNA to bring the enzyme to the region that needs to be edited which works well in the nucleus but not with mitochondria because it is surrounded by membranes. The emergence of the enzyme allowed for a more promising development with this order. The enzyme, when in contact with DNA base C, was able to convert it to a U. This was helpful because the U base acts like a T, so the enzymes that replicate DNA, copied it as a T which made a C become a T. Before, scientists had used enzymes known as cytidine deaminases to change DNA bases. However, these enzymes act on a single strand of DNA, but humans have two DNA strands wound together, so scientists had to use Cas9 enzymes to break the DNA and made a single strand of DNA for the enzymes. The enzyme(DddA) that has been discovered though is able to work on a double strand of DNA without the Cas9 and could allow for it to reach the mitochondria. Although a lot of work is needed to be done, this enzyme is the first breakthrough in fixing the mitochondrial mutations and creating a technique that differs from the already existing ones.
I read the article, “Scientists make precise gene edits to mitochondrial DNA for first time” and “Researchers uncover a critical early step of the visual process.” In the first article by Heidi Ledford, it talks about how a bacterial enzyme has now begin to allow researchers to accomplish what CRISPR couldn’t, which is a Cas9 genome-editing system. Additionally, this enzyme will apply changes to the mitochondria’s genes, which is a cell’s energy producing organelle. This, in turn, can allow researchers to make new ways to study and potentially treat diseases which are caused by mutations in the mitochondrial genome. Furthermore, researchers have also found another way to fix mutations that are in the mitochondria, by applying their knowledge that cells contain several copies of the mitochondrial genome. Michal Minczuk, who works at the University of Cambridge in UK as a mitochondrial geneticist, says that this latest technique can allow researchers to fix mutations when the mitochondria lacks normal copies of the gene. In the second article that I read, by the University of Texas Health Center at Houston, it talks about research that will lead to a better understanding of how the retina in our eyes process many signals from rods in the eye, particularly at both dawn and dusk. In addition, the communication between cones and rods in the retina is a key point to understanding how the process of visual signaling works. However, it was discovered that rods do not communicate directly with other rods and cones. Instead, most signaling occurs through communication between rods and cones. The protein, connexin36, is critical in the rod and cone gap junctions. Both Christophe P. Ribelayga, a Bernice Weingarten Chair in the Ruiz Department of Ophthalmology & Visual Science at McGovern Medical School at UTHealth, and Steve Massey, who is a research director in the Ruiz Department of Ophthalmology & Visual Science at McGovern Medical School at UTHealth, have both led to the ongoing effort to understand electrically coupled receptors, which is an important step towards better understanding how photoreceptors encode light signals and how these signals are then processed by the retina.
In the article “Scientists make precise gene edits to mitochondrial DNA for first time” by Heidi Ledford, the reader is exposed to information about how the enzyme DddA has the ability to help scientists study and possibly treat diseases which could happen due to incorrect sequences in mitochondrial DNA. Ledford explains how scientists couldn’t target mitochondrial DNA with the popular enzyme CRISPR-Cas9 because it uses RNA to guide it to the area of DNA that needs fixing, and since it uses RNA, it isn’t possible for it to enter the mitochondria because of the membranes that surround mitochondria. With the DddA enzyme, scientists can reach and change the sequence of improper mitochondrial genome without having to rely on something to support the enzyme. However, this enzyme needs to be tweaked and some changes have to be and are made for it to properly function and not get out of control and harm mitochondria instead of help it. This enzyme can prove to be extremely helpful in the future because it can provide scientists and medical workers with more research to find cures to diseases that are caused by mitochondrial DNA, which usually can be very fatal to the people who inherit these diseases because it affects major parts of one’s body, including the nervous system, the heart, and muscles. This enzyme is also very important because it can change the sequence of large amounts of incorrect mitochondrial genome, so it can prove useful in helping people who have many mitochondria with incorrect and harmful sequences. This article was fun to read because it gave a lot of information as to why we couldn’t change much in mitochondrial DNA before and how this new enzyme can make a huge impact on our knowledge of mitochondrial DNA related diseases. This article also showed how new discoveries are being made all the time and how complex and interesting our body is to research. Last but not least, this article also showed me how we still haven’t made many discoveries in the world of science, and many more are yet to come for the future.
The article “Researchers Uncover a Critical Early Step of the Visual Process,” focuses on the discovery of the components that connect light receptors and the impacts of these connections on visual processing. These light receptors are called photoreceptors, and in order to understand their connection to visual processing, researchers have been studying the main types of sensory cells, rods and cones. Prior to this study, researchers had known that electrical signals could spread between photoreceptors through gap junctions, but the details of these junctions had been widely unknown. The study started by researching communication between rods and cones in the retina. Through this research, it was surprisingly discovered that most of the gap junctions are between cones and rods as opposed to being between two cones or two rods. In order to further test this discovery and what it means for visual processing, researchers have developed genetic mouse strains. Even with this new discovery, many questions still remain regarding visual processing. In order to continue working towards finding answers to these questions, the National Institute of Health’s National Eye Institute has awarded the researchers $4 million in grants. According to Christophe P. Ribelayga, PhD, as this research continues to advance, it can be incorporated into the designs of photoreceptor or retinal implants that can be used to restore vision. This discovery lays out the foundation of electrical receptors, and is a vital step towards understanding visual processing.
In the article “Scientists Make Precise Edith to Mitochondrial DNA for the First Time” Mutations in the mitochondrial genome can be fatal and passed down through generations. These mutations can lead to heart and nervous system problems that can’t be cured. In past years we have been able to try and edit the DNA with the CRISPR-Cas9 genome editing system. With technology, researchers found a new way to base edit genes even more precisely to help with these diseases. Through trial and error, we are seeing enzymes like DddA. Ddda acts directly on double-stranded DNA, unlike relying on Cas9 enzymes to help enzymes act on a single strand. DddA can target changes to the genomes of mitochondria to the point where one day they might be able to cut off the site of harmful mutations. This could stop the population of mutated DNA in the body, and allow the repopulation of the normal (non-mutated) DNA to occur. Even with a lack of normal DNA this could be possible with the new technology found. By complementing existing methods we can build on the way we treat mitochondrial disorders. By generating animal models that have the same mitochondrial mutations, we can learn more about how to use this new found information. Over time this discovery can help thousands of people with mitochondrial diseases and through more research can become even more beneficial.
This week I read the article “Researchers uncover a critical early step of the visual process” by the University of Texas Health Science Center. I liked how the article was about photoreceptors, because it was able to establish a clear connection between biology and psychology, and those are both topics that I’m fascinated in. So,
this article was a bit of a refresher. For example, I had forgotten that rods are used for night vision and cones are used for daytime and color vision. I was surprised to find out that cones don’t directly communicate with other cones(it is rare), and instead, signaling happens via communication between rods and cones. These sensory cells rely on a protein called Cx36, which is the main component of rod/cone gap junctions. To further prove their hypothesis, the UTHealth authors are going to use mice to determine the importance of rod/cone gap junctions. By writing this article, readers can understand how photoreceptors encode light signals and how the retina processes these signals.
The first article I read was “Scientists make precise gene edits to mitochondrial DNA for first time” by Heidi Ledford. The article is about a new method that could help thousands of patients with mitochondrial mutations. Such diseases harm the heart, muscles, and nervous systems. A unique bacterial enzyme has rendered it possible for scientists to accomplish what the widely CRISPR - Cas9 genome-editing structure could not carry out: targeted modifications to mitochondrial genomes that produce important energy. This technique can be used to examine, and tend to diseases that are caused by mitochondrial modifications. Researching these diseases has been challenging since scientists lacked a way to render animal models of the same alterations to the mitochondrial genome sequence. CRISPR - Cas9 granted scientists to study and examine the nucleus, where the DNA is located. The tool they used for the nucleus, couldn’t get through the cell membranes around the mitochondria, so they needed another method to get to the mitochondria. The DddA could reach the mitochondria with the Cas9 enzyme, but they needed to be managed. Researchers have developed a method for repairing mitochondrial alterations by leveraging the fact that cells can carry thousands of duplicates of the mitochondrial genome and that only a portion of these does not carry the disease-related mutation. If this method succeeds, the way of life of thousands can be improved. Diseases such as mitochondrial myopathy, DAD, NARP, and many others could get treated.
The second article I read was “Researchers uncover a critical early step of the visual process” by the University of Texas Health Science Center at Houston. The article was about how scientists examine and study eye receptors. For the first time, the main aspects of electrical systems between photoreceptors in the eye and the impact of these connections on the initial stages of visual signal processing were recognized. Scientists usually had kept their attention to the rod and cone cells and hadn’t explored other ways, They transform basic light waves into electronic pulses, and signals are transmitted to the brain by designated pathways. Rods are used at night to see while cones are being used for day and seeing colors. Since it has been recognized for while now that electrical impulses can travel across cell processors called gap junctions between photoreceptors, structure and function have remained weakly understood. Rods do not interact directly with other rods and cones rarely communicate first hand with other cones. Most of the signaling occurs via interaction among rods and cones. Researchers also defined a particular protein named connexin36 as the main component of junctions between rod/cone gaps junctions.
I read the article, “Researchers uncover a critical early step of the visual process” which discussed the significance of the anatomy of the eye and understanding how that affects visual processing. The article is written by a group of scientists and doctors at the University of Texas Health Science Center at Houston. I found this article to be especially interesting, because these studies could affect the abilities of photoreceptor or retinal implants to restore a patient’s sight. The scientists originally believed that rods, which are responsible for night vision, and cones, which are responsible for daytime and color vision, communicate solely with other rods or cones respectively. Meaning, cones communicate with cones and rods communicate with rods. However, throughout their research they found out that there is communication between rods and cones together. This is largely thanks to a protein called connexin36. The scientists will be continuing the studies in mice to better understand the role of the rod/cone gap junctions in regards to the visual process. Thus, I think this article is important because it changed the common theory held about the communication between rods and cones and could lead to a large variety of medical advances.
We all know what CRISPR-Cas9 is; a technology that enables geneticists and medical researchers to edit parts of a genome by removing, adding, or altering sections of the DNA sequence. CRISPR was a buzz in the science world, as it allowed us to do something never done before, edit the human genome. For the first time, organisms were able to “play god” and tamper with biological mechanisms. As mentioned in “Scientists Make Precise Gene Edits to Mitochondrial DNA for the First Time” by Heidi Ledford, CRISPR failed at one of geneticists perplexing problems: targeted and controlled changes to the genomes of mDNA, or mitochondrial DNA. Now, with the discovery of a “peculiar bacterial enzyme”, scientists may be able to develop new ways to study, and perhaps even treat, diseases caused by mutations in the mitochondrial genome.
We know that there are only a small number of genes in the mitochondrial genome versus the nuclear genome, however even the slightest mishap in replication can be fatal, as these mutations particularly harm the nervous system and muscles, including the heart.
As stated, “CRISPR-Cas9 has allowed researchers to tweak genomes to their liking...but the tool uses a strand of RNA to guide the Cas9 enzyme...this works well for DNA in the nucleus, but researchers have no way to shuttle that RNA into mitochondria, which are surrounded by membranes.” In late 2018, microbiologist Joseph Mougous at the University of Washington discovered a strange enzyme; a toxin made by the bacterium Burkhholderia cenocepacia. This was a peculiar discovery, as the bacterium turned any Cytosine base it encountered into a Uracil base. Because Uracil is not common in DNA, and it behaves like Thymine, the enzymes in DNA replication (DNA Polymerase, Ligase, etc.) copy the U as a T , converting the C into a T.
The enzyme that Mougous found was called DddA, and could act directly on double-stranded DNA without relying on Cas9 to break it. This allowed scientists to penetrate the mitochondrial membrane. There was a complication. The ability to modify double-stranded DNA also makes this enzyme deadly because if set loose, it would mutate every C it came across.
This work is a long way from being used in clinics, and more studies in different cell types are needed. This technique can ultimately complement existing methods to treat mitochondrial disorders. Using this, researchers can generate animal models and expedite this process, as it’s an amazing step forward.
When I read "Scientists make precise gene edits to Mitochondrial DNA for the first time" by Heidi Ledford,In the article there is a paragraph that says "In Seattle, a team led by microbiologist Joseph Mougous at the University of Washington had discovered a strange enzyme. It was a toxin made by the bacterium Burkholderia cenocepacia — and when it encountered the DNA base C, it converted it to a U. Because U, which is not commonly found in DNA, behaves like a T, the enzymes that replicate the cell’s DNA copy it as a T, effectively converting a C in the genome sequence to a T.". When I finished reading that paragraph from the "Scientists make precise gene edits to Mitochondrial DNA for the first time", I was stunned by how the Seattle Team from the University of Washington managed to make such an extraordinary discovery of newly formed enzymes by replication of the cell's DNA copy it as a T which then effectively changed into a C in the genome sequence into a T. This discovery is shockingly amazing because what we are seeing with the enzyme is that the enzyme replicated another enzyme that is not similar to another enzyme. I think this article is important because it shows how a group/team of scientists can edit the genes of the Mitochondrial DNA.I loved reading this article because it brought me into another part of science and It showed how scientist can edit the genes/traits of the mitochondrial DNA for the first time because this type of editing for the Mitochondrial DNA has never been attempted or done.
The article I read was “ Researchers uncover a critical early step of the visual process.” The article discussed research regarding the cones and rods located inside the eye, which was done by the The University of Texas Health Science Center at Houston. In the eye, rods are used for night vision, while cones are used for daytime and color vision. The researchers talked about how their findings regarding how rods and cones communicated could affect how photoreceptors or retinal implants are designed to restore vision. Researchers initially believed that the cones in the eye communicate with other cones, while the rods communicate with the other rods, but this was later disproved by their research. They had found out that rods communicate with cones, while cones communicate with rods. These rod/cone junctions were mainly operated by a protein known as connexin36. The research that was discussed in the article brought upon a change in the way eye anatomy would be perceived, and also helped the researchers to further understand how the visual signaling process works.
The article I chose for this week's assignment was about the researchers found an early step of the visual process. In this article, I learned how light receptors are a significant influence on the development of vision. It revealed that the researches put their focus on cones and rods. Rods are cells that are used for night time, whereas the cones are used for day time and the coloration of our vision. One misconception that has been changed was that we initially thought that the communication was limited to rods and other rods, as well as cones and other cones. They were able to find out that both types of cells can communicate with each other. These cells use a protein known as connexin36, which is a protein prominent in the gap junctions between rods and cones. In fact, almost 95 percent of all signal is transmitted through rod-cone signaling. Now researchers have mice that will help them learn more about the rod-cone pathway in the retina and how it is relevant for vision.
In the article, Scientists make precise gene edits to mitochondrial DNA for the first time, scientists found a new way to DNA which could further their studies to treat diseases caused by mutations in the mitochondrial genome. It is a major improvement from CRISPr-Cas9. The procedure was called mitochondrial replacement, in which the nucleus of an egg or embryo is transplanted into a donor egg or embryo that contains healthy mitochondria. Researchers are also trying to develop a technique to correct mitochondrial mutations by taking advantage of the fact that cells can contain thousands of copies of the mitochondrial genome. The research is still in its early stage, but with time, scientists can use this to save many lives of people who inherited genetic diseases by mutations.
A life-changing advancement in DNA research has recently been discovered and is discussed in the article “Scientists Make Precise Gene Edits to Mitochondrial DNA for the First Time” by Heidi Ledford. The article explains the findings of a bacterial enzyme that can be used to make specific changes to the genome within the mitochondria of animal cells. This in turn can lead to the treatment of diseases that stem from mitochondrial DNA mutations. Mutations in this genetic sequence can result in a depleted amount of energy for the cell and damage the nervous and muscular systems. With the DNA inside the nucleus, scientists have been able to use the CRISPR-Cas9 enzyme to alter genes in many organisms. This enzyme is directed to certain sections of the DNA by a strand of RNA. However, CRISPR-Cas9 cannot be used to change the DNA inside mitochondria due to the enclosing membranes, which prevent the RNA strand from entering. Other enzymes, including cytidine deaminases, were also tested to change the DNA, but these enzymes could only make adjustments to a single strand of DNA. Eventually, a solution to these problems arose when the enzyme DddA alone was discovered to be able to alter the nitrogenous bases in mitochondrial double-stranded DNA. It would turn the base cytosine into uracil, which is not normally present in DNA. Instead, uracil would act as thymine, copying thymine during the DNA replication process. To ensure that the DddA enzyme did not change every cytosine base, it was broken into two pieces, each of which were attached to proteins that directed the DddA to specific areas of the DNA. The enzyme can then cut off the mutated section of DNA, eventually causing it to break down and giving rise to normal copies of DNA. This discovery is beneficial to fix mitochondrial mutations, but still requires further testing to prevent errors from occurring. However, it is still a huge leap forward towards saving more lives. Several more advancements are being made in the science field day by day, and this changes perspectives on how further scientists and researchers can go to develop major medical innovations.
Today I read “Scientists make precise gene edits to mitochondrial DNA for first time” by Heidi Ledford. The article discussed how scientists discovered how to edit the DNA found inside of a mitochondria. This technological advancement is extremely important because it could heal patients that suffer from diseases caused by genetic mutations in the mitochondria. Even though the nuclear genome contains many more genes than the mitochondrial genome, the mitochondrial genome can still cause mutations that can be deadly to humans. By using a method called base editing, scientists will be able to modify the mitochondrial genome with great precision. In the past, scientists were unable to use other methods, such as CRISPR–Cas9, to modify genes in the mitochondria because this technique uses RNA which cannot pass the membrane of a mitochondria. The enzyme used in CRISPR–Cas9, cytidine deaminases, can only modify a single stranded DNA. A new enzyme, called DddA, can edit double stranded DNA which means it can pass through the membrane. This opens up the opportunity for scientists to correct potentially deadly mutations found in the mitochondrial genome. Although an exciting discovery, scientists argue that it could be a long time before this technique is used clinically. It must first go under a series of regulated tests to ensure that the method is both safe and effective.
Scientists make precise gene edits to mitochondrial DNA for first time explains how researchers are now able to target changes to the genomes of a cells’ mitochondria. This has been a struggle for scientists because they lacked the ability to make animal models with the same changes to the mitochondrial genome. The technique stems from a super-precise version of gene editing called base editing which allows researchers to develop a new may to treat diseases caused by mutations in the mitochondrial genome. Even though there is a small amount of genes in the mitochondrial genome, the mutations in this part of the cell can cause harm to the nervous system and the muscles. Prior to the discovery of gene edits in the mitochondrial DNA, scientists have used CRISPR-Cas9 to tweak genomes in the cell’s nucleus because it uses a strand of RNA to guide the Cas9 enzyme to the region of DNA that scientists wish to edit. This works well in the cell’s nucleus but the strand of RNA could not be shuttled into the mitochondria. This was until chemist David Liu and microbiologist Joseph Mougous had found the enzyme DddA, which was suitable for reaching the mitochondrial genome without relying on the Cas9 enzyme to break DNA. In order to make it into a genome editing tool, it had to be split into two pieces that would change DNA only when brought together in the right orientation and to control which DNA sequence the enzyme modified. This newfound enzyme and technique could complement existing methods used to prevent or treat mitochondrial replacement.
Researchers uncover a critical early step of the visual process discusses how a connection between the key components of electrical connection between light receptions in the eye and the impact of these connections on the early steps of visual sign processing have been identified for the first time. Researchers have typically focused their attention on two key sensory cells- rods and cones- that make particles of light into electrical signals and how these signals are relayed in the brain through circuits. The nature and function that electrical signals can be spread between photoreceptors through cell connectors was a topic scientists lacked knowledge. The communication between the rods and cones in the retina is critical for understanding how the visual signaling process works. During their research, Christophe P. Ribelayga and Steve Massey had discovered a specific protein called connexin36 as the main component of rod/cone gap junctions. In 2018, researchers in Ruiz Department of Ophthalmology and Visual Science were given $4 million from the National Institute of Health’s National Eye Institute to study photoreceptor development, function and electrical interactions. Ribelayga and Massey led the effort to lay out the foundation of the network of electrically coupled receptors.
The newly discovered bacterial enzyme has created an opportunity for scientists to make changes to the genome of mitochondria. This will allow researchers to develop a deeper understanding on diseases involving a mutated mitochondrial genome. Eventually, a treat option might be introduced to those suffering from these types of diseases. A mutation in the mitochondrial genome can be detrimental to the nervous system and muscles. Previously, scientists have used a strand of RNA and the Cas9 enzyme to alter the DNA in the cell’s nucleus. However, this method proves to be difficult for mitochondria which it is surrounded by membranes. The new enzyme that has been developed has the ability to alter the gene in the mitocondria by changing the bases in the DNA. This enzyme is a toxin which changes the base C into a U, and it replicates as a T. Now the C in the genome sequence has been converted into a T. Unlike other enzymes previously used, DddA can work on both strands of the DNA. However, DddA can be extremely dangers as it is deadly. When released, it could change every C that it comes in contact with. Scientists have found a way to lower the risks by splitting the enzyme so that it can only be activated when the two parts come together in an appropriate manner. They are then attached to proteins that bind to specific locations in the genome. In order to cure diseases from mitochondrial mutations, the scientists must enter the mitochondria and cut the DNA at the site of the mutation. This will allow the mitochondria to repopulate the structure in the normal and correct way. The DddA enzyme has the ability to correct a mutation even when there aren’t many normal copies of the gene. Michal Minczuk, a mitochondrial geneticists, claims that it is a short term solution, but an amazing accomplishment. I believe that people have a higher chance of survival from a dangerous and life-threatening disease since scientists are making new discoveries. Researchers still have a long way with this new enzyme since it still needs to be tested on animal model before it can be perfected. However, victims of a mitochondrial mutation can now have hope that their cure is in the near future.
In the article, “Researches uncover a critical early step of the visual process”, the author talks about how photoreceptors, light receptors, impact the early stages of the process of vision. Researchers most l’y focused on how rods and cones, the two key sensory cells, convert elementary particles of light into electrical signals. Then, these electrical signals transfer to the brain through devoted circuits. Rods are used for night vision. Cones are used for daytime and color vision. Scientists know that the electrical signals can spread between photoreceptors through cell connectors. The cell connectors which are called gap junctions. However, researchers have prolly understood the function. Christophe P. Ribelayga explained that the understanding of how the retina processes signals from rods and cones in the eyes can help design better photoreceptor or retinal implants to restore vision. Furthermore, it is very important to understand what happens when both photoreceptor types are active under ambient lighting conditions. Coupling, communication, between rods and cones is critical for understanding how the visual signaling process works. The researchers have found pretty surprising informations. They found out that rods do not directly communicate with other rods. While, cones rarely communicate with directly with other cones. The majority of the signaling happens through the communication between rods and cones. In 2018, the Ruiz Department of Ophthalmology & Visual Science received more than $4 million in grants for researchers to study development, function, and electrical interactions.
I find CRISPR-Cas9 to be fascinating. CRISPR, as we know, is a family of DNA sequences found in the genomes of prokaryotic organisms such as bacteria and archaea. The first article talks about the base editing system. Researchers have recently been able to use base editing, which allows them to treat diseases caused by mutations in the mitochondrial genome. This is different than the CRISPR-Cas9 editing system as it can now make changes to the genomes of the mitochondria. Mutations are passed down and can be fatal, harming the nervous system and muscles. Before, scientists could not make animal models with the same changes to the mitochondrial genome. This advancement in science could potentially save lives in the future.
The base editing system was improved upon a team in Seattle, Washington, which has found a strange enzyme, made by the bacterium Burkholderia Cenocepacia. When this enzyme encountered (in the DNA base) C, it would convert to U, which does not happen in DNA. I was intrigued by this concept of a DNA base that goes against its own rules. Because of this, researchers can now change one DNA base to another. On top of that, an enzyme called DddA can act directly on a double-stranded DNA, which makes it suitable for reaching the mitochondrial genome.
The second article discusses photoreceptors. Photoreceptors are the cells in the retina that respond to light. The critical components of the electrical connections between light receptors in the eye and the impact of these connections and the early stage of visual signal processing have been identified. Researchers have focused their attention on two vital sensory cells: rods and cones. Rods are used for night vision while cones are used for day vision. These convert elementary particles of light into electrical signals. This research will lead to a better understanding of how the retina processes signals from the rods and cones in the eyes, especially under ambient lighting conditions when both photoreceptor types are active (i.e dawn and dusk). Researchers have found out that rods and cones communicate with each other, rather than interacting in their own groups. I find this interesting as it is important to comprehend how we, as humans, can see.
This article about the visual process was very interesting to read about but it also showed me how far we are from truly understanding the human body. Everyday we learn more and more things that we never knew before. Everyday we have a better understanding of the human body through the technology we create. Just in this article they discuss how people once believed that the rods and cones used electrical signals to spread information however people didn’t know how they specifically did it. However through many tests and technological advancements they were able to learn the functions and the process. They learned and developed a better understanding of photoreceptors networks. This allowed them to learn how photoreceptors had light signals which the retina processed. Researchers are able to discover new things they never did before which is clearly seen in the steps that they were able to encode in the visual process.
When studying cellular mutations, CRISPR-Cas9 “...has allowed researchers to tweak genomes...”(Ledford-4) in order to understand and treat the diseases more efficiently. Mutations can affect any part of DNA and any part of the cell. Mitochondria are energy producers for the cell, so it is easy to see why mitochondrial mutations can be detrimental to patients. However, scientists have found it difficult to study mitochondrial mutations.
CRISPR-Cas9 uses RNA to deliver the Cas9 enzyme to regions of DNA that researchers want to edit. That same technique cannot be used for mitochondrial mutations because the mitochondria contains many membranes that won’t allow the RNA through.
In 2018, microbiologist Joseph Mougous discovered a toxin enzyme DddA produced by the bacteria Burkholderia cenocepacia. The enzyme is able to breakdown double stranded DNA without the help of Cas9. However, DddA is very dangerous as it will mutate everything, so David Liu and his team split the enzyme into two parts. The enzyme is not able to work without the other half placed in the right orientation. This newfound enzyme will now allow scientists to easily study and treat mitochondrial mutations.
Anjana Kottaiveedu
I decided to read both articles that were provided this week. I found the first article, “Scientists make precise gene edits to mitochondrial DNA for first time” by Heidi Ledford, very interesting. I was fascinated by the fact that scientists have discovered an enzyme that can potentially treat deadly diseases. The enzyme accomplishes this task by targetting changes to the genomes of mitochondria, which are mutations that cause the diseases. This is something that the CRISPR–Cas9 genome-editing system couldn’t carry out, which is a technique that allows researchers to change genomes to their preference. Two teams of scientists, led by David Liu and Joseph Mougous, researched the strange enzyme, relating it to enzymes that Liu had worked on in the past. Although there is a long way for the enzyme to be used in the clinic for curing diseases, researchers have been developing and utilizing alternate techniques. I find it fascinating that scientists have been developing enzymes that enter the mitochondria and cut the DNA at the location of a harmful mutation, and rather than repairing the cut, the mitochondria will degrade the DNA that has been damaged. I also found the second article, “Researchers uncover a critical early step of the visual process” a very compelling discovery. The researchers came upon the key components of the electrical connections between light receptors located in the eye, as well as the impact it has on the visual signal process. This shows how we learn new things in our world every day, considering this is an important discovery never found before. To fully understand their findings, researchers focus on two significant sensory cells that convert particles of light into electrical signals, called rods (used for night vision) and cones (used for daytime and color vision). Researcher Christophe P. Ribelayga states that this research will overall lead to a better understanding of how the retina processes signals from the rods and cones located in the eyes. The communication between rods and cones is important to understand how the visual signaling process works. Surprisingly the researchers discovered that rods do not directly communicate with other rods, similarly to cones. But instead, the rods and cones communicate together, utilizing a specific protein that researchers identified called connexin36 (the main component of rod/cone gap junctions). These rod/cone gap junctions were labeled as the “keystone of the photoreceptor network”. Overall, from this week’s articles, I have learned many new things about what researchers and scientists are discovering in our current times.
An impactful discovery regarding the early stages of processing vision has recently been made and after reading the article “Researchers uncover a critical early step of the visual process” written by The University of Texas Health Science Center at Houston, I was able to understand how this discovery has majorly changed what we know and understand about our vision. The article opens up by discussing existing information on the topic. It explains how scientists in the field collectively understand how photoreceptors affect the early stages of the process of vision, through their research focused on rods and cones. The article explains some basic information regarding these two sensory cells then introduces the lack of knowledge concerning crucial cell connectors called gap junctions. Christophe P. Ribelayga, Ph.D., co-lead author of the study, and other individuals have been working to change this. These scientists have focused on finding a better understanding of how the retina processes signals from the rods and the cones in specific settings. The author then establishes the scientist's breakthrough,that the majority of signaling actually occurs through the communication between rods and cones specifically through the connexin36 (Cx36) protein. They elaborate by saying that every single rod has an electrical connection to a cone and that rod and cone gap junctions subjugate the network of photoreceptors. Scientists concluded that the rod and cone gap junctions are the entry points of a rod pathway through which signals of rod origin can travel across the retina. With this newfound knowledge in addition to numerous grants being inaugurated, scientists like Christophe P. Ribelayga are sure to better comprehend how photoreceptors encode light signals in relation to the electrical connections between rods and cones. In summary, after reading the article it's safe to say that even the smallest of scientific discoveries could be the cornerstone of an entire scientific field. Besides the obvious reason of providing new information, these discoveries prove to be essential in expanding its real-world possibilities and applications.
“Scientists Make Precise Edits to Mitochondrial DNA for the First Time” talks about a new enzyme that can change mitochondrial DNA. This new enzyme is especially important, since by editing mitochondrial DNA, scientists can create animal models with mitochondrial DNA mutations for research. They were unable to do this using CRISPR- Cas9, a gene editing system, since Cas9 relied on RNA to guide the enzyme. As a result of membranes around mitochondria, this wouldn’t work. Furthermore, Cas9 and most cytidine deaminases (Enzymes used for gene editing) only works on single stranded DNA, which is created when the enzyme unwinds the DNA. The new enzyme, DddA, could be used directly on double stranded DNA. Besides its implications on research, DddA also changes the way mitochondrial genome mutations, affecting the nervous system and muscles are cured. One of the ways these mutations are cured is by using enzymes to cut DNA at the sight of the mutation. Instead of repairing it, the mitochondria degrades the DNA. It will then be refilled with a normal copy of the genome. The problem with this method is that it only works in cells that have more mitochondrial genes that are not affected by the mutation. DddA could be used to edit these mutations in cells where this is not the case. It will expand the field of medicine, and help many people. In addition to medicine and research, I am personally interested in how this new enzyme will change genetic engineering, and GMO products. Further research that may occur in this field may include finding other deaminases that convert other DNA bases. DddA changes the base C into U, which acts like the base T. Another article covering the same discovery reveals that the scientist who discovered DddA believes there are enzymes that can be developed into more mitochondrial gene editing tools.
“Researchers Uncover a Critical Early Step of the Visual Process” reveals insights on new research pertaining to the visual process, specifically light receptors and early development. When researching how light receptors impact early development, scientists focus on two types of cells called rods and cones, which convert light particles into electrical signals to relay to the brain. Rods are used for night vision, and cones are used for daytime and color. This study researches how electrical signals are passed between photoreceptors by gap junctions, which is something not well understood. By understanding this process, scientists can identify how our eyes work at times like dawn and dusk, during which both rods and cones are active, which is critical for understanding the visual process. The result of the research was surprising. They discovered that rods didn’t communicate with rods, and cones rarely communicate with cones. 95% of the signaling was between rods and cones. The data collected suggested that the gap junction between cones and rods are the most important part of the photo receptor network. These gap junctions act as entry points to the pathway for signals from rods to travel across the retina. A protein called connexin36 was discovered as the main component of these gap junctions. The researchers of this study plan to further investigate this by using specifically bred mice that lack the specific gap junction. This research is important since it provides essential information for implants to restore vision. A recent article talks about an implant that restores vision in blind people by using a special pair of glasses with a camera attached. The problem with this implant is that it requires a surgery involving the brain. This is a risky and potentially dangerous procedure. The details acquired by researchers in the recent study could be used to create a better and safer implant to aid people with visual impairments.
Additional Resources:
https://www.genengnews.com/news/interbacterial-toxin-leads-scientists-to-crispr-free-method-for-precise-mitochondrial-gene-editing
https://www.technologyreview.com/2020/02/06/844908/a-new-implant-for-blind-people-jacks-directly-into-the-brain
As someone who possibly wants to go into optometry, I found the article, "Researchers uncover a critical early step of the visual process" very interesting. The article discusses how light receptors, or photoreceptors, influence the early stages of vision. Two sensory cells, rods and cones, convert particles of light to electrical signals and these signals are sent to the brain by circuits. These electrical signals and travel between photoreceptors in gap junctions, but how this happens has not been understood. Because of this, the communication between rods and cones is critical to understanding how the process works. Scientists discovered that the majority of gap junctures are between rods and cones, not rod and rod or cone and cone. Scientists are now experimenting with the rod/cone junctures to determine their importance in the processing of electrical signals. It is so surprising to me that even a body part as small as the eye has so many hidden secrets. An entire network of photoreceptors is all contained in such a small place. It's so fascinating that we all live in bodies that we do not understand completely and that there is as much to discover about our own bodies as their is everywhere else in the universe.
CRISPR-Cas9 is a genome editing system used by researchers to tweak genomes in nearly every organism, but the process itself prevents them from accessing the mitochondria. The process uses an RNA strand to guide the Cas9 enzyme down a DNA strand. Some of these enzymes were used by Liu with CRISPR-Cas9 to change the DNA base sequences, but it only worked on one DNA strand. Humans have two DNA strands, so the Cas9 enzyme had to break apart the two strands and the Cas9 dependence on the guiding RNA strand prevented them from reaching the mitochondrial genome. Joseph Mougous, from the University of Washington, discovered a similar enzyme made from the bacterium Burkholderia cencocepacia, which converted the DNA base C into U, which commonly acts like a T. This enzyme, now called DddA, could act on double stranded DNA which would mean there would be no dependence on the Cas9 enzyme and could allow them to reach the mitochondrial genome. Before this process can be used though, they have to tame the enzyme so that they can control what bases the enzyme switches into Cs. This entire process is extremely beneficial to the development of medicine because it theoretically allows us to delve into the mitochondrial genome and observe diseases passed down from the maternal DNA, and we can figure out how to correct any mitochondrial mutilation by cutting out the harmful mutilation and allowing that DNA to degrade.
This week I have decided to read the article, “Scientists Make Precise Gene Edits to Mitochondrial DNA for First Time,” by Heidi Ledford. This article is talking about the research of a bacterial enzyme which can target the genomes of mitochondria, or the powerhouse of the cell. As much of an importance the mitochondria has towards the cell, there can also be mutations brung up by the mitochondrial genomes, as well. By using the technique of base editing, which is a much more precise way of gene editing, these mitochondrial disorders might be treatable in the future. Just to sum up some information about these mitochondrial genome disorders, they can be passed down maternally which can affect the ability of the cell to generate energy. On the bright side, these mitochondrial disorderly genes have a less number compared to the nuclear genome’s genes. Since base editing is a new way of spotting and possibly treating mitochondrial genome disorders, the “old way” of conquering them was something called the CRISPR-Cas9. This tool allowed scientists to use a strand of RNA to then help the Cas9 enzyme, thus the name, to the spot of DNA which needed to be edited in order to spot and treat mitochondrial genome disorders. But, the RNA does not have a way to go into the mitochondria because of the semi-permeable membranes which only allow certain organelles to travel through. Because CRISPR-Cas9 is not 100% effective due to its lack of getting the RNA strand through the membrane, some countries have allowed something called mitochondrial replacement. To sum up this procedure, it is when a nucleus of an egg/embryo is then transplanted into a donor egg/embryo which then has a healthy mitochondria. Scientists have been using the fact that mitochondrial mutations contain many copies of that same mitochondrial genome and found out that many of them don’t even have an original connection towards the linked disease. By using this fact, scientists have been able to correct mutations such as those which lack the original or normal copies of the gene.
In the article "Scientists Make Precise Edits to Mitochondrial DNA for the First Time", Heidi Ledford describes the discovery and initial research of the toxin produced by the bacterium Burkholderia cenocepacia. This toxin is unlike CRISPR-Cas9, a well-known genetic modification tool, in that it does not require the Cas9 enzyme. Due to CRISPR's utilization of Cas-9 and its necessity on RNA, it is not a functional solution to mitochondrial genome editing. That's where DddA comes into play. DddA is able to work with double-stranded DNA and does not rely on RNA, making it a promising find for mitochondrial genome editing.
I found the section where Liu described needing to "tame the beast" that is DddA particularly interesting. This part of the article explains how the enzyme could do more harm than good without the implementation of critical steps, such as splitting the enzyme and including site-specific alterations within the genome. By including an additional layer of precision in the process, researchers controlled the outcome as much as possible and avoided a serial edit of C bases. This discovery, in tandem with other mitochondrial mutation correction techniques, is promising for the short-term issue of needing animal models for extended research.
New research has allowed scientists to finally explore uncharted fields. The CRISPR-Cas9 genome-editing system can target changes to the mitochondria. This new version of genome-editing can allow researchers to study and perhaps cure diseases caused by mutations in the mitochondria. Initially, this technique uses a strand of RNA to guide the Cas9 into the DNA where researchers would like to change. But there is no way to bring the RNA inside the mitochondria bc of it being surrounded by membranes. Liu uses enzymes that allow scientists to use parts of CRISPR-CAs9 to change the DNA bases. Cytidine Deaminases act on a single-stranded DNA, but the DNA in humans, are shaped as double helixes. Initially relying on the Cas9 enzyme that breaks the DNA to unwind it, RNA is unable to reach the genome of the mitochondria. But the newly found DddA enzyme can be used directly on double-stranded DNA without the use of the Cas9 enzyme making it suitable for the mitochondria. Now researchers are developing new ways to correct the mutations by using the numerous amounts of copies of the mitochondrial genome. Developing enzymes that can cut the DNA of a malignant mutation, and degrading the damaged DNA, instead of repairing it, can result in a healthier version of the strand, allowing it to replicate. This process is extremely beneficial to technological advancements in medicine and can allow researchers to tweak and change DNA to our advantage.
A recent discovery has been made in the world of science in which a bacterial enzyme can be used in order to alter mitochondrial genomes, possibly allowing researchers to study and treat diseases caused by mutations within the mitochondrial genome. This discovery is described in the article, “Scientists make precise gene edits to mitochondrial DNA for the first time” written by Heidi Ledfored. The aforementioned mutations are passed down and inherited by an offspring through their mother and can seriously damage the nervous system and muscles such as the heart. This new method is the first that has been able to make specific changes in the genome and might enable researchers to gain the ability to modify mitochondrial DNA.
A gene editing tool known as CRISPR-Cas9 uses a strand of RNA that leads the Cas9 enzyme to the particular area of DNA that will be edited. CRISPR-Cas9 has been used to edit genomes in a countless amount of organisms since first being discovered in 1987 by Yoshizumi Ishino and being used as a gene editing tool since 2012. The CRISPR sequence was found to protect cells from surrounding viruses and bacteria, essentially anything that could potentially cause an infection. The associating Cas9 enzymes would recognize the DNA sequences of the virus or the bacteria and essentially break them apart. The way that the CRISPR-Cas9 worked made it ideal for usage as a gene editing tool. This tool however, is difficult to use in regards to mitochondria due to the membranes surrounding it making it hard for the RNA used by the CRISPR-Cas9 to get past. Despite this, researchers have found an enzyme known as DddA which may be able to efficiently reach the mitochondrial genome and be converted into a tool much like the CRISPR-Cas9.
DddA was found after a microbiologist known as Joseph Mougous discovered an enzyme that was produced by a bacterium called Burkholderia cenocepacia that was able to convert the DNA base of Cytosine into Uracil which is a base typically found in RNA, not DNA. Since Uracil has the same function as the DNA base Thymine , enzymes that were involved within replication copied it as Thymine meaning the original base of Cytosine was replaced with Thymine in the DNA sequence. Normally, cytidine deaminases alongside CRISPR-Cas9 replace DNA bases with the Cas9 enzymes breaking apart the DNA strands and the cytidine deaminases act upon a singular strand of DNA. Once again, the RNA used by CRISPR-Cas9 means the CRISPR-Cas9 method cannot be used. However, DddA can act upon double strands of DNA without needing Cas9 which makes it ideal for reaching and editing the mitochondrial genome . The threat to using this enzyme was that it could alter more bases than needed if allowed to run rampant. So the scientists split the Ddda into two pieces that only work when they are together and binded them to proteins that activate only at specific areas. This technique is not yet perfected but it could be exceptionally beneficial in treating diseases when it is.
In the first article, “Scientists Make Precise Edits to Mitochondrial DNA for the First Time,” Heidi Ledford explains the new method of gene editing in the mitochondria. The CRISPR-Cas9 has allowed scientists to change the genomes in organisms by using an RNA strand to lead the Cas9 enzyme. However, the RNA strand can not go into the mitochondria due to the surrounding membranes. A new enzyme, cytidine deaminases, was found to change the DNA bases; however, it only worked on single strands. They used the Cas9 enzyme to unwind the DNA and created a single strand for the enzyme to work on. The technique still couldn’t work on the mitochondria due to the RNA strand that guides the Cas9 enzyme. Mougous’s team found an enzyme, called DddA, that could directly work on the double-stranded DNA. This eliminated the necessity for the CAs9 enzyme to separate the DNA and made it possible to enter the mitochondria. The enzyme was considered a “beast” because it could mutate every c base if not controlled. The enzyme was split into two pieces, only when brought together they could change the DNA. Half of the DddA were linked to proteins that were created to bind to specific sites. This method could stop and treat disorders in the mitochondria. Researchers have also been developing a way to remove the damaged DNA altogether, allowing the normal DNA to replicate.
In the article, “Researches Uncover a Crucial Early Step of the Visual Process,” by the University of Texas Health Science Center explains the connections between light receptors and the impact during the initial step of visual signaling. Two sensory cells, rods and cones, are used to convert the light particles into electrical signals, which are delivered to the brain by circuits. In order to better understand the signaling process, we need to learn about the communication between the rods and the cone. As opposed to what was previously believed, rods and cones communicate with each other rather than two rods and two cones. Researchers found a protein connexin36, which is the base of the rod/cone gap junctions. I find it interesting how they use mouse strains to acquire more about the rod and cone pathways. Through future experiments, we will be able to learn how photoreceptors convert light signals and what helps the retina to process the signals.
In the article, “Researchers uncover a critical early step of the visual process,” the research is centered around visual transduction, which takes place in the retina, and the relationship between the photoreceptors and its respective connections that allow this processing to take place. The typical focus in research surrounding vision is usually subjected to the photoreceptors, rods and cones. Rods are highly light-sensitive, but color-insensitive, unlike the cones which are meant to distinguish color. These photoreceptors in turn, contain photopigments, which essentially convert light into neural activity. Though this knowledge is available, researchers have yet to identify how the retina processes signals from the rods and cones, under conditions in which the photoreceptors can be activated. It was interesting to find that in order for this electrical signal to be conveyed, it was not the rods communicating with other rods, or cones with other cones, but it is through a joint communication between the rods and cones that occupy the network. The researchers, Steve Massey and Elizabeth Morford Chair had discovered a protein, connexin 36, as a central segment of the rod/cone gap junctions. I had learned in psychology that there was a difference in the distribution of the rods and cones in the eye, and that the cones were mainly concentrated in the center of the retina, known as the fovea, where visual acuity is prominent. Meanwhile there is an increasing amount of rods straying from the fovea. Because of this knowledge of the location and the purpose, it was not apparent to me that signaling happens between the two, which was quite intriguing.
The first article "Scientists make precise gene edits to mitochondrial DNA for first time" highlights an exciting development in the genetic world. CRISPR - Cas9, a DNA editing method, has been around for some time and has allowed experimentation on DNA found in the nucleus. However, this method utilizes the Cas9 enzyme to unwind the DNA because the enzyme cytidine deaminases (used to edit the genes) can only act on single-stranded DNA. Due to the membranes surrounding the mitochondrion, RNA strands are hard to guide into this crucial organelle. Recently, an enzyme called DddA was discovered that can act on double-stranded DNA. It converts C bases to U bases, allowing human-made edits to the mitochondria's genetic makeup. Unlike a previous technique, utilizing DddA will allow researchers to correct mutations in the mitochondria's genome even if there were no normal copies present. I am intrigued to see how this technique will be developed and deployed in order to correct genetic disorders rooted in the mitochondria.
The second article "Researchers uncover a critical early step of the visual process" reveals an exciting development in to world of optometry. A study revealed that a majority of signal communication occurs between rods and cones. These two sensory cells rarely transmit signals to themselves, but rather they communicate with the other type of cell. It also has been understood that 95% of all gap junctions (cell connectors in the eye) are rod and cone gap junctions. Further research will be conducted with mice that have had their gap junctions between rods and cones eliminated. Findings from this research can be used to design better photoreceptor and retinal implants to restore vision.
I read "Scientists Make Precise Edits to Mitochondrial DNA for the First Time" and it got me very interested but worried about the future. There are a lot of genetic diseases that used to be incurable or at least not preventable for centuries. If you were found to have the mutation for the disease early on, then the baby or child will be able to have that mutation in their mitochondria taken away from them with the Ddda enzyme early on and have a much lower to nonexistent risk of getting said disease. That in itself is an amazing discovery that will lead to a more developed and futuristic humanity that will have less to worry about when it comes to inheritable diseases. However, it brings about the question of ethics, which is why it also makes me worry for the future of human beings. CRISPR-Cas9, the original gene editing system, was initially used for the same purpose as Ddda: to fix and stop deadly inheritable diseases before the baby is even born. However, this quickly escalated into the very controversial topic of designer babies, where CRISPR can now cut and alter genes to make the baby become more intelligent, have blue eyes and blond hair, become stronger, etc. There were some aspects to these traits, however, that could not be altered or mutated with CRISPR, but with the development and usage of this enzyme, these traits will most likely be able to be altered as well, leaving the future of humans as beings to be designed like machines by their parents to be a very close reality. In my opinion, that future terrifies me because it just further proves to us that humans are nothing special to this world, just meat machines walking around the Earth whose issues can be solved like programmers do on faulty computers. It makes me worry that our existence on this planet is unnecessary, which it very well might be, and that our lives will end up depending on these "doctors" who hold all the power in the world with their ability to change your DNA. In my opinion, although this gene editing enzyme is being used for good now, it won't be once doctors and scientists figure out how to manipulate it and cause even more discrimination in this world (for example, having people ask for their babies to have blue eyes and blond hair and making them the superior traits and discriminating against the other traits). Although it is being used for good, I do not know if it is wise to mess with the way our bodies are from that early on in our life cycle since we also do not know the impacts of messing with one particular gene, as we do not know if one gene is responsible for more than one trait or not. The uncertainties this brings about is enough for me to back away from this technology and not participate in the furthering of this knowledge.
We, as students, must learn and understand the new advances in the medical field as we will one day be at the forefront of this research. In the article “Researchers uncover a critical early step of the visual process,” new information about the visual signaling process is uncovered.The research in Science Advances by The University of Texas Health Science Center at Houston discusses a groundbreaking discovery. For the first time, the science community has identified that early steps of visual signal processing are impacted by electrical connections between light receptors in the eye. Before breaking down the new information the center learned, the author writes about what the community already knew about photoreceptors. To begin with, researchers closely worked with two sensory cells, called rods and cones. The rods and cones transform light particles into electrical signals that are then processed by brain circuits. Furthermore, rods are used for night vision, whereas cones are used during the day and for color vision. Researchers have also known that the electrical signals spread between photoreceptors by utilizing gap junctions, however, the nature and function remained a mystery. The communication between rods and cones in the retina is crucial in order to comprehend how the process works. The new research sheds light on a surprising topic, the rods do not directly communicate with other rods and cones directly. Instead, the communication is linked by a protein called connexin36 (Cx36). Cx36 is a major component of gap junctions. As a whole, the study’s important implications are how photoreceptors encode light signals and how the retina processes these signals. Science changes as new advances occur, and it is our duty to know about these fascinating new discoveries that help us understand the process that our body does daily.
In the article “Scientists Make Precise Edits to Mitochondrial DNA for the First Time”, the author talks about how chemical biologist David Liu received an email from Joseph Mougous, a microbiologist, saying that they had discovered an interesting enzyme. The toxin, when in contact with DNA base C, would change into a U. This enzyme that Mougous and his team had discovered was called DddA. This enzyme was an important discovery for the scientists because it was a breakthrough in their research for finding something suitable to reach the mitochondrial genome. DddA was also a beneficial discovery because with further research, it could help treat mitochondrial disorders that occur due to incorrect or different sequences in the mitochondrial genome. This discovery could lead to many cures to different disorders which could make life easier for many different people. With these cures, more scientists can work on researching cures or treatments for other disorders. This article shows that there are many different enzymes still to be discovered that could help with different disorders. This enzyme that was discovered can help with mitochondrial disorders. It also shows how there are scientific discoveries made often even if we don’t get to know about them. In the article “Researchers Uncover a Critical Early Step of the Visual Process” scientists discover and explain how photoreceptors, which impact the process of vision in the beginning, and two sensory cells, rods and cones, work. Rods are used at night while cones are used during the day and to see colors. Researchers were shocked to learn that rods don’t communicate with other rods. In fact, rods communicate with cones. Cx36 was identified as the main element of the gap junctions for the rods and cones. The scientists and researchers developed mice to help them decide the importance of the rod/cone pathway in the retinal processing. This article shows how interesting the human body is and only in one part: the eyes. They are still making interesting discoveries to see how it can benefit or disadvantage a person by testing on mice. Both of these articles show just how much research is still being done on the human body and how there is still so much that is being discovered. It is so interesting to learn all of the different aspects of the human body and how there is even more being discovered to help people.
The article titled “ Researchers uncover a critical early step of the visual process” was particularly interesting to me, as I learnt about the process of vision last year in AP Psychology. In this article, the author first discusses the impact photoreceptors have in the early stages of vision. Rods and cones are sensory cells that convert light into electrical signals, allowing our brain to comprehend visual stimulus and ultimately allow us to see. Rods specialize in dark environments, while cones are used in lighter settings and color vision. Research conducted by the University of Texas Health Science Center at Houston (UTHealth) has identified key components of the electrical connections between light receptors in the eye and their impact on the early stages of vision. This information can be used to find out how the retina processes information coming from rods and cones at the same time. In addition to this, researchers discovered that rods and cones very rarely communicate with one another, instead, rods communicate with cones thanks to a protein called connexin36. These junctions of rods and cones will now be further researched in mice to understand their importance. After reading this article, I’m excited to see the results of this research. Thanks to my prior knowledge about the topic of this article, I really enjoyed reading this article. I never knew about the junctions between rods and cones, and always assumed they only communicated among themselves. It’s amazing how something as small as an eyeball has so much going on inside of it just to allow us to see, something we take for granted.
Upon first reading “Researchers uncover a critical early step of the visual process,” I found it interesting that the visual process continues to grow more and more precise as new research comes out. As read in the article, rods and cones are two critical photoreceptors in the process of converting light into signals. Research has already been conducted which has proved these signals spread between rods and cones throughout gap junctions. The nature and function of gap junctions, until now, have been misunderstood as the lack of research provided little viable information. The impact that electrical connections have on the beginning of the visual signaling process is being more holistically understood due to the research published in Science Advances by UTHealth. According to Cristophe P. Ribelayga, the information this research puts forth, which allows for a more complete understanding of how the retina retains the signals from photoreceptors, is crucial for the creation of implants that can aid vision. The middle of the article discusses a discovery that was shocking, which is that rods and cones more commonly communicate with each other instead of rods with rods and cones with cones. Upon further research, the protein connexin36 has a prominent role in gap junctions, which allow rods and cones to communicate. It is extremely rare for cone on cone gap junctions to appear, evident by the 95% rod to cone gap junction rate which statistically proves the rarity. This shocking discovery was further tested using genetic mouse strains that were bred together in hopes of reducing the gap junctions with the two photoreceptors. The gap junctions between rods and cones are extremely important as they serve as an entrance for signals (from rods) to be transported across the retina. The testing of the discovery described in this article ultimately produced mice without this “entrance,” which can be useful in upcoming studies to determine how important these gap junctions are in retinal processing. I found the article extremely interesting as I thought I had a decent knowledge of the visual process from when I learned the sensory processes in psychology, but this article opened my eyes to how complex, intricate and detailed the visual (and all other sensory) processes are.
This week I decided to read the article “Scientists make precise gene edits to mitochondrial DNA for the first time”. I found this article very interesting because, as stated in the first paragraph of the article, this is something that wasn’t even achievable with the widely known CRISPR technology. This technique would allow scientists to study these genes in new and maybe more accurate ways. This may allow for easier ways to study and learn about different diseases that were far too difficult before. CRSIPR allowed scientists to make slight changes or little tweaks in genomes to how they wanted in almost any organism. This technique, though, uses an RNA strand which is fine for most parts of the cell but not for when working with the mitochondria. Studies in late 2018 from chemical biologist David Liu resulted in the finding of the toxin made by the bacterium Burkholderia cenocepacia. This toxin allows for the base C, in DNA, that converts to a base U, not found in DNA, to be copied over as a base T. It does this by behaving as a base T so when the enzyme replicates the DNA it copies over as a base T. The same researcher had done something similar in base editing. Researchers could use parts of CRISPR to do the same thing. The problem was that it only worked on single stranded DNA. Mougous’s team found DddA, which would act directly on double stranded DNA. To be able to use DddA, one would have to be very careful because this could make the enzyme deadly. If not kept under control, it could mutate every base C it came across. To contain this, the team split the enzyme into two pieces. It would only be able to change the DNA when they were brought together again. This whole process was quite interesting to me because it just shows that there’s always more to learn and do and also than any solution always has its flaws. Over all this new method can help a lot in studying various diseases and maybe helping find other solutions in the future.
This week, I read both articles; one discussed a breakthrough in gene editing mitochondrial DNA while the other talked about a vital step of the visual process. The first article, titled “Scientists make precise gene edits to mitochondrial DNA for the first time”, highlights a strange bacterial enzyme that allowed researchers to make changes to the genomes of mitochondria. Even the CRISPR-Cas9 genome-editing system, which has allowed for the tweaking of genomes of almost every organism it has been tested with, is unable to manage changes made to cells’ energy-producing structures. Since CRISPR-Cas9 uses an RNA strand to guide the enzyme to the target region of DNA, scientists had not discovered a way to transport the RNA into mitochondria. Furthermore, cytidine deaminases, an example of an enzyme used in base editing, only act on single-stranded DNA. Since humans have double-stranded DNA, the Cas9 enzyme had to break the DNA in order for the enzymes to be able to make edits. However, Joseph Mougous and his team at the University of Washington in Seattle, discovered an enzyme called DddA. This enzyme is capable of acting directly on double-stranded DNA without the help of the CRISPR-Cas9 enzyme to break it, making it suitable for genome edits on mitochondria. I found this article particularly interesting as it opens up a range of possibilities in terms of preventing or even treating mitochondrial disorders. Even though the use of this enzyme is quite a long way from being used in the clinic, this recent discovery could allow researchers to correct mutations even if the mitochondria lack the appropriate amount of normal copies of the genes.
The first article, “Scientists make precise gene edits to mitochondrial DNA for the first time” by Heidi Ledford talks about the discovery of a bacterial enzyme that can be used to edit the mitochondrial genome. This is necessary in order for scientists to be able to study the mitochondrial genome and diseases that occur as a result of mutations within the genome. In comparison to the nuclear genome, there are a very small number of genes within the mitochondrial genome. This means that it is “rarer” for a mutation to occur however when it does occur it is very impactful. A mutation in the mitochondrial genome can cause diseases that strongly affect the nervous system and heart, often times being fatal. Because there have only been failed attempts at editing the genome, there is barely any research strong enough to help scientists make animal models of the genome to study the diseases, let alone find treatment. There have been many attempts to edit the mitochondrial genome in the past but none have been successful, until now. Even attempts with the CRISPR-Cas9 genome editing system were unable to succeed because the RNA strand that guides the Cas-9 enzyme was not able to get past the membrane surrounding the mitochondrial genome. A microbiologist, Joseph Mougous, and his team discovered a toxin made by a bacterium called Burkholderia Cenocepacia that is able to convert the base C to U, but since U acts like T, base T is replicated instead. This means that the enzyme is able to successfully convert base C to base T. Biologist David Liu harnessed similar (non-toxic) enzymes for base editing called cytidine deaminase, but they were only able to work on single stranded DNA and relied on the RNA that guided the CRISPR-Cas9 system. So, like other attempts, it was unsuccessful. Finally, Mougous and his team discovered an enzyme called Ddda which is able to act directly on the double stranded DNA. This enzyme’s ability to convert the bases makes it deadly so they have split it into two parts, allowing it only to function in a specific orientation. It is too early in the research for medical application however now animal models to study the mutations can finally be created after years of failure. With diseases like these, life-expectancy is short, and judging from the article, there is barely any research on the true function of these diseases, making it even scarier for patients to face the disease. Mougous’s discovery is huge. These enzymes will now allow researchers to study the diseases at the root of their cause, with a possibility of eventually leading to treatment of these life-threatening mitochondrial genome diseases helping thousands live another day.
The article “Scientists Make Precise Gene Edits to Mitochondrial DNA for the first time,” by Heidi Ledford sheds light on a new enzyme that has allowed researchers to study and treat diseases caused by mutations in the mitochondrial genome through a technique called base editing. I find this technique especially interesting because it gives researchers the ability to modify mitochondrial DNA. The discovered enzyme DddA could act directly on double-stranded DNA which is why Liu and Mougous have said that it could reach the mitochondrial genome. This is so groundbreaking because the CRISPR-Cas9 genome-editing system, a popular method to modify genomes uses a strand of RNA to guide the Cas9 enzyme and researchers can’t find a way to move that into the mitochondria because of the surrounding membranes. The process that was necessary to turn the DddA enzyme into a genome-editing tool also captured my attention as Liu and his team needed to split the enzyme into two pieces that would change the DNA and then had to link each half of the enzyme to proteins that were engineered to bind to specific sites in the genome. Although the discovery of DddA is groundbreaking and extremely beneficial, the ability to modify double-stranded DNA is also deadly and could mutate every C it comes across if it’s set loose. As a result, there are many more studies that need to be conducted before this technique could be used clinically. Nevertheless, this method could be used to prevent or treat mitochondrial disorders which is tremendous progress.
In the article “Researchers uncover a critical early step of the visual process” it discusses the importance of the electrical connections between light receptors and their impact on the early stages of the process of vision. Humans' sense of vision within the nervous system is built up of photoreceptors with the sensory cells of rods and cones. Through transduction these cells convert light energy into electrical signals that are related to the brain. Scientists know that through gap junctions the signals can spread however there is still so much unknown about these signals abilities and function. If scientists gain a better understanding of these signals and its processes then they will have more success in designing photoreceptors or retinal implants to help restore people’s vision. To gain a better understanding scientists must first understand the communication between rods and cones, in which a majority of the signals move between with the help of the protein connexin36 (Cx36). Scientists have discovered that most of the gap junctions are between rods and cones, and continue to research these connections. Most of their studies and results are found by eliminating the rod/cone junction and seeing the overall effect in its absence. These studies have been conducted in mice and with more money being granted to the Ruiz Department of Ophthalmology & Visual Science, scientists can continue to work for a complete understanding of the visual process.
The article discussing a critical early step in the visual process piqued my interest, as vision was something I covered in psychology last year. When learning about the photoreceptors, I considered cones and rods to function entirely on their own. Since cones are responsible for color vision and rods are responsible for our sensitivity to light, I assumed that eyes use only cones in the daytime and only rods in the nighttime. It didn’t occur to me that there is a short period of time when both are used during dawn/dusk, which is important when studying rod/cone gap junctions. The interaction of rods and cones when transferring light energy helped me understand that while we witness the daytime in color, we forget that rods help with the amount of shadows that contributes to images we see everyday. To further understand this phenomenon, researchers decided to genetically eliminate gap junctions in mice to see how vision was affected. The strain didn’t allow electrical signals from rods to travel across the retina, meaning the energy would never reach the optic nerve, and allow the brain to process vision. Learning the massive effects of a small elimination in the visual process showed me how intricate the eye truly was.
The first article, “Scientists make precise gene edits to mitochondrial DNA for first time,” it discussed the discovery of mitochondrial genome editing opening several doorways for base editing and possible cures for diseases which stem from mutated mitochondrion. Previous studies of the CRISPR-Cas9 enzyme would not be effective when working with the mitochondrial genome, though recent studies found an enzyme they call, ‘DddA’ can successfully manipulate the mitochondrion. Although this can be combined with other techniques for combating disease, scientists caution that this is not ready to be used in clinics yet. The possibilities of DddA are endless, and hopefully they are integrated into practice soon. The second article, “Researchers uncover a critical early step of the visual process,” the author discusses the new discoveries on photoreceptors. They introduce the importance of understanding the function of gap junctions between rods (night vision) and cones (color and day vision). Something I found it interesting is how rods don’t actually communicate with other rods, but they communicate with cones. Scientists have actually estimated that 95% of all gap junctions are rod/cone junctions. In order to better understand the complexities of gap junctions in the retina, they have used genetic mouse strains. As they continue their research, they receive grants that keep their practice alive. The overall impact of their study can create better retinal implants and other technologies.
The first article, “Scientists make precise gene edits to mitochondrial DNA for the first time,” brings to light a new technique that has been discovered which can target changes in the genomes of the mitochondria. This technique was needed because there are some edits that the CRISPR–Cas9 genome-editing system can’t complete and mitochondria edits are one of them. However a discovery of a new enzyme, DddA, might be the missing piece for Cas9 to reach the mitochondria as it can act directly on DNA. This is because there isn’t a way to transfer RNA into the mitochondria. This new technique will help with studying mitochondrial disorders which was difficult to do before this breakthrough because there wasn’t a way to replicate the mitochondrial disorders in animals. There aren’t any optimal ways to treat mitochondrial disorders and this was a needed step towards a better treatment option despite the technique being far from perfection. The second article, “Researchers uncover a critical early step of the visual process,” illustrates the importance of rods and cones when it comes to understanding photoreceptors. It was discovered that most communication isn’t rod to rod or cone to cone; the communication occurred between rods and cones. Now the studies are being focused on the photoreceptors’ development, function and electrical interactions. These studies will be completed by using developed genetic mouse strains that were bred to eliminate gap junctions in either rods or cones. Without these gap junctions rods and cones won’t be able to communicate which allows the researchers to figure out how important communication between rods and cones are.
The first article, “Scientists make precise gene edits to mitochondrial DNA for the first time” by Heidi Ledford elaborates on a new enzyme known as DddA that has the capability to edit incorrect base pairs within the mitochondrial DNA to treat deadly diseases caused by mutations. The common genome editing system, CRISPR-Cas9 is unable to edit mitochondrial DNA because it uses RNA to guide the Cas9 enzyme to the section of the DNA that scientists wish to edit. However, the RNA can’t be shuttled into the mitochondria because the mitochondria is surrounded by membranes that prevent the RNA from entering it. DddA can act directly upon the mitochondrial DNA because it can bypass the outer membrane of the mitochondria since it has nothing guiding it, unlike the Cas9 enzyme. Although the DddA enzyme has foreseeable benefits that could help treat many diseases, this enzyme has the capability to cause more harm than good if it is not properly tweaked to allow scientists to control the enzyme. If the enzyme is set loose, it has the ability to convert every cytosine base pair it comes across to a uracil base pair—equivalent to a thymine base pair in DNA. This is extremely detrimental to the human body and could quite easily cause mutations throughout the mitochondrial DNA sequence. The scientists were able to tweak the enzyme by splitting it into two pieces so that the enzyme would only mutate the DNA when it was in the right orientation. The discovery of this enzyme is a major scientific breakthrough as this enzyme will allow scientists to treat many diseases related to mutations in the mitochondrial DNA. Diseases affecting the nervous system, muscles, and the heart are all caused by mutations within the mitochondrial DNA and can now be treated for the first time. Consequently, the discovery of this enzyme was a step forward in the field of medicine and will have many future uses.
The article, "Scientists make precise gene edits to mitochondrial DNA for first time" by Heidi Ledford explains the possible applications of the newly discovered DddA enzyme and how those applications could be achieved. Scientists working on this enzyme such as David Liu need to modify the enzyme so the enzyme doesn't destroy the person's DNA sequence from the inside. The enzyme was discovered by a University of Washington team led by Joseph Mougous. It converts C bases into U bases. U bases aren't typically found in DNA and instead are typically found in RNA. Before this enzyme was discovered scientists had been able to edit DNA but they were unable to edit DNA in the mitochondria. However, the new enzyme doesn't need the DNA to be split to edit it therefore allowing it to be useful in the mitochondria.
Since the beginning of civilization, this world has adapted to and cherished several famous discoveries through geniuses like Leonardo da Vinci to Albert Einstein, Stephen Hawking, Bill Gates and many more intelligent minds. The beauty about the nature of science is that there will never come a time where someone can accurately conclude that “this is it, this is all there is to science.” The more we grow as a society, the greater discoveries that we approach as a generation. However, each discovery has its own process toward accuracy. The first article, “Scientists make precise gene edits to mitochondrial DNA for the first time” by Heidi Ledford, discusses an enzyme known as DddA (founded by Jospeh Mougous and his team), which could surpass the inability of Cas9 to normally function and alter two strands of DNA (instead of one strand). This enzyme functions to mutate every cytosine into a uracil, which can effectively be converted to a thymine. Like a mutation could cause an old cell to become an uncontrollable cancer cell that abnormally divides and invades the body, DddA could also uncontrollably mutate every cytosine into a uracil without reason. Like every new discovery, there will be alterations. Yes, the research team has found an enzyme that could potentially (with extensive collaboration and further research) cure diseases. However, the weak points of this enzyme needed to also be tackled, and with such precision, they were. By splitting DddA into two pieces that can only function when met together and placing these split enzymes onto proteins that code only for specific DNA sequences, the team was able to limit the function of DddA and improve its effectiveness. This enzyme is far from being applied in real life surgeries involving mitochondrial errors, but by furthering this research and creating a problem-solution chain, we take a step toward extraordinary cures that will alter the face of mitochondrial DNA. From there, new questions will follow greater discoveries through involved minds.
The first article I read for this week’s assignment was entitled, “Scientists make precise gene edits to mitochondrial DNA for first time” by Heidi Ledford. The article revolved around a new mechanism of gene editing which allowed for direct editing of mitochondrial DNA. The CRISPR-Cas9 system has been regarded as the most revolutionary tool for gene editing we have ever seen. However, even CRISPR has its limitations due to its purpose when it was engineered. The Cas9 enzyme present in this system creates mandatory breaks in the double stranded nuclear DNA and allows geneticists to edit the genome however they see fit. The issue with this and getting into mitochondrial DNA is the fact that RNA is used to guide that Cas9 enzyme in the nucleus, but scientists have no way to bring the guide RNA into the mitochondria. Recently, though a team of scientists at the University of Washington, led by microbiologist Joseph Mougous discovered a new enzyme called DddA which could convert cytosine into uracil which is inferred by DNA replicating enzymes as thymine, essentially converting cytosine and thymines. While enzymes like DddA which altered base pairs were used in CRISPR editing mechanisms, what was unique about this specific enzyme was that it can act directly on a double stranded molecule of DNA, essentially bypassing the RNA needed to guide the Cas9 enzyme. Mutations present in the mitochondria can cause cells to lower their ability to produce energy, harming the nervous system and muscles including fatal damage to the heart. Finally, there is a way to combat these mutations but the enzyme needs to be kept under control in order to prevent a cancer like spread of base changes. To prevent this from happening the team split the enzyme and made it so that only if it combines in a specific way, will it work. Other mechanisms of mitochondrial editing involve cutting out mutated strands and allowing the thousands of other copies of the genome to help fix the issue, and in the latest news, scientists are trying to find a way to fix mutations without the help of other genomes at all. These discoveries of editing mitochondrial DNA could help save millions of lives who previously had no possible way of solving their condition. However, the issue is that there is a lack of experimentation done with these forms of treatment so there is no way of knowing if it is 100% viable and safe for everyone at the moment. When that process is completed, the life changing mitochondrial editing process may occur. I particularly enjoyed reading this article as I have a great deal of interest in the field of genetic engineering mechanisms like the seemingly primitive at this point, zinc finger nucleases and TALENS, to the more modern CRISPR-Cas9 systems. The varying uses for these systems also have caught my attention as it can range from fixing genetic ailments to possibly helping produce vaccines for current viruses.
The first article I read for this week’s assignment was entitled, “Scientists make precise gene edits to mitochondrial DNA for first time” by Heidi Ledford. The article revolved around a new mechanism of gene editing which allowed for direct editing of mitochondrial DNA. The CRISPR-Cas9 system has been regarded as the most revolutionary tool for gene editing we have ever seen. However, even CRISPR has its limitations due to its purpose when it was engineered. The Cas9 enzyme present in this system creates mandatory breaks in the double stranded nuclear DNA and allows geneticists to edit the genome however they see fit. The issue with this and getting into mitochondrial DNA is the fact that RNA is used to guide that Cas9 enzyme in the nucleus, but scientists have no way to bring the guide RNA into the mitochondria. Recently, though a team of scientists at the University of Washington, led by microbiologist Joseph Mougous discovered a new enzyme called DddA which could convert cytosine into uracil which is inferred by DNA replicating enzymes as thymine, essentially converting cytosine and thymines. While enzymes like DddA which altered base pairs were used in CRISPR editing mechanisms, what was unique about this specific enzyme was that it can act directly on a double stranded molecule of DNA, essentially bypassing the RNA needed to guide the Cas9 enzyme. Mutations present in the mitochondria can cause cells to lower their ability to produce energy, harming the nervous system and muscles including fatal damage to the heart. Finally, there is a way to combat these mutations but the enzyme needs to be kept under control in order to prevent a cancer like spread of base changes. To prevent this from happening the team split the enzyme and made it so that only if it combines in a specific way, will it work. Other mechanisms of mitochondrial editing involve cutting out mutated strands and allowing the thousands of other copies of the genome to help fix the issue, and in the latest news, scientists are trying to find a way to fix mutations without the help of other genomes at all. These discoveries of editing mitochondrial DNA could help save millions of lives who previously had no possible way of solving their condition. However, the issue is that there is a lack of experimentation done with these forms of treatment so there is no way of knowing if it is 100% viable and safe for everyone at the moment. When that process is completed, the life changing mitochondrial editing process may occur. I particularly enjoyed reading this article as I have a great deal of interest in the field of genetic engineering mechanisms like the seemingly primitive at this point, zinc finger nucleases and TALENS, to the more modern CRISPR-Cas9 systems. The varying uses for these systems also have caught my attention as it can range from fixing genetic ailments to possibly helping produce vaccines for current viruses.
The first article, “Scientists make precise gene edits to mitochondrial DNA for the first time” by Heidi Ledford discusses how their ability to now make precise gene edits to mitochondrial could now allow researchers to develop new ways to study, and even treat, diseases caused by mutations in the mitochondrial genome. The article continues on how it was a difficult task to study such disorders, because scientists lacked a way to make animal models with the same changes to the mitochondrial genome. Later on in the same article Liu warns people that the work is a long way from being used in the clinic. He says this although the technique could ultimately complement existing methods used to prevent or treat mitochondrial disorders. The second article is titled “ Researchers uncover a critical early step of the visual process“ by the
UNIVERSITY OF TEXAS HEALTH SCIENCE CENTER AT HOUSTON. The article begins by The University of Texas Health Science Center at Houston explaining the early steps of visual signal processing and how the key components of electrical connections between light receptors in the eye and the impact of these connections have been identified for the first time. The article then continues on how photoreceptors impact the early stages of the process of vision, although researchers have traditionally focused their attention on how two key sensory cells convert elementary particles of light into electrical signals and how these signals are relayed to the brain through devoted circuits. The article also continues to say how the previous information will lead to a better understanding of how the retina processes signals from the rods and the cones in the eyes, in particular under ambient lighting conditions when both photoreceptor types are active, such as at dawn and dusk. communication between rods and cones in the retina is critical for understanding how the visual signaling process works. But what to the researchers surprise rods do not directly communicate with other rods and cones seldom communicate directly with other cones. Instead, the majority of signaling happens through communication between rods and cones. They discovered a specific protein called connexin36 (Cx36) as the main component of rod/cone gap junctions. They used genetic mouse strains to better help researchers understand how the photoreceptor network is organized. The article ends with with in 2018, researchers in the Ruiz Department of Ophthalmology & Visual Science received more than $4 million in grants from the National Institutes of Health's National Eye Institute to study photoreceptor development, function, and electrical interactions. Ribelayga and Massey led the effort to lay out the architecture of the network of electrically coupled receptors, a critical step toward a better understanding of how photoreceptors encode light signals and how the retina processes these signals.
After reading the article “Researchers uncover a critical early step of the visual process,” I have been able to expand my knowledge of visual perception. I learned a lot about the vision process in psychology, so it is interesting to learn that researchers are still uncovering pieces to the puzzle today. Prior to reading the article, I knew that the two primary receptors were rods and cones. The eye uses rods to perceive black and white (or non colored) objects, while cones are used to perceive colors. I found it interesting that the rods and cones primarily communicate between each other, rather than within each photoreceptor. The protein connexin36 (Cx36) was discovered and allows for the communication between rods and cones. Researchers set up a study on the rod/cone gap junctions of a mouse eye to identify that rod signals pass through it and across the retina. This information will be beneficial towards future research, which will study the rod/cone pathway’s functional importance.
Although I found both articles truly fascinating, I found "Scientists make precise gene edits to mitochondrial DNA for the first time," by Heidi Ledford, to be more interesting. The thing that fascinates me is that in a way using this new technology we are even closer to having full control over our DNA, and when one has control over this, they may be able to change many things about a person. This power can be used in many ways, some being positive and others being negative. CRISPR-Cas9 is unable to edit mitochondrial DNA since it uses RNA to guide the Cas9 enzyme to the section of DNA scientists wish to edit. DddA is a new enzyme that is capable of editing incorrect base pairs within the mitochondrial DNA in order to treat mutation related diseases. DddA can act directly to edit Mitochondrial DNA since it has the ability to pass through the mitochondrial membrane. This enzyme is not yet ready to be used significantly since it is under testing and scientists are learning to control the enzyme. If used improperly, it can convert every Cytosine to a Uracil pair. And when the DNA replication enzymes copy it it becomes a T. Scientists then split the enzyme into two pieces so that it would only change DNA sequences when in the correct orientation. The power that scientists now hold will lead them closer to being able to reduce mutation caused diseases, and ultimately possibly lengthen the average lifespan of a human being. In conclusion, this a groundbreaking discovery that may forever change the field of genetic engineering.
This week I decided to read “Scientists make precise gene edits to mitochondrial DNA for the first time”. The article is split up into 2 parts. Expanding Toolbox and Exploring Diseases. This article highlighted how scientists have found out how to edit the energy-producing cell with a bacterial enzyme (far more precisely than the popular gene editing system CRISPR-Cas9). The article even explained how the CRISPR-Cas9 system worked. It works with a strand of RNA that guides the Cas9 enzyme to the area of DNA that scientists wanted to edit. A team of scientists led by Joseph Mougous found that the bacterium Burkholderia cenocepacia effectively converted a C in the genome sequence to a T. It then goes on to explain how CRISPR-Cas9 can not effect the mitochondrion genome because of its reliance on RNA. The article then finishes out by explaining how this new base editing system could even be used without a proper copy of the gene. This article has peaked my interest about how gene editing can be used to fix genetic diseases.
In “Scientists make precise gene edits to mitochondrial DNA for the first time,” Heidi Ledford describes how a specific enzyme allows researchers to treat/discover possible solutions to diseases that CRISPR-Cas9 couldn’t crack. The conditions were caused by mutations n the “mitochondrial genome,” and these mutations can hurt the nervous system and muscles, causing a fatality. Scientists wanted to research this issue and try to avoid death by trying to modify genes. However, CRISPR–Cas9 has allowed researchers to alter individual genomes to fit better genomes. CRISPR–Cas9 wasn’t able to work correctly, so a team led by microbiologist Joseph Mougous at the University of Washington had discovered an enzyme called Burkholderia cenocepacia. The enzyme that Mougous’s team had found, called DddA, could act directly on double-stranded DNA without relying on the Cas9 enzyme to break it. Both Liu and Mougous split the enzyme into two pieces that would change DNA only when brought together in the right orientation. And to control which DNA sequence the enzyme-modified, the team then linked each half of DddA to proteins that were engineered to bind to specific sites in the genome. This led to the discovery of mitochondrial replacement and other mitochondrial mutation techniques used worldwide.
In “Researchers uncover a critical early step of the visual process,” UTHealth authors identified critical components of electrical connections between light receptors in the eye and the impact of these connections on the early steps of visual signal processing. Researchers focused on the rods and cones in the eyes to lead to a better understanding of how the retina processes signal, particularly under ambient lighting conditions when both photoreceptor types are active(dawn and dusk). The researchers discovered that rods do not directly communicate with other rods, and cones only communicate directly with other cones. A specific protein called connexin36 was involved in the gap junctions between the rods/cones. To eliminate gap junctions, they developed genetic mouse strains. However, The mouse strains were not helping the problem. The data showed that The rod/cone gap junction is the entry of a rod pathway through which signals of rod origin can travel across the retina.
“Scientists make precise gene edits to mitochondrial DNA for first time” by Heidi Ledford proposes intriguing research regarding the mitochondrial DNA. According to the research a bacterial enzyme allows researchers to manipulate the mitochondrial genome which in turn can allow researchers to treat diseases caused by mutations that occur within the genome itself. Furthermore, the mutation can be passed down either maternally or paternally which will harm the nervous system, and muscles, including the heart, and can be life threatening to the ones who inherit it. Moving on CRISPR-Cas9 was vital and added great benefits to researchers when they wanted to tweak genomes to their liking in any organism. An RNA strand guides the Cas9 enzyme to the DNA that scientists want to change. Unfortunately, this only works for DNA that is located in the cell’s nucleus because researchers are unable to figure out how to shuttle the RNA into the mitochondria as it’s surrounded by membranes. Later, a toxin formulated from bacterium, Burkholderia cenocepacia, was proven to be able to convert DNA base C into U when they interacted. Due to the fact that U is rarely spotted in DNA, it shifts its behavior into a T. This results in the C being converted effectively into a T in the genome sequence. Now it is available for researchers to use components of CRISPR-Cas9 to change one DNA base to another. It was very interesting to have a first hand experience in witnessing how researchers discovered the bacterial enzyme. With this new discovery we will be able to treat many diseases caused by mutations within the mitochondrial DNA and is a huge step forward for the field of medicine.
“Scientists make precise gene edits to mitochondrial DNA for first time” by Heidi Ledford proposes intriguing research regarding the mitochondrial DNA. According to the research a bacterial enzyme allows researchers to manipulate the mitochondrial genome which in turn can allow researchers to treat diseases caused by mutations that occur within the genome itself. Furthermore, the mutation can be passed down either maternally or paternally which will harm the nervous system, and muscles, including the heart, and can be life threatening to the ones who inherit it. Moving on CRISPR-Cas9 was vital and added great benefits to researchers when they wanted to tweak genomes to their liking in any organism. An RNA strand guides the Cas9 enzyme to the DNA that scientists want to change. Unfortunately, this only works for DNA that is located in the cell’s nucleus because researchers are unable to figure out how to shuttle the RNA into the mitochondria as it’s surrounded by membranes. Later, a toxin formulated from bacterium, Burkholderia cenocepacia, was proven to be able to convert DNA base C into U when they interacted. Due to the fact that U is rarely spotted in DNA, it shifts its behavior into a T. This results in the C being converted effectively into a T in the genome sequence. Now it is available for researchers to use components of CRISPR-Cas9 to change one DNA base to another. It was very interesting to have a first hand experience in witnessing how researchers discovered the bacterial enzyme. With this new discovery we will be able to treat many diseases caused by mutations within the mitochondrial DNA and is a huge step forward for the field of medicine.
Since the beginning of civilization, this world has adapted to and cherished several famous discoveries through geniuses like Leonardo da Vinci to Albert Einstein, Stephen Hawking, Bill Gates and many more intelligent minds. The beauty about the nature of science is that there will never come a time where someone can accurately conclude that “this is it, this is all there is to science.” The more we grow as a society, the greater discoveries that we approach as a generation. However, each discovery has its own process toward accuracy. The first article, “Scientists make precise gene edits to mitochondrial DNA for the first time” by Heidi Ledford, discusses an enzyme known as DddA (founded by Jospeh Mougous and his team), which could surpass the inability of Cas9 to normally function and alter two strands of DNA (instead of one strand). This enzyme functions to mutate every cytosine into a uracil, which can effectively be converted to a thymine. Like a mutation could cause an old cell to become an uncontrollable cancer cell that abnormally divides and invades the body, DddA could also uncontrollably mutate every cytosine into a uracil without reason. Like every new discovery, there will be alterations. Yes, the research team has found an enzyme that could potentially (with extensive collaboration and further research) cure diseases. However, the weak points of this enzyme needed to also be tackled, and with such precision, they were. By splitting DddA into two pieces that can only function when met together and placing these split enzymes onto proteins that code only for specific DNA sequences, the team was able to limit the function of DddA and improve its effectiveness. This enzyme is far from being applied in real life surgeries involving mitochondrial errors, but by furthering this research and creating a problem-solution chain, we can come closer to an extraordinary cure that will alter the face of mitochondrial DNA. From there, new questions will follow greater discoveries through involved minds.
This week, I decided to read the article “Scientists Make Precise Gene Edits to Mitochondrial DNA for First Time.” As the title entails, this article focuses on the advances scientists have made in regards to editing the genomes of mitochondria—something that even the CRISPR-Cas9 has never been able to do. CRISPR-9 itself is a unique technology that scientists use to edit parts of the genome by removing, adding, or altering sections of the DNA sequence. Now, scientists have uncovered a new bacterial enzyme that permits them to do the same thing to mitochondrial genomes. I was very enraptured by reading this article because there are many diseases caused by mutations in the mitochondrial genome that have no explicit cure and this new technique paves the road to potentially correcting mitochondrial mutations. The way that scientists would be able to do this would be by using the toxin made by the Burkholderia cenocepacia bacterium to reach the mitochondrial genome. This bacteria, when in contact with the DNA base C, converts it to DNA base U. But usually, the base U is never found in the DNA sequence, (mostly in RNA), so the base behaves like a T and is also copied as a T by the enzymes that replicate the cell’s DNA and ultimately convert a C in the genome sequence to a T. This enzyme could act directly on DNA without the aid of the CRISPR technology and thus, scientists Liu and Mougous argued, could allow the enzyme, DddA, to reach the mitochondrial genome. Though this new mitochondrial editing tool is far from perfect and still has to be tweaked, it is a scientific breakthrough that may cure all mitochondrial diseases by editing and correcting mutations in the mitochondrial genome that cause such diseases.
In the article “Scientists Make Precise Edits to Mitochondrial DNA for the First Time,” scientists have been able to achieve something that even the CRISPR-Cas9 genome-editing system was not able to do: make targeted changes to the genome of a mitochondria. This presents a major advancement in the field of genome editing. Mutations in the mitochondrial genome can be fatal and may be passed down through generations. These mutations can lead to a multitude of health issues in the future. Genome editing has been been achieved using the CRISPR-Cas9 system but this new method has allowed for more precise base editing of a genome. A big part of this is the enzyme Ddda, which acts directly on double stranded DNA without relying on Cas9 to break it first. The Ddda enzyme is so precise that we may be able to cut off the site of harmful mutations. This could potentially mean that mutated DNA will stop populating in the body and can be replaced by normal non-mutated DNA. Further testing is required but this is definitely huge for genome-editing and science. Personally, I think that this is very cool and I am happy that this development has the potential to help and save many lives.
The article "Researchers uncover a critical early step of the visual process" explains the relationship between rods and cones and their affect on the early stages of the visual process. This is important because by understanding how rods and cones communicate, it helps the understanding of the visual process as a whole. Researchers discovered that majority of the gap junction communications are between rods and cones as opposed to rods and rods or cones and cones. In these rod/cone gap junctions they discovered the protein connexin36 (Cx36). I thought it was especially interesting to learn that during dusk and dawn, both rods and cones are actively used. The retina then processes these signals between sensory cells and transmits it to the brain. This made me wonder what role the rods and cones played in worsening eyesight. I wondered if bad eyesight was caused by weak signals between the sensory cells, if it occurs in earlier stages at the lens or some other reason. This study also made me wonder what the visual process is when looking at a single bright object in a dark environment, such as a screen in a dark room or the moon in the sky. I wondered what the circumstances for cone/cone or rod/rod gap junctions, and what makes it uncommon.
After reading the article “Researchers uncover a critical early step of the visual process”, I now have a better understanding of the early stages of the vision process. Photoreceptors mainly impact the process and researchers focus on rods and cones which convert light particles into electrical signals. Rods are used for night vision while cones are used for daytime and color vision. The communication of rods and cones in the retina is important to understand how the vision process works. Researchers discovered that rods don’t directly communicate with rods and cones sometimes directly with other cones. Researchers created genetic mouse strains for the work to eliminate gap in rods or cones. They found that rod/cone gap junction is the entry of rod pathway and then signals of rod origin can travel across the retina. This article explained what the early stages of visual process is like and how researchers are looking to find more information about it.
Science is always so fascinating because one day or another, discoveries are made that change the way that we operate. The article "Scientists make precise gene edits to mitochondrial DNA for the first time," by Heidi Ledford describes how a new enzyme may help with scientific research to cure deadly diseases. This bacterial enzyme may even allow researchers to do certain things that CRISPR-Cas9 couldn't do. CRISPR-Cas9 is a genome editing system, but it couldn't manage to do targeted changes to the genomes of mitochondria. The tool uses a strand of RNA to guide the Cas9 enzyme to the region of DNA being changed. It works well with DNA, but the RNA can't go through the mitochondria that is surrounded by a membrane. The mitochondria are the cell's energy-producing structure, and the new enzyme may be able to edit it. This editing is a super precise version of gene editing called base editing. Therefore with this type of editing, mutations in that mitochondrial genome can be treated. These disorders are most often passed down maternally, and not allow the cell to create energy. Since scientists lacked a way to make models of the mutated mitochondrial genome, it has been difficult to study. This new enzyme is made by the bacterium Burkholderia cenocepacia. When this encounters the DNA base C it converts it into a U. U is not commonly found in DNA, so it acts like a T. The enzyme that replicates the cells DNA copies it as a T, therefore converting the C in the sequence to a T. The similar enzymes in CRISPR- Cas9 also do that, but those enzymes known as cytidine deaminases act on only a single-stranded DNA. Human DNA consists of two strands, so scientists had to rely on the Cas9 enzyme to break the double-stranded DNA into single-stranded DNA for the enzyme to work on. As expected, this technique does not reach the mitochondrial genome as well. However, the new enzyme called DddA could act directly on double stranding DNA without using the Cas9 enzyme to break it. That is why DddA may be suitable for reaching the mitochondrial genome. Before experimenting with this, scientists need to be very careful. Although this enzyme can be helpful, it can also be very deadly by mutating every C it came across. To prevent this, the enzyme would be split into two pieces that would change the DNA only with brought together in the correct orientation. The research team also linked each half of DddA to proteins that were created to bind to specific sites in the genome, so the DNA sequence that the enzyme modifies can be controlled. This new technology can save so many lives, but that will take some time. Reading this article was so interesting, and I can't wait to see what this technology will do for us.
Both of the articles were intriguing, but the article that interested me more was "Scientists make precise gene edits to mitochondrial DNA for first time" by Heidi Ledford. This is because technology in medicine has always been an engaging topic for me. With every new scientific discovery we are getting closer to unlocking the secrets that DNA hold. Since DNA is the blueprint of all known life on earth, understanding it and manipulating it can tell us a lot about ourselves and the power that we hold inside of us. The popular gene editing tool known as CRISPR/Cas9 was very useful, until later on when it was figured out that it could not precisely edit mitochondrial DNA yet. This is because CRISPR/Cas9 used a Guide RNA to guide the Cas9 protein, to then edit the gene. A new enzyme called DddA, can edit specific base pairs, that are located inside mitochondrial DNA. This new enzyme can prevent further genetic diseases to occur down the bloodline of the patient. The reason DddA works is because it can easily pass. through the mitochondrial membrane, which will then allow it to edit base pairs. As of now this newly developed enzyme is not ready to test/use in human beings. When not controlled the enzyme can go haywire, and turn every Cytosine into a Uracil, which can severely damage an individuals cells. over time scientists are learning on how to control the enzyme so it can correct mitochondrial DNA. With this new enzyme it will most likely make the quality of life better, add a significant lifespan to people, and eliminate mutations causing horrible diseases to occur. This new scientific discovery will possibly be in history books as one of the most important scientific discoveries of its time.
- [x] Today I read the article “Researchers uncover a critical early step of the visual process”, and I learned about the vision process. The process evolves around photoreceptors which transfer what we see to our brains, giving us exact ideas of what is in our field of vision. The mixture of rods( Night) and cones (day), help decipher between objects during the day and the night. The rods and cones both interact with each other to help depict objects, which is essential to the vision process. The protein connexin36 helps differentiate and bond the rods and cones together in this process. Within the retina, rods and cones interchange with each other to work with a variety of different types of other cones and rods. Overall, the article explained the vision process, what can be done to disrupt it, how it works, and why it’s essential to everyday life.
I read the article, “Researchers uncover a critical early step of the visual process,” written by a group of researchers at the University of Texas Health Science Center at Houston. This article discusses how new information was brought to light regarding how light receptors impacted the early stages of vision. After reading this article, I have learned that in the past, researchers struggled to understand how the retina processed signals from the rods and cones. They were particularly confused by how it worked when both rods and cones were active. The researchers had to understand how the communication between the rods and cones in the retina worked, for them to figure out the process of visual signaling. They found out that rods and cones communicated directly with each other and not just with their respective group. This was mainly done through the protein named connexin36, which made up the majority of gap junctions between rods and cones. To understand the organization of the photoreceptor network, they created genetic mouse trains made to get rid of the gap junctions between rods or cones. Since rods and cones are the main focus of photoreceptor networks, their gap junction is how signals move through the retina. They found that the mice could not go through this pathway. Researchers are continuing to study photoreceptor development, their functions and interactions, with a grant of 4 million dollars in the Ruiz Department of Ophthalmology and Visual Science. This is important to the overall advancements and knowledge about these signals.
This week I chose to read the article "A New Theory of Dreaming". This article talked about a theory why humans dream when they sleep. The theory was proposed by David M. Eagleman and Don A. Vaughn who claimed that the reason that we dream is to make sure that the visual cortex in the brains optical lobe is active while we are sleeping. This is because if the visual cortex is not active while we sleep it might degrade. In addition they claim that if the optical lobe where the visual cortex is located is deprived other senses might take over. This is shown with blind people because their sense of touch is sent to the optical lobe because of the lack of sight. Eagleman and Vaughn also proposed that neuroplasticity is a threat. Neuroplasticity it when the brain is re-wires less used part of the brain. They then said that if we did not dream then neuroplasticity would happen to the optical lobe because we do not use is when we sleep. Though some people do not agree with this because of REM sleep which stimulates the optical lobe. For their theory to be proven there would need to be further testing because the is some evidence that is not entirely proven.
In the article, “Researchers uncover a critical early step of the visual process”, the authors at University of Texas Health Science Center talk about how photoreceptors, otherwise known as light receptors, impact the early stages of the process of vision. In the past, researchers mainly focused on how rods and cones, two key sensory cells, convert particles of light into electrical signals which transfer to the brain through devoted circuits. Rods are used for night vision, while cones are used for daytime and color vision. Scientists know that the electrical signals can spread between photoreceptors through cell connectors, which are a type of gap junctions. However, researchers have now they work. TChristophe P. Ribelayga explained that the understanding of how the retina processes signals from rods and cones in the eyes can help design better photo receptor or retinal implants to restore vision. Furthermore, it is very important to understand what happens when both photo receptor types are active under ambient lighting conditions. Coupling, communication, between rods and cones is critical for understanding how the visual signaling process works. The researchers have found pretty surprising information. They found out that rods do not directly communicate with other rods. Cones rarely communicate directly with other cones. The majority of the signaling happens through the communication between rods and cones. In 2018, the Ruiz Department of Ophthalmology & Visual Science received more than $4 million in grants for researchers to study development, function, and electrical interactions.
In the article, “Researchers uncover a critical early step of the visual process,” I learned of the method that rods and cone cells within eyes help see in different lighting conditions. Two sensory cells called rods and cones turn light particles into electrical signals that are sent to the brain. Rod cells are used to see in dark conditions and cone cells are used to see in light conditions and color. The signals from photoreceptors travel through gap junctions to send the signal. There is also communication between rod and cone cells that allows for visual processing and there is one on one connection between each rod and cone cell. The protein connexin36 is involved in the gap junctions between the rods and cones. There is often never a connection between a cone cell with another cone cell and that a majority of the gap junctions are rod and cone gap junction. To better understand the network of photoreceptors, they experimented with mice and bred some of them to not have rod and cone gap junctions. This research will help scientists understand the photoreceptors interactions with signals.
A particular enzyme, a peculiar bacterial, allows researchers to find the changes in the mitochondria part of the cell. it allows researchers to find new ways to study and treat the diseases caused in the mutations that are placed in the mitochondria. It’s hard to study some disorders because they test on animals first and since some animal genomes are different from human ones, it’s hard to find what will cure mutations. When a DNA base C is converted to a U a bacterium toxin is formed called Burkholderia cenocepacia. A common problem found in gene editing is that more studies are required. Some techniques are available where the nucleus of an egg can be transplanted into a donor egg that has a healthy mitochondria. Till this day they try to find more advanced way to cure the diseases created by mutations in the mitochondria.
I read the article “Researchers Uncover a Critical Early Step of the Visual Process” by the University of Texas Health Science Center at Houston. This article states how the electrical connections between light receptors in the eye affect the early steps of visual signal processing. It was discovered that rods (which are used for night vision) and cones (which are used for daytime vision and color vision) don’t really communicate with themselves, and instead most of the signaling happens between rods/cones, with the protein connexin36 (Cx36) being the main element of the rod/cone gap junction. To really understand how the vision process works, it’s important to figure out how rods and cones connect and signal to each other, and how the retina takes these signals and processes them to enable us to see. I also thought it was interesting to find out that at dusk/dawn, both rods and cones are used to help us see.
I read the article "Scientists make precise gene edits to mitochondrial DNA for first time" by Heidi Ledford. It gave a lot of insight on the building blocks of life and genes, DNA. The article spoke about how to edit the DNA in a Mitochondria. The CRISPR-Cas9 is allowing scientists to change the genomes of organisms by using an RNA strand to lead the Cas9 enzyme. However, the RNA strand can not go into the mitochondria due to the surrounding membranes. A new enzyme, cytidine deaminases, was found to change the DNA bases. Also, it was deadly to modify it cause if it was let loose, it would mutate every C it came across. To prevent this, they split the enzyme into 2 pieces that would come together as DNA when set in the right orientation.
The article, “Scientists make precise gene edits to mitochondrial DNA for the first time” by Heidi Ledford. It gave me a lot more vision on DNA and it also allowed me to learn how DNA is structured. I also learned that how mitochondrial DNA was edited. The RNA Strand cannot go into the mitochrondria due to its surroundings. A new enzyme was also discovered. It was a horrible change as it would lead to a genetic mutation.
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