BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: DNA (Page 3 of 8)

Researchers at UT Austin tweak cas9 to make CRISPR gene-editing 4,000x less error-prone

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On March 16, 2022

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A huge stride in ensuring the efficacy of CRISPR genome-editing has been made by researchers at the University of Texas at Austin. The CRISPR gene editing tool is a new genetic engineering technique that can, by using an enzyme called Cas9, correct problematic genomes in a person’s DNA. It finds the genome that its programmed to and cuts it out of the DNA, leaving the organism without that DNA, and inhibiting the organism from spreading that gene to their offspring. There have been studies have shown CRISPR has been effective in editing genomes that may cause disease. In a study where the Cas9 enzyme was injected into the bloodstream of six people with a rare and fatal condition called transthyretin amyloidosis, those who received the higher dose saw a decline around 87% in production of the misshapen protein that causes this condition.

For many diseases, Gene therapy is the “Holy Grail”. For treatment of Sickle-Cell Anemia, CRISPR has been thought of as a definitive cure. In 2017, it was reported that a 13-year-old boy with HbSS disease had been cured with gene therapy. This treatment also allows the carrier of this gene to reproduce without any risk of their offspring being affected by SCD.

GRNA-Cas9However, there are concerns that when performing the genome editing, the wrong segment of DNA could be targeted by scientists and removed, resulting in potentially drastic consequences. Another concern is that editing out certain genes is societally damaging, as it is considered unnatural to be able to edit the genomes of human bei

ngs. Another major safety concern is mosaicism (when some cells carry the edit but others do not); this could result in many different side effects. Due to the many uncertain aspects around the danger of genome-editing, there has been delay in passing legislation approving genome-editing.

 

In a study published on March 2nd 2022 at the University of Texas at Austin, researchers have found a previously unknown structure in the Cas9 protein that is thought to attribute to these genetic mistakes. When using cryo-electron microscopy to observe the Cas9 protein at work, the researching team noticed a strange finger-like structure that stabilized the off-target gene section to be edited instead of editing the target gene.

The researchers at the University of Texas at Austin were able to tweak the protein, preventing Cas9 from editing the wrong sequence. This change has made the tool 4,000 times less likely to produce unintentional mutations; the team calls the new protein ‘SuperFi-Cas9’.

While other researchers have made similar edits to make the Cas9 protein more accurate in its editing, these often result in slowing down the genome editing process. At UT Austin, the researchers say that SuperFi-Cas9 still is able to make edits at the normal speed.

The researchers plan to test SuperFi-Cas9 further in living cells as opposed to the testing thats been done with DNA in test tubes. Hopefully they’re able to cement the accuracy of SuperFi-Cas9, and that this may accelerate us on our way to implementing CRISPR gene editing in the current medical world. Let us know in the comments below what your thoughts are on CRISPR editing, and if you think we should continue researching it!

Can Gene Edited Tomatoes Save Your Life?

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On March 16, 2022

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In a new invention by Hiroshi Ezura, the chief technology officer at Sanatech and molecular biologist, Tomatoes can now lead to lower blood pressure and higher relaxation.

This invention is based off a new phenomenon that is becoming more and more popular in Japan, food that is genetically edited using CRISPR technology. This technology is used to increase the amount of GABA in foods. GAMA, or gamma-aminobutyric acid, is a neurotransmitter and amino acid that “blocks impulses between nerve cells in the brain” (Waltz, Scientific American).

GAMA is being tested by many groups, including Ezura and his crew, for positive correlations between available GAMA, and health benefits. So far, there have not been any confirmed guaranteed health benefits, but the data from other genetically modified foods shows generally there are health benefits. People eating the food should feel more relaxed. Other tests have been done in the human, or animal bodies. GAMA is a natural substance found in humans, so the genetic mutations do not add a foreign substance to the body – it is safe to consume.

CRISPR technology is at the heart of this. This is a genetics technology in which one can add, take away, or alter sections of DNA. DNA is a double helix which consists of the nucleotide bases, Adenine, Cytosine, Guanine, and Thymine. When certain sections of the genetic code, represented in letters, are replaced by others, certain genes can change. Genes are certain pieces of DNA that carry genetic information which can alter how someone looks or functions. When worked on a tomato, it is able to alter a gene that gets rid of a pathway called the GABA shunt, which through a series of events limits GABA in cells.

Basepairs Graphic Public Domain

This technique has been used before, but it is so special because this is the first time it has been a commercial food product. This is exciting; genetic engineering can have negative effects in some areas, but so far the data shows that it is effective. Personally, I hope there is a rigorous series of tests that has to be conducted in the future for each CRISPR modified food to be commercially produced and sold.

New research further advances the understanding of DNA repair

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On March 16, 2022

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In a study recently published in Nature Cell Biology, there’s been a discovery that alters our understanding of how the body’s DNA repair process works and may lead to new chemotherapy treatments for cancer and other disorders. Because DNA is the repository of genetic information in each living cell, its integrity and stability are essential to life. DNA, however, is not inert. Rather, it is a chemical entity subject to abuse from the environment and any resulting damage, if not repaired, will lead to mutation and possibly disease.

File:DNA polymerase.png

DNA Polymerase

The fact that DNA can be repaired after it has been damaged is one of the great mysteries of medical science, but pathways involved in the repair process vary during different stages of the cell life cycle. In one of the repair pathways known as base excision repair (BER), the damaged material is removed, and a combination of proteins and enzymes work together to create DNA to fill in and then seal the gaps. In addition to genetic insults caused by the environment, the very process of DNA replication during cell division is prone to error. The rate at which DNA polymerase adds incorrect nucleotides during DNA replication is a major factor in determining the spontaneous mutation rate in an organism.

Researchers discovered that BER has a built-in mechanism to increase its effectiveness, it just needs to be captured at a very precise point in the cell life cycle. In BER, an enzyme called polymerase beta (PolyB) fulfills two functions: It creates DNA, and it initiates a reaction to clean up the leftover chemical waste. Through five years of study, scientists learned that by capturing PolyB when it is naturally cross-linked with DNA, the enzyme will create new genetic material at a speed 17 times faster than when the two are not cross-linked. This suggests that the two functions of PolyB are interlocked, not independent, during BER.

Cancer cells replicate at high speed, and their DNA endures a lot of damage. When a doctor uses certain drugs to attack cancer cells’ DNA, the cancer cells must cope with additional DNA damage. If the cancer cells cannot rapidly fix DNA damage, they will die. Otherwise, the cancer cells survive, and drug resistance appears. This research examined naturally cross-linked PolyB and DNA, unlike previous research that mimicked the process. Prior to this study, researchers had identified the enzymes involved in BER but didn’t fully understand how they work together. This research improves the understanding of cellular genomic stability, drug efficacy, and resistance associated with chemotherapy, which, as previously stated, can lead to new chemotherapy treatments for cancer and other disorders.

CRISPR Gene Editing: The Future of Food?

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On March 16, 2022

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Biology class has taught me a lot about genes and DNA – I know genes code for certain traits, DNA is the code that makes up genes, and that genes are found on chromosomes. I could even tell two parents, with enough information, the probabilities of different eye colors in their children! However, even with all this information, when I first heard “gene editing technology,” I thought, “parents editing what their children will look like,” and while this may be encapsulated in the CRISPR gene editing technology, it is far from its purpose! So, if you’re like me when I first started my CRISPR research, you have a lot to learn! Let’s dive right in!

CRISPR

Firstly, what is CRISPR Gene Editing? It is a genetic engineering technique that “edits genes by precisely cutting DNA and then letting natural DNA repair processes to take over” (http://www.crisprtx.com/gene-editing/crispr-cas9).  Depending on the cut of DNA, three different genetic edits can occur: if a single cut in the DNA is made, a gene can be inactivated; if two separate DNA sites are cut, the middle part of DNA will be deleted, and the separate cuts will join together; and if the same two separate pieces of DNA are cut, but a DNA template is added, the middle part of DNA that would have been deleted can either be corrected or completely replaced. This technology allows for endless possibilities of advancements, from reducing toxic protein to fighting cancer, due to the countless ways it can be applied. Check out this link for some other incredible ways to apply CRISPR technology!

In this blog post however, we will focus on my favorite topic, food! Just a few months ago, the first CRISPR gene-edited food went on the market! In Japan, Sicilian Rouge tomatoes are now being sold after the Tokyo-based company, Sanatech Seed, edited them to contain an increased amount of y-aminobutyric acid (GABA). “GABA is an amino acid and neurotransmitter that blocks impulses between nerve cells in the brain” (https://www.scientificamerican.com/article/crispr-edited-tomatoes-are-supposed-to-help-you-chill-out/). It supposedly (there is scarce scientific evidence of its role as a health supplement) lowers blood pressure and promotes relaxation. In the past, bioengineers have used CRISPR technology to “develop non-browning mushrooms, drought-tolerant soybeans and a host of other creative traits in plants,” but this is the first time the creation is being sold to consumers on the market (https://www.scientificamerican.com/article/crispr-edited-tomatoes-are-supposed-to-help-you-chill-out/)!

Tomatoes

So, how did Sanatech Seed do it? They took the gene editing approach of disabling a gene with the first method described above, making a single cut in the DNA. By doing so, Sanatech’s researchers inactivated the gene that “encodes calmodulin-binding domain (CaMBD)” in order to increase the “activity of the enzyme glutamic acid decarboxylase, which catalyzes the decarboxylation of glutamate to GABA, thus raising levels of the molecule” (https://www.scientificamerican.com/article/crispr-edited-tomatoes-are-supposed-to-help-you-chill-out/). These may seem like big words, but we know from biology that enzymes speed up reactions and decarboxylation is the removal of carbon dioxide from organic acids so you are already familiar with most of the vocabulary! Essentially, bioengineers made a single cut in DNA inside of the GABA shunt (a metabolic pathway) using CRISPR technology. They were therefore able to disable the gene that encodes the protein CaMBD, and by disabling this gene a certain enzyme (glutamic acid decarboxylase) that helps create GABA from glutamate, was stimulated. Thus, more activity of the enzyme that catalyzes the reaction of glutamate to GABA means more GABA! If you are still a little confused, check out this article to read more about how glutamate becomes GABA which will help you better understand this whole process – I know it can be hard to grasp!

After reading all of this research, I am sure you are wondering if you will soon see more CRISPR-edited food come onto the market! The answer is, it depends on where you are asking from! Bioengineered crops are already hard to sell – many countries have regulations against such food and restrictions about what traits can actually be altered in food. Currently, there are some nutritionally enhanced food on the market like soybeans and canola, and many genetically modified organisms (GMOs), but no other genome-edited ones! The US, Brazil, Argentina, and Australia have “repeatedly ruled that genome-edited crops fall outside of its purview” and “Europe has essentially banned genome-edited foods” (https://www.scientificamerican.com/article/crispr-edited-tomatoes-are-supposed-to-help-you-chill-out/). However, if you are in Japan, where the tomatoes are currently being sold, expect to see many more genome edited foods! I know I am now hoping to take a trip to Japan soon!

Thank you so much for reading! If you have any questions, please ask them below!

Do Genetics Play A Role In Attraction?

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On February 25, 2022

In Student Post

Have you ever met someone with whom you instantly wanted to be friends but couldn’t put your finger on why or how you felt so drawn to them? There is a reason why you might be drawn to a specific person or group of people that may be explained by biology.

Double stranded DNA with coloured basesChromosome Terminology

According to a book by a well-known author, Malcolm Gladwell, a “unconscious” region of the human brain helps us to digest information spontaneously while encountering someone or something for the first time or making a rash decision. The University of Maryland School of Medicine has expanded on this hypothesis with a new study, indicating that these reactions may have a biological foundation related to heredity. The experiment was carried out on a group of mice. Variations in a particular enzyme discovered in a portion of the brain that affects mood and drive appear to influence which mice desire to actively engage with other mice; genetically related mice favored one another. Similar circumstances, such as disorders linked with social withdrawal, such as schizophrenia or autism, might also influence people’s decisions. Consequently, researchers do not agree with the phrase “opposites attract,” because genetics have a significant role in attraction. Instead, experts propose that we choose friends based only on their similarities to ourselves. Unlike the concept of “opposites attracting,” the expression “people like their own kind” is accurate. While genes definitely contribute to an individual’s attractiveness, they only account for around one-third of the reasons why we choose someone else to be our friend.

In a separate study, researchers examined a range of variables, that often are most inheritable and those that are less inheritable, to evaluate the role genes function in our human conduct, and they discovered that “people are genetically inclined to choose as social partners those who resemble themselves on a genetic level.” Rushton discovered in this study that humans prefer to choose partners based on inheritable attributes, even when we are unaware that such characteristics are genetically determined. For example, the middle-finger length is inherited, although the upper-arm circumference is not. Spouses who took part in the study had identical middle finger lengths but not the same upper-arm circumference. The function of heredity also influences personality, which explains why “people like their own kind.” What you inherited biologically from your parents, which is defined by the genes in your DNA, is the key to personality traits. Genetic heredity accounts for almost half of our cognitive differences, from personality to mental capabilities.

Love-heart-hands

Genetics is the scientific study of genes and heredity, which transfer particular characteristics from parents to offspring due to variations in DNA sequences. The genome contains all of an organism’s genetic code, including its genes and additional components that govern the activation of those genes. We are drawn to others because of the features that we share with them through genetic material. Our DNA is stored in chromosomes, and each of the 23 pairs of chromosomes has the same genes that are handed down from parent to offspring. When a baby is being formed, DNA is handed down, and each parent sends half of their chromosomes to their kid, thus each of your parents contributes 50% of your DNA. The term “genetic love” refers to the idea of matching partners for romantic relationships based on their biological compatibility. “Genetic love” describes the notion of attraction based on heredity.

Difference DNA RNA-EN

Is it possible that you want to be friends with someone of the same genetics as yourself? Yes! It is! However, it is not the only thing that accounts for maintaining a friendship.

Do Mitochondria contribute to neurological and psychiatric disorders?

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On February 17, 2022

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Mitochondria have had a deep history through the evolution of eukaryotic cells. A primitive bacterium was engulfed by another free floating prokaryotic cell. Many think that this was originally how eukaryotic cells were formed and why mitochondria have their own DNA different from a their cells nucleus. Endosymbiotic theory has been used to understand the intricacies of Mitochondria and leaves many clues as to how their relationship with their cell affects its overall performance  The mutually beneficial relationship between both has lasted for over two billion years by fueling the processes for everyday life.

Mitochondria are membrane-bound cell organelles which generate majority of the chemical energy needed to power a cell’s biochemical reactions. Cell, Mitochondria, Biology, Organelle, ScientificChemical energy produced by the mitochondria is stored in a small molecule called adenosine triphosphate or ATP. This is only one of the many essential jobs mitochondrion hold as an organelles in our cells.

Since mitochondria have their own set of DNA different from their cells, it makes it both a critical element of our cells and a potential source of problems. Mitochondrial DNA can harbor mutations similarly to ones in our nuclei. These can either be detrimental to their function powering our bodies or have little to no effect whatsoever. Age, stress and other factors may disrupt mitochondria’s many functions. On top of that, mitochondrial injury can release molecules that, due to their similarities to those made by bacteria, can be mistaken by our immune system as foreign invaders, triggering a harmful inflammatory response against our own cells.

One of our most important organs, the brain, needs mitochondria the most for its power driven functions. “The more energetically demanding a cell is, the more mitochondria they have, and the more critical that mitochondria health is — so there’s more potential for things to go wrong,” says Andrew Moehlman, postdoctoral researcher who studies neurodegeneration at the US National Institute of Neurological Disorders and Stroke (NINDS). Some estimates assume that each neuron can have up to two million mitochondria meanwhile there are eighty-six billion neurons in our brain.

Researchers have then linked dozens of disorders to alterations in mitochondrial DNA and nuclear DNA related to mitochondrial function. The majority of these are either neurological in nature or have some effect on the brain because of how dominant mitochondria is in the brain. According to Douglas Wallace, a doctoral student at Yale University, despite making up only 2 percent of a human’s body weight, the brain uses roughly a fifth of the body’s energy. These small reductions in mitochondrial function can have large effects on the brain, Wallace explains.

ATP gives us the energy we need for our body to function as we learned through our cellular respiration unit. Without this form of energy, our body simply cannot function which is why mitochondria play a key role in brain function. Mutations which affect the flow of ATP synthase seem most detrimental to cell function and as we know is where ADP and a Phosphorus join together to create ATP. Mitochondria’s own set of DNA makes it difficult to pinpoint a mutation and leaves animals vulnerable to neurological disorders.

New research exposes and demonstrates how damaged cells survive the cell cycle

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On February 15, 2022

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In recent news, the Center for Cancer Research have recently discovered a previously unknown phenomenon, which allows certain cells to continue through the cell cycle despite experiencing DNA damage. This also includes past natural safety checkpoints within the cell cycle that are designed to stop the problem from occurring. On January 13, 2021 researchers, in Science Advances, suggested that the timing of DNA damage was crucial for determining whether a faulty cell would survive the cycle.

File:The Cell Cycle.svg

The Cell Cycle

When cells begin to divide and replicate as part of their natural cycle, they transition from their resting state to one called the G1 phase. In this phase, cells have several important checkpoint mechanisms to ensure that the cell is healthy enough to proceed onto the next stage of the cell cycle. If/when these mechanisms fail due to genetic mutations, cells can progress through the G1 phase unobstructed, which can ultimately lead to cancer.

It was previously believed that cells with DNA damage could not pass through these safety checkpoints in the G1 phase and that the cells would either repair the DNA damage or die. However, scientists helped uncover evidence proving that cells with damaged DNA can actually progress past these critical checkpoints. A team of scientists studied individual cells for days at a time, using live cell time-lapse microscopy, single-cell tracking software, and fluorescent biosensors to detect the cell’s safety checkpoint mechanisms. They added a substance to induce DNA damage for cells of different ages in the cell cycle. Strikingly, the majority of cells seemed to ignore the DNA damage because they failed to trigger the checkpoint between G1 and the next phase, and proceeded into the next phase anyway.

File:Damaged DNA.png

Damaged DNA

Further investigation revealed that the timing of DNA damage during the cell cycle influenced the likelihood that damaged cells would slip past the checkpoints. The researchers found that the cell’s response to DNA damage is relatively slow compared to the speed of the cell cycle. This means if cells were already very close to the next phase of the cell cycle at the time DNA damage happened, they were more likely to continue into that phase. If the cells were still early in the G1 phase, they were more likely to revert back to a resting state. These observations are a form of inertia, where the cell will continue moving towards the next phase regardless of safety checkpoint signals.

It was also discovered that cells which were genetically identical were more likely to share the same cell cycle fate than non-identical cells. This suggests that factors specific to the cells themselves influence their fate during the cycle, rather than random chance. More studies are needed to understand how these findings apply to cancer. Testing is also extremely important in order to fully understand what the long-term consequences of the checkpoint failures are and find out if the cells that entered the next phase despite considerable DNA damage can become cancerous and eventually form a tumor, which, in my opinion and most likely the opinion of others, will be groundbreaking for cancer research.

Could These Blood Proteins Be The Key To Extending Human Lifespan?

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On February 15, 2022

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All around the world, companies profit off of the idea of “anti-aging” products; but could these various serums, skincare products, and supplements even have an impact? A study from the University of Edinburgh, in which researchers analyzed six different genetic studies surrounding human aging, suggests otherwise. Instead, after analyzing 857 proteins from genetic information from hundreds of thousands of people, scientists have reason to believe that two distinct blood proteins have negative effects on aging. As we know from AP Bio, different individuals naturally have higher or lower levels of certain proteins depending on their genetics, and the DNA they inherit from their parents. Additionally, we know that each parent provides 23 chromosomes, which encode the same genes, totaling to 46. This means that if your parent has high levels of specific proteins, you have a significant chance of inheriting that.

Ácido desoxirribonucleico (DNA)

 In the case of these two blood proteins, LPA and VCAM1, people who inherited DNA that causes raised levels of these proteins were overall much more weak, unhealthy, and less likely to live a long life. Lipoprotein (a), a lipoprotein variant containing a protein called Apolipoprotein (a), is made in the liver. High levels of this protein are associated with a vast increase in the risk of atherosclerosis, which is a cardiovascular disease in which there is a​​ thickening or hardening of the arteries caused by a buildup of fatty substances in the inner lining of the arteries. Additionally, LPA is also linked to coronary heart disease and strokes. The second protein, vascular cell adhesion protein 1, or VCAM1,  is a protein found mainly on endothelial cells lining the blood vessels. It primarily controls blood vessel expansion and retraction. Elevated levels of VCAM1 are associated with long-term risk of heart failure.

Currently, there are clinical trials working to reduce the risk of heart disease through testing a drug to lower LPA. While there are no trials surrounding VCAM1 at the moment, there has been some animal testing done on mice to see the effects of lowering this protein. In these tests, researchers found that antibodies lowering VCAM1 levels improved cognition in old age for the mice.

The scientific progress and research regarding these two blood proteins is profoundly important, for it has revealed two key targets for future drugs to extend the lifespan of humans who aren’t genetically blessed. It is medical progress and news like this that continuously help us remain hopeful as we, and our loved ones, age.

How are new COVID variants identified?

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On January 4, 2022

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COVID variants are of high concern for scientists studying the disease. Some variants can be more infectious or cause more severe illness. Additionally, some variants can evade vaccines by having different surface proteins than the variant the vaccine was created for. This causes the antibodies produced from the vaccine to be less effective against other variants. In AP Biology class we discussed how the Delta Variant, first identified in December 2020, has a different spike protein structure than the original virus from which the vaccine was created from. This allows the variant to be more infectious, and make the vaccine less effective against it. But, what are COVID variants? And how are they discovered? Hand with surgical latex gloves holding Coronavirus and A Variant of Concern text

COVID variants are “versions” of the virus with a different genetic code than the original one discovered. However, not every mutation leads to a new variant. This is because the genetic code of the virus codes for proteins. Some mutations will not change the structure of the protein and thus not change the virus. So, COVID variants can be defined as versions of the virus with a significantly different genetic code than the original virus.

To detect new COVID variants, scientists sequence the genetic code of virus which appears in positive COVID tests. Scientists look at the similarity of the genetic sequences they find. Then, if many of the sequences they get look very similar to each other, but different to any other known virus, a variant has been discovered.

To sequence the RNA of the virus, scientists use what is called Next Generation Sequencing (NGS). To understand how NGS works, it is best to start with what is called Sanger Sequencing. Sanger Sequencing utilizes a modified PCR reaction called chain-termination PCR to generate DNA or RNA fragments of varying length. The ending nucleotide of each sequence is called a ddNTP, which contains a florescent die corresponding to the type of nucleotide. The addition of a ddNTP also terminates the copying of the particular sequence. The goal of this PCR reaction is to generate a fragment of every length from the start to the end of the sequence. The sequences can then be sorted by length using a specialized form of gel electrophoresis. The sequence is then read by using a laser to check the color of the fluorescent die at the end of each sequence. Based on the color and size, the nucleotide at that position of the genomic sequence can be found.

Sanger Sequencing Example

The difference with NGS is that many sequences can be done in parallel, allowing for very high throughput. In other words, with NGS many COVID tests can be sequenced in once.

Quit Hogging All the Kidneys

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On November 1, 2021

In Student Post

Xenotransplantation is defined as the process of transplanting organs between members of different species. Saying it out loud it sounds like mad science but the it’s not as crazy you might think. Xenotransplantation has actually been a process that has been used for many years, even dating back to the 1960s. This journey began with apes and monkeys. Scientists believe that it would make the most amount of sense to use because they were essentially the most promising source of organs and tissue due to their being primates. However, this unraveled into a series of problems that were due to them being contaminated with viruses that are pathogenic to human beings. Baby monkeys were also researched but the idea was dismissed due to ethical reasons. This consequently led to the study of pig tissue.

We have actually been utilizing things from pigs that most people may not even be aware of. One example of this is pig insulin. It would replace the insulin that your body would usually make in order to get blood sugar into your cells. We obviously can’t take just any part of a pig and use it. We can, however, utilize a pig’s kidneys and transplant it into a human body. On September 25th, scientists and researchers  successfully transplanted a kidney from a genetically altered pig into a human patient and discovered that it functioned normally.

Little piggies

How Did It Work?

According to the an article by the New York Times, the pig needed to be genetically altered in order to be transplanted into the patient. What was altered? Essentially the kidney in the procedure was obtained by removing a pig gene that encodes a sugar molecule that elicits an aggressive human rejection response. Interestingly enough, the genetic difference between pig DNA and human DNA is 98 percent.

What Were The Risks?

While pigs and humans may share a lot of DNA, they are not a match right away. A non altered pig would cause many risks if any part of it were transplanted into the human body. A way it could pose an issue is through the viruses they may contain. Pig viruses may not cause disease in pigs, but they can in fact be pathogenic to humans. The human proteins that are expressed onto the transgenic pig cells can be receptors for viruses. An article on pig DNA from PMC explains that CD55 is a receptor for human Coxsackie B and ECHO viruses (these are relatives of poliovirus), and these cause a disease called myocarditis. The protein CD46 can act as as a receptor for the measles virus, so it is possible that morbilliviruses of animals could be preadapted in the same pigs used for xenotransplantation.

Another way that these transgenic pigs may heighten risk of virus is through viruses with lipid envelopes that are from host cell membranes would be less likely to inactivated by human compliment. What could have been a protective mechanism against infections from viruses derived from farm animals could be broken down in attempts to make xenografts for humans (The tissue or organ being transplanted from the other species).

Slide4kkk

Diagram of a pig kidney

The future of xenotransplantation looks promising. While it may have worked, scientists are still doing studies and still trying to find out more about the viruses pigs may carry. While we can weed out the viruses we are aware of, we still can’t account for the ones we don’t know exist. There is a reason this topic is somewhat new and that is because of ethics. Apes and Monkeys could’ve actually been genetically altered the same way these pigs were, however it was deemed unethical. I personally agree that apes and monkeys shouldn’t be harvested, but that begs the question of whether harvesting organs from pigs is ethical. And with that I ask you what you ate for breakfast, lunch or dinner. Pigs and other animals are already being harvested for food and I believe that if there is a problem with xenotransplants, there would be a problem with the food industry. With that being said, if you’re ever in the market for a kidney, you have options.

Are Artificial Chromosomes the Key to Future Medicine?

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On October 31, 2021

In Student Post

Our DNA is packaged intricately by proteins in order to make up chromatin. If DNA were like a thread, these proteins are the spools that the DNA thread winds around to keep itself neat, organized, and compact inside of a microscopic cell. If a foreign, naked DNA thread with no spool is introduced into the environment, the cell is armed and ready to supply this new thread with its own self-made spools, allowing this naked DNA thread to be stably maintained in the cellular environment as part of the cell’s new collection. This process is known as artificial chromosome formation.

Royalty-free dna photos free download | Pxfuel

DNA Double Helix

Prospects for the Use of Artificial Chromosomes include the potential to overcome problems in gene therapy protocols such as immunogenicity, insertional mutagenesis, oncogene activation, or limitations in capacity for transgene expression. One case where artificial chromosomes can be useful is found with someone dealing with Cystic Fibrosis. This fatal chronic lung disease is caused by a mutation in the CFTR gene and is currently a disease without a known cure. Scientists have been studying the use of bacterial and yeast artificial chromosomes as a transmitter to implement the normal functioning CFTR gene and overcome the defective CFTR gene in patient cells.

File:Cell division according to E. Strasburger (1875).png

Cell Division

Almost two trillion cells divide every day in an average human body. This means that two trillion cells have to make a perfect copy of themselves every time. In our class, we’ve gone over the importance of cell division and have discussed the Mitochondria and Chloroplast’s ability to replicate independently within cells. The cost of cell division that comes short of flawlessness is undoubtedly humankind’s worst enemy yet: cancer, in which many are characterized by chromosome instability. One important player in ensuring the inheritance of our chromosomes during cell division is the centromere. The current studies of artificial chromosomes provide novel insights into the chromosomal processes required for de novo centromere formation and chromosome maintenance.

Ultimately, the results of these studies could help advance the synthetic biology field by exploring how some characteristics can be designed to optimize the establishment of an artificial chromosome by improving the efficiency of de novo centromere formation through accurate segregation to improve the applications of artificial chromosomes as large-capacity transmitters for cloning and gene therapies.

 

A New Way to “Tangle” with Diseases? British Scientists Think They’ve Stumbled Upon the Future

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On October 27, 2021

In Student Post

A team of scientist from the Universities of Bath and Birmingham have made a discovery that is making noise in the world of Biology. Ironically, they had the realization while studying silent mutations in DNA. What they found is a new method of evolution. Well not a new method per say as the scientists predict this method is being used in all forms of life; however, new in the sense that it was only recently realized. What they have discovered is a trend of tangles in DNA strands. This tangling occurs in DNA strands that are not in a double helix as DNA typically is. However The DNA strands are separated during copying. This task is done by DNA polymerase enzymes. During the copying process, the enzymes are often disrupted by the tangles in the strand. The resulting skipping of genes causes specific mutations to the DNA.

DNA replication split horizontal

The scientists then tested their hypothesis by way of experiment. They did so by studying the evolution of soil bacteria called Pseudomonas fluorescens (SBW25 and Pf0-1). They began by removing the gene that give the bacteria the ability to swim. They then observed the re-evolution of the strains to regain the ability swim. Both strains evolved quickly; however, there was a clear differences in predictability. One strain (SBW25) mutated the same part of a particular gene in every trial. The other strain (Pf0-1) varied in which gene and where the mutation occurred in each trial. Upon further observation, this contrast coincided with a hair-pin shaped tangle in the SBW25 strain. As the DNA polymerase enzymes would pass this tangle they would be effected in a predictable manner that would disrupt copying of DNA and result in a mutation that allows for the bacteria to swim. The scientists tested the theory by removing the tangle. They did so using 6 silent mutations so that the DNA sequence would not have a relevant change. The trials after the change showed that both strains showed inconsistent areas being mutated.

 

DNA are the dictators of protein synthesis in the body. The DNA sequences code for the types of proteins that are created. Proteins perform many of the bodies function. This means that even the slightest change in the sequencing of DNA can have major effects on the functioning of a human body or any organism. The process of evolution was thought to be caused by random errors in DNA sequencing that coincidentally gave an organism a survival advantage. These mutations would then be tested in the concept of survival of the fittest. While this is still thought to be the most prevalent form of evolution, especially with eukaryotic organisms, the tangling of DNA strands proposes a form of evolution that would be easier to study and predict.

 

The predictability of such a phenomenon is where the intrigue in viruses arises. “If we knew where the potential mutational hotspots in bacteria or viruses were, it might help us to predict how these microbes could mutate under selective pressure.” says Dr. Tiffany Taylor, from the Milner Centre for Evolution. Mutational hotspots have already been found in cancer, and the new information on their significance is getting scientists excited about the opportunities present. The new ways to understand and predict evolution of bacteria and viruses may allow scientists to be a step ahead on vaccines and be able to anticipate and understand new variants. It’s hard not to think this information would’ve been nice before the rise of SARS-CoV-2.

Is Junk DNA Really Junk?

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On October 27, 2021

In Student Post

DNA is the base code of all living creatures. It is in every plant, animal, and single-cell organism, yet  50% of human DNA is seen to be irrelevant to bodily function. While some DNA is responsible for synthesizing materials within cells, much of it is in essence, spare genes, or ancient viruses that have become part of the human genome over time. Moreover, it has been debated whether the 50% of DNA that is not seen to be relevant is truly essential for survival. That is, can humans live without unused genetic code, or is it vital to the survival of the species?

Ácido desoxirribonucleico (DNA)

One specific element of junk DNA is transposons. Transposons are sequences of DNA that have the ability to mutate a cell or change its function as a whole. A study was conducted at the University of California, Berkley, and Washington University on transposons, as written in the So-called Junk DNA – Genetic “Dark Matter” – Is Actually Critical to Survival in Mammals, by the University of California, Berkley. The studies looked at a specific transposon in mice called MT2B2, one that controlled the growth rate of cells in a fertilized embryo, and when the embryo would implant in the uterus of the mother by initiating the short gene Cdk2ap1. When the researchers disabled the MT2B2 transposon using CRISPR-EZ, the mice created a longer version of the gene Cdk2ap2. This new version of the gene decreased cell growth and increased the period of implantation. The teams found that half of the baby mice died before birth without this transposon in their DNA. When the transposon was disabled, the mice sort randomly instead of uniformly in the uterus, and some may cause the death of a developed fetus and or the mother.

The team at Washington University researched the transposons turned on before embryos are impacted into the uterus in humans, rhesus monkeys, marmosets, mice, goats, cows, pigs, and opossums. The team used scRNA-seq, which records messenger RNA levels to indicate which genes are being used. With this technique,  the team saw that in every animal, a group of species-specific transposons was turned on. While the transposons were different for each species, the result of their use was nearly the same for all eight cases. Moreover, the gene Cdk2ap1 was expressed by all eight animals, but the amount of short and long versions of the gene expressed was unique for each one. While an animal that needs fast implantation uses more of the short version of the gene, like the mouse, animals with little to none of the shorter version of Cdk2ap1 took two weeks to longer for implantation to occur, like the cow.

Baby Mouse Rehabber

For these transposons to be promoting the expression of the Cdk2ap1 gene, at a certain point in history, a virus entered the organism and eventually part in a mutually beneficial symbiotic relationship with the organism until it evolved into the current iteration of the transposon. When viruses blend into the DNA of a species, they can be used to regulate and perform tasks that the cell could not previously perform. This can create a wide range of evolutionary options in species. Additionally, the main difference between the different genomes of species is the regulation of genes. By studying transposons, scientists can better understand differences in the genome of one species to another. With the understanding of this transposon, scientists could now begin searching further into junk DNA, as the removal of the transposon studies by the two universities proved lethal 50% of the time. Moreover, undiagnosed patients could have junk DNA mutations that lead to health problems, but those cases are currently a mystery to the medical world. Transposons are just the beginning of scientists dive into junk DNA, and who knows what wonders they will find next?

“I Wanna Live Forever Young”

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On October 27, 2021

In Student Post

Aging: the inevitable… or so we thought. Don’t get too excited, aging is apart of every living organisms’ life, and it always will be. Besides growing old as a downside itself, the real worry of aging is all of the diseases that you grow prone too. But what if there was a way to change that? What if there was a way to grow old healthily? In this blog post, I am going to be explaining how cellular modifications can potentially change the future of aging forever.

In order to understand how to prevent aging, we must understand how aging occurs in the first place. One of the main causes of aging roots from the mitochondria. The mitochondria is the source of energy for the cell and is responsible for cellular respiration. It also is independent from the cell, so it has its own DNA known as mtDNA. As time goes on, exposure to toxic products within the cell begins to cause the mitochondria’s DNA (mtDNA) to mutate. The build up of this mutation in mtDNA eventually causes the cell to function improperly, causing respiratory chain disfunction and many cell degenerative diseases. Common diseases due to mtDNA mutations are Parkinson’s disease, Alzheimers, and Huntington’s disease. Mitochondrial dysfunction can also lead to the damaging of nerve function- another side effect of old age. In our AP Biology class, we learned about the significant role the mitochondria has on cell function and how it came to be apart of the cell through the Endosymbiont Theory. This theory mentions the mitochondria’s own DNA, which we are diving into today to understand the effects of genetic mutation in the mitochondria and how we might combat it.

Mitochondrion (standalone version)-en

 

Professor and disease research specialist Ming Guo dives into how we can achieve healthier aging by combating mtDNA mutation. The only way to do this would be to rid the cell of mutant mtDNA and restore mitochondrial function. In order to understand how to do this, Guo conducts an experiment with Professor Bruce Hay involving fruit flies. Fruit flies share 80% of their disease genetics with humans, making them a viable option to begin testing on. Guo observed that by forcing the cell into autophagy, the cell will remove damaged cell parts and therefore restore proper cell function. By starving the cell, the cell is forced to eat damaged parts of itself, including mutated mitochondrial DNA, in order to survive. The term “autophagy” can be broken in to two terms: “auto” and “phagy”. “Auto” refers to “self” and “phagy” means “eat”. In essence, autophagy means, “self eating”, as seen through the cells digestion of its own damaged parts. This gets inevitably prevents mutations of the cell that damage cognitive function and mobility that usually come with old age. In our AP Bio class, we also discussed autophagy, or the removal of waste from a cell through the use of lysosomes.

The findings of this study shed light on how to counter mtDNA mutation through triggering cellular processes, such as autophagy, at a more efficient level than the cell previously had.  On average, triggering autophagy in a cell gets rid of 95% of its mutated mitochondrial DNA. Guo and Hay’s findings are only just the beginning. Now that it is understood how to prevent mitochondrial DNA mutation, scientists must discover specific drugs on how to activate the cellular processes in a way that is safe, easy to administer, and available to the public. The answer to healthy aging, and longer lasting cognitive function that goes with it, is just around the corner!

I chose this topic because aging is inevitable for everybody, therefore it is relevant to every single person. Also, being that my family has a history with age related diseases, this topic particularly interests me. Ever since I was a kid, I would hear things like “You’ll be able to live to 200 the way technology is advancing” all of the time. This discovery is a huge step on making that statement a reality. Hopefully aging will soon become a less dreadful concept and people will live to be happier and healthier.

 

 

 

 

Your Inner Chimpanzee

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On October 27, 2021

In Student Post

 

Chimpanzees

What is the closest living relative we have (evolutionary speaking)? That’s right, chimpanzees!! Our evolutionary paths separated us about five to six million years ago leading to the chimpanzee of today, and us humans of the 21st century, but we still have much in common. Like humans, Chimpanzees use body language to communicate. They often kiss, hug, pat each other on the back, hold hands and shake their fists. They even laugh when they get tickled. At the same time, a lot has also changed. Not only do we stand on two legs and are relatively hairless, but we also have brains that function differently. 

 

Recent research from Lund University has found the answer to what in our DNA makes our brains different. Created by Shinya Yamanaka, the study used a revolutionary stem cell technique. Yamanaka discovered that if reprogrammed specialized cells can be developed into all types of body tissue. It was even recognized by the 2012 Nobel Prize in Physiology or Medicine. 

 

The researchers used stem cells grown in a lab. Their partners in Germany, the US, and Japan reprogrammed the skin cells. Then Johan Jakobsson, professor of neuroscience at Lund University, and his partners examined the stem cells that they had developed into brain cells. Using the stem cells, the researchers specifically grew brain cells from humans and chimpanzees and compared the two cell types. The researchers then found that humans and chimpanzees use a part of their DNA in different ways. This appears to play a significant role in the development of our brains.

 

What the researchers learned was different in part of our DNA they and I found so unexpected. Unlike previous research in the part of the DNA where the protein-producing genes are — about roughly two percent of our entire DNA, the difference that was found indicated that the differences between chimpanzees and humans appear to lie outside the protein-coding genes. The research found that it is actually located a so-called structural variant of DNA in what has been labeled as “junk DNA,” a long repetitive DNA string that has long been deemed to have no function. This was thought to have no function. 

 

This data suggests that the basis for the human brain’s evolution is a lot more complex than previously throughout genetic mechanisms, as it was supposed that the answer was in that 2 percent of the genetic DNA. These results indicate that the overlooked 98 percent is what has been significant for the brain’s development is instead perhaps hidden in, which appears to be important. 

 

Researchers hope to answer that question one day. But there is a long way to go before they reach that point. The question that now remains is instead of carrying out further research on the two percent of coded DNA should they delve deeper into all 100 percent. Even though exploring the missed ninety-eight percent is a considerably more complicated task for research. 

 

One question that also definitely still remains is why did the researchers want to investigate the difference between humans and chimpanzees in the first place?  

 

Well, Johan Jakobsson believes that in the future the new findings will prove his belief that the brain is the key to understanding what it is that makes humans human. How did it come about that humans can use their brains in such a way that they can build societies, educate their children and develop advanced technology? It is fascinating!” (Lund University). He hopes that this research will contribute to answers about things like genetically-based questions about psychiatric disorders, such as schizophrenia. As for me, I wonder if this continued research will tell us anything about how Chimpanzees will evolve. 

 

 

Mutation in the Nation

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On January 12, 2021

In Student Post

We constantly think of SARS-CoV-2, the virus that causes COVID-19, as a single virus, one enemy that we all need to work together to fight against. However, the reality of the situation is the SARS-CoV-2, like many other viruses, is constantly mutating. Throughout the last year, over 100,000 SARS-CoV-2 genomes have been studied by scientists around the globe. And while when we hear the word mutation, we imagine a major change to how an organism functions, a mutation is just a change in the genome. The changes normally change little to nothing about how the actual virus functions. While the changes are happening all the time since the virus is always replicating, two viruses from anywhere in the world normally only differ by 10 letters in the genome. This means that the virus we called SARS-CoV-2 is not actually one species, but is a quasi-species of several different genetic variants of the original Wuhan-1 genome.

The most notable mutation that has occurred in SARS-CoV-2 swapped a single amino acid in the SARS-CoV-2 spike protein. This caused SARS-CoV-2 to become significantly more infective, but not more severe. It has caused the R0 of the virus, the number of people an infected person will spread to, to go up. This value is a key number in determining how many people will be infected during an outbreak, and what measures must be taken to mitigate the spread. This mutation is now found in 80% of SARS-CoV-2 genomes, making it the most common mutation in every infection.

Glycoproteins are proteins that have an oligosaccharide chain connect to them. They serve a number of purposes in a wide variety of organisms, one of the main ones being the ability to identify cells of the same organism.  The spike protein is a glycoprotein that is found on the phospholipid bilayer of SARS-CoV-2 and it is the main tool utilized in infecting the body. The spike protein is used to bind to host cells, so the bilayers of the virus fuse with the cell, injecting the virus’s genetic material into the cell. This is why a mutation that makes the spike protein more efficient in binding to host cells can be so detrimental to stopping the virus.

In my opinion, I find mutations to be fascinating and terrifying. The idea that the change of one letter in the sequence of 30,000 letters in the SARS-CoV-2 genome can have a drastic effect on how the virus works is awfully daunting. However, SARS-CoV-2 is mutating fairly slowly in comparison to other viruses, and with vaccines rolling out, these mutations start to seem much less scary by the day.

 

File:New COVID19 mutant.jpg - Wikimedia Commons

Diagram of the SARS-Cov-2 mutation

What is Nanotechnology, and How is it Transforming Vaccine Development for SARS-CoV-2?

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On December 30, 2020

In Student Post

1,000+ Free Covid-19 & Coronavirus Illustrations - PixabayCOVID-19 Spike Protein

In an era of mask-wearing and social distancing, the big question on everyone’s mind is when will things go back to normal? Scientists all over the world have been working quickly and intensely to develop a solution–one that is safe. 

Nanotechnology is the process of manipulating atoms and molecules on a microscopic scale. According to a UC San Diego ScienceDaily Article, scientists have been using this technique to design vaccine candidates for COVID-19. Nicole Steinmetz, a nanoengineering professor at UC San Diego, has been one such scientist. Instead of relying on older vaccine models, such as live-attenuated or inactivated strains of the virus itself, these “next-generation vaccines” are more stable, easier to manufacture, and easier to administer. 

Since June 1 of 2020, there have been more than one-hundred vaccines in play, with more than a few triumphing through clinical trials. Although many may be years away from deployment, the act of their development will prepare our nations’ leaders for future pandemics. 

There are three forms of these novel vaccines in the mix: peptide-based, nucleic-acid based, and subunit vaccines. All of these are alternatives to classic vaccines, which are slower to produce and sometimes pose the threat of inducing allergic responses.

scientist, microbiologist, virus, molecular biology, laboratory, coronavirus testing, COVID-19Vaccine Development

Peptide-Based Vaccines

Peptides are short chains made up of amino acid monomers. Simple and easily manufactured, peptide-based vaccines are typically made from VPLs, or virus-like particles, which come from bacteriophages or plant viruses. They are composed of peptide antigens, and mimic the patterns of pathogens, making those patterns visible to the immune system. However, they do not produce a strong enough immune response on their own, and thus must be accompanied by adjuvants.

Nucleic-acid Based Vaccines

In the midst of a fast-spreading pandemic, the world needs a vaccine that can be both developed and deployed rapidly. DNA and mRNA vaccines have this potential. DNA vaccines contain small, circular pieces of bacterial plasmids that are engineered to target the nucleus and produce parts of the virus’s proteins. They have a lot of stability, however, they also pose the risk of messing up a person’s pre-existing DNA, leading to mutations. In contrast, mRNA-based vaccines release mRNA into the cytoplasm, which the host cell then translates into a full-length protein of the virus. Because it is non-integrating, it does not have the same mutation risks as DNA-based vaccines.  

Subunit Vaccines 

Subunit vaccines have minimal structural parts of the pathogenic virus, meaning either the virus’s proteins or VLPs. These vaccines do not have genetic material, and instead, mimic the topical features of the virus to induce an immune response. 

The Power of Masks

Delivery Development

One of the most important aspects of a vaccine is accessibility and deployment. In the past, when dealing with live or inactivated vaccines, the lack of healthcare workers to administer the vaccines emerged as a significant concern. Yet, through nanotechnology, researchers have developed devices and platforms to ease these previous issues. They have created single-dose, slow-release implants and patches that can be self-administered, removing pressure from health care workers. Open reporting and the mass culmination of data has allowed for this rapid development of vaccine technologies. Because of these revolutionary advancements, some researchers optimistically predict that COVID-19 has the potential to become merely another seasonal flu-like disease over time.

What Lies Ahead

In these bleak times, it is promising to look at such amazing scientific developments. While a good portion of the general public feels skepticism towards the speed at which these COVID-19 vaccines are being produced, and thus claim they will not take it, I believe that the work of these scientists will not go to waste. As a nation, and as a global community, we will get past it, and come out stronger than ever on the other side. 

Now, ask yourself, would you take a COVID-19 vaccine? 

Shocking Connection Between Ancient Neanderthals and COVID-19

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On October 27, 2020

In Student Post

As stated in an article that details the shocking discoveries of an investigation led by Professors Svante Pääbo and Hugo Zeberg, genetic material from our neanderthal ancestors can be linked to the development of severe COVID-19. COVID-19, as I am sure you are all aware, is the disease ravaging the world and is caused by the newly

discovered coronavirus. While most people only have mild reactions to the disease and recover relatively easily, some people with underlying conditions may have a severe reaction to the disease and require hospitalization. However, this new study indicates that certain people may be genetically predisposed to a severe COVID-19 reaction, and it all links back to our 60,000-year-old Neanderthal ancestors.

The study that discovered this connection analyzed the genetic material of 3,000 patients who had both severe and mild COVID-19. The study identified a section of the chromosome that contained the genetic material responsible for the severe COVID-19. Chromosomes are tiny structures located in the nucleus of cells and these structures hold the genetic material that determines virtually everything about the cell. This genetic material is made up of nucleic acids that — when combined into a double-strand helix by covalent bonds between the phosphate, sugar, and base groups– create DNA. The order of the bases in the chain determines the amino acid sequence. We inherit our genetic material from our parents, and chromosomes are present in pairs, with one part of the pair inherited from each parent. This means that you hold genetic information from your earliest ancestors, which could potentially include Neanderthals. Neanderthals were archaic humanoids that were eventually assimilated into the homo sapien species.  However, cross-breeding was required to absorb the Neanderthals into our species, which means that most of the people alive today have a percentage of Neanderthal DNA. If a person holds one of the thirteen variants that are present in Neanderthal DNA, they are far more likely to have severe COVID-19.

Professors Pääbo and Zeberg proved this to be true by discovering that the Neanderthal variants distinctly matched the variants associated with severe COVID-19. However, they discovered that the genetic material only originated from Neanderthals located in southern Europe. Therefore, they concluded that when the Neanderthals of southern Europe merged with present-day people 60,000 years ago, they introduced the DNA region responsible for severe cases of COVID-19. Additionally, the people who possess these Neanderthal variants today are three times more likely to have severe COVID-19. The fact that I found the most interesting is how dramatically the presence of the variants vary in different parts of the world. For example, in South Asia, 50% of the population holds the variants, but in East Asia, almost nobody has them. I also think that it is rather tragic how genetic material that has not had any effect on the world for 60,000 years is just now becoming active. What do you think about this discovery? Why do you believe Neanderthal DNA is causing these extreme cases?

 

A Sweet Post About Sourdough!

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On October 25, 2020

In Student Post

When Covid-19 hit the US, some of the biggest quarantine coping mechanisms all revolved around a fan favorite carbohydrate: bread. With the copious amount of time on people’s hands, baking sourdough bread was the perfect activity.

Unlike any other bread, it’s hard to get the perfect tasting sourdough. Research has found that there are biological reasons behind sourdough bread and its taste, but before doing so, it’s important to learn what sourdough bread is made up of, and how it’s made. To help learn more about the process of making sourdough bread from scratch, I got a mini crash course from Little Spoon Farm. The starter (initial mixture) contains flour and water and sometimes salt, which will eventually grow into a diverse selection of microbes (these are tiny living organisms, which in this case are bacteria). The starter has to sit for 7-14 days, and within that time, the starter grows through the flour by eating the sugars within itself. With that growth comes bacteria/microbes and lactic acid, which eventually will allow the bread to be able to leaven in the oven.

Recent studies have shown that each starter is made up of different microbes. One study had 18 professional bakers from all around the globe make their sourdough, and send it to a lab in Belgium, where DNA sequencing was used to identify the microbes in the different starters. Although there were common yeasts and acids found like Saccharomyces cerevisiae and Lactobacillus, the strands and amount of each differed according to the starter. Another study done by Elizabeth Landis, at Tufts University, looked at 560 different starters submitted from all around the world. Through doing so, she found recurring microbe groups within these different sequences. There is still no definitive reason behind the microbe groupings, and why exactly they differ for each starter, but Landis mentioned that certain yeasts “specialize in feeding on distinct sugars,” due to the fact that they are made of different sugar mixtures. Some yeast also lack certain enzymes, which as we learned in class, help break down molecules. In this specific situation, the enzymes within different yeasts feed on and break down sugars. Differing yeasts could also be a reason why sourdough bread has different flavors. (Keep in mind that Landis’ findings are still under review, so there are still limited details on this experiment and not definitive reasoning).

Microbial ecologist, Erin McKenny, further elaborates on how “each microbial community can produce its own unique flavor profile.” For example, when more acetic acid is present in the starter, the bread will have a more sharp and vinegary taste. When the starter produces more lactic acid, it has a more sour and yogurt like taste. Metabolic byproducts within the starter could also potentially add to the complexity of the sourdoughs’ taste. In addition to each microbial community, scientists have identified other features that influence the taste of the bread like temperature. When lactic acid ferments in a warmer area, the bread has a more sour taste, and when it ferments in a colder area, the bread has a more fruity taste.

After looking at multiple articles showing how bakers get their sourdough to have a certain taste, I have learned how important the specifics are when it comes down to making sourdough. One article that gave tips on how to manipulate the taste of sourdough reinforces everything that the main article helped explain, and talks about the importance of keeping a warmer, dry climate to ensure that the bread tastes sour. It turns out that a quarantine treat may be a bit more complex than it appears. It’s interesting to see how biology plays a key role in one of the most prominent foods, and next time you consider making sourdough or get a bread basket from the Cheesecake Factory, you’ll now know the biology behind it.

Some People Can’t Smell Stinky Fish?!

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On October 19, 2020

In Student Post

A New York Times article has just reported a new “mutant superpower.” In Iceland, a brand new genetic trait was discovered, in which 2% of the population can’t smell the stinky odor of fish. 

A study of 11,326 Icelanders was conducted, in which each participant was given six “Sniffin’ Sticks (pens imbued with synthetic odors)” of cinnamon, peppermint, banana, licorice, lemon, and fish. The participants were then asked to identify the odors based on how strong each smell was and how good each Sniffin’ Stick smelled. Across the majority, the fish was rated the lowest in pleasantness. However, a small group of people actually enjoyed the scent, noting that it smelled like caramel or even a rose. 

This small group of participants was discovered to have a genetic mutation that enables the TAAR5 gene to form. TAAR5 (Trace Amine Associated Receptor 5) aids in making proteins that recognize trimethylamine (TMA), a chemical found in rotten and fermented fish, and some bodily fluids, including sweat and urine.  TAAR5 is also a G Protein, meaning that it binds guanine nucleotides. And, like other coding proteins, TAAR5 is a quaternary structured protein that has three subunits. Because this protein is incapable of binding guanine nucleotides, it means that there will be at least one “broken” copy of the gene that codes for the inability to smell fish. 

To simplify: TAAR5 recognizes the chemical of smell in fish (TMA), however, with the mutation that prevents the TAAR5 from forming, the smell of fish (TMA) is unrecognizable.

Interestingly, research has shown that this mutation may be a reaction to the customs of Iceland and a possible next step in the evolution of the region. In Iceland, fish takes a prominent place on most menus including dishes like “rotten shark.” These cultural and possibly smelly dishes may explain why this mutation is much more prominent in Iceland compared to Sweden, Southern Europe, and Africa (where the study was repeated). Bettina Malnic, an olfaction expert at the University of Sao Paulo in Brazil, commented on the luck of the region study took place, saying, “if they hadn’t looked at this population, they might not have found the variant [of TAAR5].”

I am VERY sensitive to smell and, at the same time, a lover of sushi, so it definitely fascinates me that there are people out there who don’t have to deal with the odor of smelly fish. This mutation is definitely one I wish I obtained. What do you think about this? Do you think you could have this mutation?!

 

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