BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: genetics (Page 1 of 4)

Are You Predisposed to Being Overweight? New Genetic Variations Say Yes.

Recent studies composed by researchers from the Spanish National Cancer Research Centre and the IMDEA Food Institute show that people with a specific variation or version of a gene crucial to cell nutrition tend to accumulate less fat. This means that those with a particular change or alteration in this gene may be inclined to store less fat in their bodies. Prior research has shown that genetics only play a role in 20% of our body weight for the general population. This means that other external factors such as diet, exercise, and overall lifestyle have much more of an impact on body weight.

Past research has identified nearly 100 genetic variants which slightly increase one’s likelihood of having a high BMI. This new research identifies one additional variant. Typically genetic variations are only slightly different versions of a gene and often do not result in visible changes. But, this new variation challenges this idea. It affects the amount of fat the body stores, something which can strongly alter one’s physical appearance. What’s more, the researchers of this gene have found that it is more prevalent in Europe with just under 60% of the population having it.

Ácido desoxirribonucleico (DNA)

 

According to Alejo Efeyan, the head of CNIO’s Metabolism and Cell Signalling Group, the new research can help us to further understand the role which genes play in obesity, body weight, and fat accumulation. Efeyan says, “the finding is a step forward in the understanding of the genetic components of obesity.” Additionally, Ana Ramirez de Molina, the director of the IMDEA Food Institute, claims that a key understanding of cell pathways regarding cell nutrition may affect and spur the creation of not only obesity prevention but also personalized treatments. Essentially, understanding the new gene can help us to target obesity and body weight on an individual level rather than the population as a whole. She believes, “a deep knowledge of the involvement of the cellular nutrient-sensing pathway in obesity may have implications for the development and application of personalized strategies in the prevention and treatment of obesity.”

To find and research the genetic variant which influences fat storage and obesity a team from the IMDEA Food institute collected a variety of data from 790 healthy volunteers. This included body weight, muscle mass, genetic material, and more. The researchers found a “significant correlation between one of these variants in the FNIP2 gene and many of these obesity-related parameters.” Essentially their research proved that there is a connection between the specific gene and factors of obesity. The study has also been published in the scientific journal of Genome Biology. Although this gene may play a role in keeping body fat storage lower than others, it is important to note that it is not entirely a preventative measure against obesity or fat gain. Efeyan clarifies, “It is not at all the case that people with this genetic variant can overeat without getting fat.”

The genetic variation is present in a gene that specifically partakes in a signaling pathway that tells the cell what nutrients are available and needed. The gene signals to the cell what nutrition is necessary at a given moment. In our AP Bio class, we learned the intricacies of cell communication; how and why it can occur, the stages of it, and even the differences in the distances of communication. Connecting back to our AP Bio class, I wonder whether the gene interacts in an adjacent, paracrine, or long-distance manner. Also, how the distance can affect the communication of the gene to the cell regarding cell nutrition. We also learned about how genes in the nucleus of our cells can code for specific factors in our bodies and how they are a sort of ‘instructions’ for us to carry out. This connects to the research as we can see that a change in a gene can alter our body’s fat storage and connection to obesity. The genetic variation changed the ‘instructions’ for weight, fat storage, and obesity disposition. Additionally, the research stated that 60% percent of Europeans have genetic variation, I wonder what may have caused this. Was it a result of their diets, lineage, geography, or just a scientific anomaly? I invite any and all comments with a perspective and an idea as to what may have caused this, along with any comments regarding this research as a whole.

Obesity-waist circumference

 

 

COVID-19 on the Genetic Level

Similar to any other virus, the symptoms of COVID-19 are amplified in patients who are of old age, have additional complications, or are unvaccinated. For instance, researchers found that unvaccinated individuals ages 50 and older are 12 times more likely to die from COVID-19 than individuals who are vaccinated with boosters (Hesman Saey). Additionally, cancer patients, especially those who are immunosuppressed, are at a higher risk of facing the serious impacts of COVID-19. Research suggests that baseline immunosuppression increases the risk of a cytokine storm. Cytokine storms result in extreme immune responses towards a pathogen which can result in harmful conditions for the body or inSARS-CoV-2 without background​​​ some cases death. 

These factors play an important role in the severity of COVID-19, however, there are still some severe cases that are unaccounted for. Throughout the COVID-19 pandemic, one question that has perplexed many scientists is: why do certain healthy patients contract severe cases of COVID-19 while others merely experience the symptoms of the common cold? Recent research has found that genetics may be the answer. Studies have revealed that genes passed down from our ancient ancestors can both help and hurt individuals infected with COVID-19. A global study that took DNA samples from 28,000 patients infected with Covid-19 and about 600,000 healthy patients confirms this theory.

The two main genes taken i3D Structure of Legumin Proteinnto account are toll-like receptor 7 (TLR7) and TYK2. Variants in these genes are what can control the severity of a COVID-19 case. TLR7 is a gene whose protein is responsible for initiating an immune response by sending signals to other cells that a pathogen has invaded the body. If this process is not operating correctly, it is more difficult for the body to defend against a virus. So, if SARS-CoV-2 enters the body, a variation in TLR7 can cause a more severe case of COVID-19. TYK2 is responsible for producing interferons. A variation in TYK2 can cause an overproduction of interferons. When there is a virus present, such as SARS-CoV-2, the production of interferons can be helpful in the body’s defense. 

The processes impacted by TRL7 and TYK2 directly relate to the body’s innate immune process. Innate immunity is the body’s first line of defense once a virus has passed through our innate immune system. The innate immune process involves mast cells which release histamines and macrophages which release cytokines. Interferons work in a similar way. All parts of innate immunity are focused on keeping the pathogen from advancing. Cell signaling is central to innate adaptive immunity, so any alterations in it would result in a less effective defense and therefore a more severe case of COVID-19. 

I found this COVID-19 study to be intriguing because this past January a few members of my household were infected with COVID-19. However, only one experienced extreme symptoms. Since all were vaccinated, it may be possible that the alterations in TLR7 and TYK2 are the reason for the differences in reactions among my family.

Would You Have Survived the Black Death?!?!

New research from McMaster University, the University of Chicago, the Pasteur Institute, and other organizations suggests that during the Black Death, 700 years ago, there were select individuals whose genes actually PROTECTED them from the devastating population-crushing Bubonic Plague.

Model of bubonic plague bacteria - Smithsonian Museum of Natural History - 2012-05-17

The Bubonic Plague, later nicknamed the Black Death after many realised people would develop blackened tissue on their body postmortem, due gangrene(the death of tissue due to lack of blood flow). “It remains the single greatest human mortality event in recorded history, killing upwards of 50 per cent of the people in what were then some of the most densely populated parts of the world.” (ScienceDaily.com)

The team researching this genetic phenomena collected DNA from the deceased 100 years before, during and after the Black Death. They collected samples from the greater London area, as well as some parts of Denmark to accurately represent Upon searching for evidence of genetic adaptation, they found 4 different genes prevalent in the pandemic survivors, all of which are protein-making genes that are used in our immune systems, and found that versions of those genes, called alleles, either protected or rendered one susceptible to plague. We in AP Biology will soon learn more about alleles in higher depth, for they are imperative in the genetics of almost every DNA-carrying organism’s survival.

People with two identical copies of a gene named ERAP2 were able to survive the Black Plague at significantly higher rates than those who lacked that specific gene. “When a pandemic of this nature …  occurs, there is bound to be selection for protective alleles in humans … Even a slight advantage means the difference between surviving or passing. Of course, those survivors who are of breeding age will pass on their genes”.- evolutionary geneticist Hendrik Poinar. Mr. Poinar’s analysis of this research poses a unique and interesting question. Does the natural selection that occurred during the Bubonic Plague mean that you and I have a higher chance of having this gene in our DNA? If another plague with a similar biological makeup to the Black Death, would our bodies be better suited to find it?

Scientists Discover Super-Protein Involved in Gene Replication

For over 50 years, it has been believed all factors that control gene activation in humans were identified and known to scientists. However, researchers from the University of California San Diego and Rutger’s have proved this theory wrong. 

Collegiate professors, and now pivotal contributors to modern science Dr. Jia Fei and James Kadonaga, have discovered a new protein that is involved in the regulation of RNA polymerase. Called NDF (nucleosome destabilizing factor), this gene-building molecule not only unravels nucleosomes, but also “turbocharges” RNA polymerase as it works its way along the DNA strand, improving the synthesis of replicating RNA.

But that’s not all this protein has to offer: NDF has also been found to be in an array of species and organisms, ranging from yeast particles to mammals. This widespread presence suggests that NDF is an ancient factor in the process of gene activation, and has been here since the very beginning. 

NDF works by first interacting with nucleosomes in cells, and then goes on to facilitate transcription– in other words, to replicate strands of RNA. Enzymes called RNA polymerases then come into play, and copy the RNA via dehydration synthesis. This process includes removing oxygen molecules and hydroxides from each nucleotide to covalently bind them together, producing a waste product of water molecules and, finally, a copy of the RNA strand. 

While this newly discovered protein is crucial for the elongation of RNA strands in many organisms, it is especially abundant in humans. Kadanoga reports that it is “present in all [our] tissues,” particularly in stem and breast cells. This makes sense, as NDF has actually been linked to breast cancer; Abnormally high levels of this protein lead to hyperactivity in gene synthesization, which increases the chance of a mutation occurring, and thus cancer. 

With all the remarkable characteristics of NDF, it is crucial that scientists today continue to explore the capabilities and effects of this gene-activating protein, and use it as a basis for studying diseases and phenomenons that occur in the process of gene replication.

RNA recognition motif in TDP-43 (4BS2)

Depiction of RNA strand.

CRISPR Mini | New Territory Unlocked

For over a million years, DNA has centered itself as the building block of life. On one hand, DNA (and the genes DNA makes up) shapes organisms with regard to physical appearance or ways one perceives the world through such senses as vision. However, DNA may also prove problematic, causing sickness/disease either through inherited traits or mutations. For many years, scientists have focused on remedies that indirectly target these harmful mutations. For example, a mutation that causes cancer may be treated through chemotherapy or radiation, where both good and bad cells are killed to stop unchecked cell replication. However, a new area of research, CRISPR, approaches such problems with a new perspective.

The treatment CRISPR arose to answer the question: what if scientists could edit DNA? This technology involves two key components – a guide RNA and a CAS9 protein. Scientists design a guide RNA that locates a specific target area on a strand of DNA. This guide RNA is attached to a CAS9 protein, a molecular scissor that removes the desired DNA nucleotides upon locating them. Thus, this method unlocks the door to edit and replace sequences in DNA and, subsequently, the ways such coding physically manifests itself. Moreover, researchers at Stanford University believe they have further broadened CRISPR’s horizon with their discovery of a way to engineer a smaller and more accessible CRISPR technology.

This study aimed to fix one of CRISPR’s major flaws – it is too large to function in smaller cells, tissues, and organisms. Specifically, the focus of the study was finding a smaller Cas protein that was still effective in mammalian cells. The CRISPR system generally uses a Cas9 protein, which is made of 1000-1500 amino acids. However, researchers experimented with a Cas12f protein which contained only 400-700 amino acids. Here, the new CasMINI only had 529 amino acids. Still, the researchers needed to figure out if this simple protein, which had only existed in Archaea, could be effective in mammals that had more complicated DNA.

To determine whether Cas12f could function in mammals, researchers located mutations in the protein that seemed promising for CRISPR. The goal was for a variant to activate a protein in a cell, turning it green, as this signaled a working variant. After heavy bioengineering, almost all the cells turned green under a microscope. Thus, put together with a guide RNA, CasMINI has been found to work in lab experiments with editing human cells. Indeed, the system was effective throughout the vast majority of tests. While there are still pushes to shrink the mini CRISPR further through a focus on creating a smaller guide RNA, this new technology has already opened the door to a variety of opportunities. I am hopeful that this new system will better the general well-being as a widespread cure to sickness and disease. Though CRISPR, and especially its mini version, are new tools in need of much experimentation, their early findings hint at a future where humans can pave a new path forward in science.

What do you think? Does this small CRISPR technology unlock a new realm of possibility or does it merely shed light on scientists’ lack of control over the world around us?

Unnatural Selection: The Future of The Future?

Imagine it’s Saturday night, you are snowed in until the morning and you need a way to pass the time. Like many people, you resort to Netflix. Upon browsing through the vast selection of horror, comedy, and romantic films, you decide you are in the mood for a documentary. Scrolling through the options, you stop at a title that grabs your attention: Unnatural Selection.

Since you are an AP Biology student, you immediately connect the words “Natural Selection” to the work of Charles Darwin, the study of genetics, and most importantly: evolution. In brief, natural selection is the survival and reproduction of the fittest, the idea that organisms with traits better suited to living in a specific environment will survive to reproduce offspring with similar traits. Those with unfavorable traits may not be able to reproduce, and therefore those traits are no longer passed down through that species. Natural selection is a mechanism for genetic diversity in evolution, and it is how species adapt to certain environments over many generations.

If genetic diversity enables natural selection, then what enables unnatural selection? Well, If natural selection eradicates unfavorable traits naturally, then unnatural selection essentially eradicates unfavorable traits or promotes favorable traits artificially.

The Netflix docuseries “Unnatural Selection” focuses on the emergence of a new gene-editing technology named CRISPR (an acronym for “Clustered regularly interspaced short palindromic repeats”). CRISPR is a revolutionary new method of DNA editing, which could help cure both patients with genetic diseases and patients who are at risk of inheriting unwanted genetic diseases. The two pioneers of this technology, Emmanuelle Charpentier and Jennifer Doudna, recently won Nobel Prizes in Chemistry for their work on CRISPR.

CRISPR illustration gif animation 1

Animation of CRISPR using guide RNA to identify where to cut the DNA, and cutting the DNA using the Cas9 enzyme

CRISPR works with the Cas9 enzyme to locate and cut a specific segment of DNA. Scientists first identify the sequence of the human genome, and locates a specific region that needs to be altered. Using that sequence, they design a guide RNA strand that will help the Cas9 enzyme, otherwise known as the “molecular scissors” to locate the specific gene, and then make precision cuts. With the affected region removed, scientists can now insert a correct sequence in its place.

Using the bacterial quirk that is CRISPR, scientists have essentially given anyone with a micropipette and an internet connection the power to manipulate the genetic code of any living thing.

Megan Molteni / WIRED

CRISPR is just the beginning of gene editing, introducing a new field of potential gene editing research and applications. But with great power comes great responsibility — and great controversy. Aside from the obvious concerns, people speculating the safety, research, and trials of this new treatment, CRISPR headlines are dominated by a hefty ethical dilemma. On one hand, treating a patient for sickle cell anemia will rid them of pain and suffering, and allows their offspring to enjoy a normal life as well. However, by eliminating the passing down of this trait, sickle cell anemia is slowly eliminated from the human gene pool. Rather than natural selection choosing the path of human evolution — we are. We are selecting which traits we deem “abnormal” and are removing them scientifically. Although CRISPR treatment is intended to help people enjoy normal lives and have equally as happy children, putting evolution into the hands of those evolving can result in more drastic effects in the future.

For our generation, CRISPR seems like a magical cure for genetic diseases. But for future generations, CRISPR could very well be seen as the source of many problems such as overpopulation, low genetic diversity, and future alterations such as “designer babies.” Humans have reached the point where we are capable of our future. Is CRISPR going to solve all of our problems, or put an end to the diverse human race as we know it? Comment how you feel down in the comments.

 

Paving The Way For Discovery: Gene Editing In Ticks

What is something that reminds you of summer and your childhood? For me, it is ticks. I know it sounds strange, but the constant reminders from my parents to “check for ticks” after long summer walks are ingrained in my memory. Although the practice of checking for ticks is common, we don’t often stop to question why, or take a moment to expand our knowledge as to just how dangerous a summer walk in long grass could be. Ticks, although tiny, are powerful, disease ridden organisms and have the potential to spread diseases to humans such as Lyme’s disease, Babesiosis, Anaplasmosis, Tularemia, etc. 

tick

Despite their ability to pass on such a vast variety of pathogens, research on ticks is extremely limited, especially in comparison to similar organisms like mosquitoes. The challenge when it comes to gene editing in ticks is that tick embryos are very difficult to inject due to high pressure in the eggs, a hard outer shell on the egg, and a wax layer outside the embryo created by Gene’s organ. In a recent study published in iScience, researchers developed a tick-embryo injection protocol that aimed to target gene disruption with CRISPR-Cas9 (using both embryo injection and Receptor-Mediated Ovary Transduction of Cargo. In this technique, researchers removed Gene’s organ to prevent the wax coating along with treating the eggs with chemicals such as benzalkonium chloride and sodium chloride to remove the outer shell and relieve the inner pressure. Gulia-Nuss, the co-author of the study and a molecular biologist at the University of Nevada, states: “Another major challenge was understanding the timing of tick embryo development. So little is known about tick embryology that we needed to determine the precise time when to introduce CRISPR-Cas9 to ensure the greatest chance of inducing genetic changes.”

Essentially, the CRISPR-Cas9 system consists of two main molecules that introduce a mutation to the DNA. The first is an enzyme known as Cas9. The function of this enzyme is to cut the strands of DNA at a specific location in order for pieces to be added or removed. As we learned in AP Bio, enzymes are key when it comes to DNA and DNA replication, for they play a variety of roles that allow DNA to replicate the way it does. For example, helicase untwists the double helix at the replication fork, topoisomerase relieves the strain of twisted DNA strands by breaking and rejoining them, and primase synthesizes short RNA strands that act as a primer. Without these enzymes and their very specific purposes, DNA would not be able to replicate. In the case of Cas9, it performs the essential job of cutting DNA in order for gene editing to occur. The second piece of the system is a piece of RNA called guide RNA. The guide RNA binds to a specific sequence in the DNA due to its RNA bases that are complementary to those of the DNA sequence. 

Prior to this study, no lab had displayed the possibility for gene editing in ticks, due to the daunting technical difficulties of such a task. This study is proof to embrace the difficulty and the challenges, in life and in science, for often the most difficult of tasks lead to the greatest outcome. In the case of this study, the discovery of ways in which to target the disruption of genes in ticks will pave the way to the uncovering of the molecular biology of tick-pathogen-host interactions, hopefully in the long run creating ways to prevent and control tick-borne diseases, a process that has the potential to save lives.

Do Genetics Play A Role In Attraction?

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.

How are new COVID variants identified?

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.

Spotlight: Sharon Strauss and Evolution of Organisms in Barren Habitats

Sharon Strauss is an evolutionary ecologist at the University of California, Davis (UC Davis) where she has been conducting research on the evolution of plants and the ways in which they interact with other species. As a woman in a STEM environment, Strauss has faced opposition due to her gender. It took her 5 years longer than the regular time trajectory to obtain a job in her field, subtle obstacles such as invitations to work with groups, and also simply not being taken seriously or personally asked to contribute to group conversations. Although she has faced challenges, Strauss has done phenomenal research on the ecology and evolution of plants and her efforts, both her research and her job as a professor, have been rewarded.

One of her largest and most well known projects was called Nowhere to run, nowhere to hide. During this project, she and her team were studying how wildlife adapted to a barren environment. During this expedition, Strauss and her team explored the possible connection between attack rates and visibility. They followed 160 seedlings of a few different species from the genus Streptanthus and observed how they grew and what their current condition was depending on the amount of bare ground and leaf coloration. Additionally, they formed small clay models of caterpillars to act as an undefended population of prey in order to measure attack rates on visible animal species. They measured this by checking the area around the caterpillars to see if there were beak or tooth marks of a predator attempting to eat it. Strauss was able to conclude that attacks on both animals and plants were connected to how apparent or visible they were in their environment. For this reason, certain plants and animals had adapted by changing their color in order to blend into their barren environment.

Since this project mainly involved studying adaption and evolution, it is not very similar to anything we have learned in class yet. However, there is a connection between evolution and genes, which we are currently learning about. Every organism that sexually reproduces passes genes down to their offspring via the sperm and the egg. The physical features of the offspring are determined by the genes they are composed of. Typically, these genes are passed down by the parents to the offspring; however, it is also possible for an error in DNA replication to occur or exposure to chemical or radiation damage that can cause a mutation. This connects to evolution since there will always be variety within a population. A certain trait could prove to be more successful in survival than another so gradually, over many generations, that trait will be passed down since the members of the population that have that gene have a higher chance at surviving and reproducing as proposed in Darwin’s Theory of Evolution.

I admire the hard work and the effort that Sharon Strauss has put into her career and passion to get where she is now and to have achieved what she has. Despite the barriers that were placed in front of her, she continued on since biology was her passion. I also have a passion for biology, specifically zoology, and as a girl, I may face similar obstacles. Even if I change my mind or find a new passion, I hope to carry the same spirit that Sharon Strauss did to push through any barriers that I may face.

Melanin: Breaking Down Barriers

In a post written by Susan Eckert (teacher) and Shannon Huhn (student), the complex and complicated construct of race is broken down to reveal the true essence of society: genetics and the genetics of the skin. 

Skin is one of the most important parts of our body. Firstly, as we studied in our immune system unit, we know that the skin protects us from sickness and from possible foreign invaders through the non-specific/innate bodily response. Specifically, however, our skin protects us from damage caused by UV light all because of melanin. 

Although we may be familiar with this term as it is oftentimes involved in the conversation of race, research shows that the concept of race is not actually backed by science and the genetics of melanin. Before we can get into this conversation, we must learn about the science behind melanin. Importantly, our bodies contain cells called Melanocytes that produce the pigment called melanin. Through the process of melanogenesis, tyrosine is oxidized, which as we know from class means that it is losing electrons, and enzymes are utilized to produce two kinds of melanin: eumelanin which causes the skin to be dark, and phaeomelanin which causes the skin to be light. Although all of our bodies have the same amount of melanocytes, our skin color is determined by how much eumelanin and/or phaeomelanin is produced. 

 

With this knowledge, it is easier to engage in conversation on race. Throughout history, skin color has been used to fuel general racial inequalities. Darker skin, whose genetic purpose is to be able to absorb more light, has been wrongfully associated with inferiority while lighter skin, whose genetic purpose doesn’t involve absorbing a lot of light, has been associated with superiority, both based on the grounds of their appearances. Making these assumptions based solely on the physical color of the skin without acknowledging or thinking about the explanatory science should automatically negate these wrongful and incorrect accusations. According to Tiskoff and Kidd, “Humans are ∼98.8% similar to chimpanzees at the nucleotide level and are considerably more similar to each other”. Of course, we must take into consideration the confidence level and margin of error in this statistic, but nevertheless, the percentage is high, showing that race doesn’t make one inferior/superior as we are all essentially the same except for minor genes which produce specific skin colors. In general, it comes down to the production of pigments all based on necessary function.

We must combine what we know about melanin, genetics, skin, and race to move forward in our society. Although all are socially and genetically unique, we are all human on a genetic and molecular level. Conducting research and getting down to the science of various topics carries the necessary substantial weight to create change. What would you like to research next?

Mutation in the Nation

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.

 

Mice Maintain Muscle in Microgravity

Scientists recently found a molecule that can maintain, and even augment, the muscle mass and bone density of space-faring mice.

That might sound irrelevant (why would mice need to maintain muscle mass in space?), but this could actually help astronauts with a common problem with space travel. Astronauts in space must exercise regularly and intensely to avoid muscle atrophy; due to the microgravity, astronauts have little regular physical exertion and quickly lose muscle mass otherwise. Studies have shown that space journeys as brief as 5 to 11 days lead to a 20% loss of muscle mass for astronauts. The calf muscles, quadriceps, and back and neck muscles (which can be collectively termed antigravity muscles) require minimal contraction for astronauts to move around in space, allowing the muscles to weaken rapidly.

Muscle atrophy isn’t only a problem for astronauts, though. Others to benefit from this research could include “people who are bedridden or in a wheelchair, as well as people with cancer, chronic obstructive pulmonary disease or other causes of muscle wasting.” 

The main focus of this study was the gene myostatin, common to various species, including mice, cattle, and humans. Myostatin plays a role in both the number of muscle fibers in the developing animal and the level of fiber growth in the adult stage, negatively regulating muscle growth in species from dogs to humans. Several studies have shown that myostatin inhibition can help with disorders that cause wasting of the muscles by increasing muscle mass. Some evidence even suggests that myostatin inhibition might increase muscle strength as well. This study, however, targeted a different cause of muscle atrophy.

Study author Se-Jin Lee eliminated the myostatin gene from mice, allowing them to achieve double the muscle mass of regular mice. In December 2019, the mice were launched on a SpaceX craft from Florida’s Kennedy Space Center for a 33 day space journey. In contrast to the normal mice, that lost muscle mass, the myostatin-inhibited mice maintained their augmented muscle mass.

On the left, a regular mouse, and on the right, a myostatin inhibited mouse with about double the muscle mass.

Of course, eliminating the gene from human astronauts is not a feasible approach. To better model a treatment that could be applied to humans, Lee’s team came up with a solution to inhibit myostatin’s expression. Myostatin prohibits growth by attaching to a specific receptor on muscle cells. To prevent this binding, the researchers came up with a molecule that was a “decoy” receptor to be injected into the mice’s bloodstreams, capturing myostatin proteins and activin A proteins, which prevent both muscle and bone growth. The unique chemical structure and folding of the receptor allows it to bind to these two proteins for this effect, and as we learned in class, the shape is very important to the functionality. The mice in the International Space Station injected with this molecule experienced bone and muscle growth while still in space. The treatment also recovered bone and muscle mass for untreated mice landing from space.

Treatments inspired by this research could hopefully be used to help astronauts maintain bone density and muscle mass in space. Though myostatin inhibition alone has not proven effective in humans, such a treatment that inhibits other proteins, like activin A, as well may be plausible.

The Problems with Ancestry Tests (23andMe, Ancestry.com, etc.)

Over the past five years or so, ancestry and DNA tests have risen in popularity due to people’s desire to find out what medical conditions they are at risk for, or where their ancestors are from.  The most common concern I have heard about as a result of these tests was that the companies would sell your DNA to third parties or the government (while there is a chance this could be true this will not be the focus of this article).  However, the true problems are not conspiracy driven, yet they are scientifically driven and verifiably true.

Many people using these tests do not realize how these tests actually work and the wrong information they present at times.  The first issue resides in the health screenings of these ancestry tests.  They claim to use your ancestry to see if you are at risk for Alzheimers, certain types of cancer, Parkinson’s, or what type of body type you have.  These companies are not completely lying, however the tests can omit certain things and it is no substitute for going to an actual doctor.

Everything they search for is compared to a reference population, therefore your genes are merely compared to other people who are considered healthy or unhealthy.  These tests do not have access to medical history in order to look for other clinical factors that could accelerate or further exacerbate this potential condition, thus explaining why it is irresponsible to tell people they are at risk for a debilitating disease because someone with similar genetics reported developing a disease that could have resulted from his or her specific lifestyle.

The issue with self-reporting in ancestry tests also can be seen in testing for heritage.  The data these companies use are based off of reference populations (many of which are self-reported especially in the early years of the tests), therefore the same person can receive different results at different times.  The database is constantly changing (which isn’t necessarily only a bad thing) so if the same person takes the test three times in three different years, they are likely to get different results.  If the company recently expands to selling DNA kits in a new area of the world, a person with mixed heritage from the United States can receive different results because the test population of a certain region was extremely small and unspecific before, whereas now they have more of a test population that can change “how Vietnamese you are” (or whatever region that applies to you).

Have you ever known someone who took the DNA test and found out they were not as Greek or Russian (insert anything) as they thought they were? These results are problematic on so many levels when breaking down ancestry.  The first example is that when comparing extremely similar populations, your heritage might not reflect your ancestry that the test finds.  For example: modern English, Scottish, and Irish people have vastly similar results in these tests because they are very similar genetically and geographically, therefore a person can find out they are 50/50 Irish and English, however all of their known relatives can be traced back to 1870s Ireland.  The person is not “less Irish than they thought”; it merely means that centuries of migration and conquering in the region of the British Isles could blend the gene pools even if this person’s family tree of the last two-hundred years can be traced back to one specific town.

Something else important to consider is that ancestry and heritage are not nearly synonymous terms.  Furthermore, two twins could receive different genes from the same parents which could lead to slight changes in genetic makeup.  Your sibling is not “more Swedish than you” in terms of heritage and the culture you were raised in.  The sibling might receive a certain gene from your parents that you did not.

While there are a myriad of problems and hypotheticals to bring up, I will leave you with one last problem. Groups of people that live in diaspora such as Jews, Romani, and Armenians could have problems with these tests.  Ashkenazi Jews from Eastern Europe live in diaspora and have been a migratory group for centuries, leading them to mix in with various gene pools that they settle in.  When an Ashkenazi Jew or Romani (who similarly lived a migratory history) takes an ancestry test, they could feel completely related to their Ashkenazi or Romani heritage, however the intermixing of people over centuries (because they settled in so many places) could come up in the test even though they feel like they have no relationship to the heritage at all.  Romani people also are difficult to pinpoint to one specific region of origin which demonstrates another potential problem with the tests.

While these tests can be a fun activity to do with your friends, make sure you take the results with a grain of salt because you are not necessarily  “less French than you thought”.

 

Does Exposure to Toxins In the Environment Affect One’s Offspring’s Immune System?

A study has recently surfaced stating that maternal exposure to industrial pollution may harm the immune system of one’s offspring and that this impairment is then passed from generation to generation, resulting in weak body defenses against viruses.

Paige Lawrence, Ph.D., with the University of Rochester Medical Center’s Department of Environmental Medicine, led the study and conducted research in mice, which have similar immune system functions as humans. Previously, studies have shown that exposure to toxins in the environment can have effects on the respiratory, reproductive, and nervous system function among generations; however, Lawrence’s research is the first study to declare that the immune system is also impacted.

“The old adage ‘you are what you eat’ is a touchstone for many aspects of human health,” said Lawrence. “But in terms of the body’s ability to fights off infections, this study suggests that, to a certain extent, you may also be what your great-grandmother ate.”

“When you are infected or receive a flu vaccine, the immune system ramps up production of specific kinds of white blood cells in response,” said Lawrence. “The larger the response, the larger the army of white blood cells, enhancing the ability of the body to successfully fight off an infection. Having a smaller size army — which we see across multiple generations of mice in this study — means that you’re at risk for not fighting the infection as effectively.”

In the study, researchers exposed pregnant mice to environmentally relevant levels of a chemical called dioxin, which is a common by-product of industrial production and wast incineration, and is also found in some consumer products. These chemicals eventually are consumed by humans as a result of them getting into the food system, mainly found in animal-based food products.

The scientists found the production and function of the mice’s white blood cells was impaired after being infected with the influenza A virus. Researchers observed the immune response in the offspring of the mice whose mothers were exposed to dioxin. Additionally, the immune response was also found in the following generations, as fas as the great-grandchildren (or great- grandmice). It was also found that this immune response was greater in female mice.  This discovery now allows researchers to have more information and evidence to be able to more accurately create a claim about this theory.

As a result of the study, researchers were able to state that the exposure to dioxin alters the transcription of genetic instructions. According to the researchers, the environmental exposure to pollutants does not trigger a genetic mutation. Instead, ones cellular machinery is changed and the immune response is passed down generation to generation. This discovery explains information that was originally unexplainable. It is obviously difficult to just avoid how much toxins you are exposed to in the environment, but it is definitely interesting to see the extent of the immune responses in subsequent generations. We can only hope that this new information, and further discoveries, help people adjust what they release into this world that results in these harmful toxins humans are exposed to, and their offsprings.

 

 

 

Is Training Your Dog Useless?

For about 100 years, humans have been trying to train the domestic animals, such as dogs, that they live with. They put in lots of time and effort for teach their dogs simple tricks such as sitting, lying down, and staying in place. While it is rewarding to have a dog listen to commands after teaching and training them, this may not as great of an accomplishment as previously thought. As a dog owner myself, this had me worried, but as a recent ScienceNews post says, the answer to how to train a dog may just lie in their genetics. 

Training Dogs May Be an Outdated Practice

This was the hypothesis that Noah Snyder-Mackler had as he and a few other colleagues from the University of Washington in Seattle attempted to prove its legitimacy. Primarily, the group collected data about 101 different breeds of dogs from two dog genotypes databases and a survey titled C-BARQ, a survey where dog owners submit information about behavior from their dogs such as aggressiveness or ability to listen. As the data came in, there were over 14,000 submissions and they were all scored on 14 different traits. Overall, Snyder-Mackler and his group found that poodles and border collies had higher traits of trainability and Chihuahuas and dachshunds had higher traits of aggressiveness. However this does not means that training a dog is rendered useless since there was about a small correlation, 50%, between energy level and fearfulness.

Aggression Could Have Been Caused from Genetics

Next the researchers tried to see if certain traits correlated with certain genes. After doing more research they found that no genes specially aligned with a breeds behaviors, but this does not mean that the research is useless since even though this  does not show that a gene brings about a behavioral trait, but it shows that this subject needs more research to be able to determine the validity of Snyder-Mackler’s original hypothesis.

Dogs are very complex genetically and therefore behavioral traits are both a combination of genetics and training. As Carlos Alvarez, a researcher at the Nationwide Children’s Hospital in Columbus, Ohio, says, “Dogs are a really powerful system to investigate the genetics of many traits and diseases because generations of domestication and breeding have simplified their genomes. This study shows that behavior is no different.” Overall while this research is just the start and is incomplete in totality, it shows that there is much more to discover regarding this topic. If you have any traits that you think correlate with either your dog’s genes or breed, please post a comment a explain why.

 

The Rice That Can Clone Itself

A team of scientists has discovered that through the use of CRISPR, they were able to create a rice plant that can asexually reproduce. The problem with previous strands of genetically modified rice plants, those bread to have a higher yield, is that their progeny did not always carry this desired trait. So farmers have to buy new genetically modified seeds every year to ensure that they will get that same yield.

Image result for rice grains

That is where the magic of CRISPR comes into the equation. The first step in the process was editing the eggs of the plant by implanting a promoter that allows the egg to start the embryo growing process without a sperm. One issue still lingered, the process of meiosis that was occurring could not produce viable offspring because it only had half of the genetic material that the progeny would need. Another team of scientists from the French National Institute for Agricultural Technology discovered that by using CRISPR to turn off three specific genes they could stop the meiosis process and allow the plant to reproduce asexually.

Image result for rice plant

This process is still only 30% efficient at this stage. However, the offspring they do produce are able to asexually produce more clones of themselves. Now the process starts to try and make this process more efficient. I think these plants could have a major impact on the agricultural industry, especially with food shortages becoming more present as the human population rapidly increases.

What do you think? Have we overstepped our bounds by editing nature? Or have we pioneered a new solution for the world hunger question on everyone’s minds?

CRISPR Research into HIV Immunity Might Also Improve Human Cognition

In the quest to genetically master human immunity to HIV, Chinese CRISPR researchers may have come across a way to control human intelligence as well.

Specifically, the trial of deleting the CCR5 gene in twin girls Lulu and Nana has lead to a scarily powerful discovery that scientists are within reach of being able to genetically modify human brain function. Scientists were initially interested in deleting the CCR5 gene because it codes for a beta chemokine receptor membrane protein which the HIV virus hijacks to enter red blood cells. However, when this alteration was tested on mice embryos in California, the resulting offspring showed evidence of improved mental capacity.

https://pixabay.com/illustrations/dna-genetic-material-helix-proteins-3539309/

After this unexpected result, scientists investigated further how the alteration would impact human function with the twins’ lives in mind. Experiments yielded evidence of improved brain recovery after a stroke and potential greater learning capacity in school. Scientists at UCLA uncovered an alternative role for the CCR5 gene in memory and suppressing the formation of new connections in the brain. The absence of this gene in the human genome would likely make memory formation easier via more efficient neural connections.

Although the mice experiment suggested that CCR5’s deletion would improve mental capacity rather than harm it, scientists cannot be sure how the alteration has impacted Lulu’s and Nana’s cognitive function. Some also fear that this discovery may have been the first Chinese attempt to genetically create superior intelligence, despite their claim to the MIT Technology Review that the true purpose of the study was to investigate HIV immunity. Although the Hong Kong scientists who engineered the twins did not publicly intend to improve human cognition, they confirmed a familiarity with UCLA’s discovered connections between CCR5 and human cognition all throughout their trial.

Are we within reach of a time when we can play with the circuit board of the human genome to raise a person’s IQ? Quite possibly. But only time and research will tell.

CRISPR/Cas9: Controlling Genetic Inheritance in Mammals

Often the subject of debate, CRISPR/Cas 9 has come to the forefront of the scientific community as its development bridges the worlds of Sci-Fi and reality. Yet while CRISPR/Cas9 has been successfully used in altering the genetic inheritance of insects, applying the same technology to mammals has proven to be significantly more complex. With the recent development of active genetics technology in mice by UC San Diego researchers, a huge stride has been made for the much contested future of gene technology.

Releasing their findings in January, the team led by Assistant Professor Kimberly Cooper engineered a copycat DNA element into the Tyrosinase gene controlling fur color. The copycat DNA results in mice that would have been black appearing white. Over two years they determined the copycat element could be copied from one chromosome to another, repairing breaks targeted by CRISPR.  Ultimately, the genotype was converted from heterozygous to homozygous.

Following the success of her lab’s single gene experiment, Cooper hopes to use the technology to control the inheritance of multiple genes and traits in mice. Her experiment, the first active genetic success in mammals, has biologists hopeful for  future development of gene drive technologies to balance biodiversity and mitigate the adverse effect of invasive species.

Strong Genes Equal Strong Immune System

Although scientists have long agreed that antibodies are in integral part of building up the body’s immune system, there is new evidence that strongly suggests genetic factors play a large role in determining how well the immune system builds and uses these antibodies when fighting disease.

https://commons.wikimedia.org/wiki/File:Redhead_twins.jpg

In a recent study, “researchers from James Cook University’s Australian Institute of Tropical Health and Medicine (AITHM) and the University of Queensland’s (UQ) Diamantina Institute have analyzed blood samples from 1835 twins and thousands of their siblings.” The team looked at the body’s immune response to “six common human viruses, including the Human Herpes virus, Parvovirus, Epstein Barr virus and the Coxsackie virus.” The team determined that genes passed down by parents are the major factor in how powerfully an immune system responds to diseases. “These genes determine whether you mount an intense or weak immune response when confronted with a viral infection,” says Associate Professor Miles.

“Demonstrating that antibody response is heritable is the first step in the eventual identification of individual genes that affect antibody response.” The researchers’ next goal is to identify the superior genes in order to, “imitate ‘super defenders’,” and “design next generation vaccines.”

 

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