AP Biology class blog for discussing current research in Biology

Author: catebolism

CRISPR Causes Cancer, Sort Of

          Scientific researchers are always looking for ways to improve modern science and help create new treatments. Currently, CRISPR, “a powerful tool for editing genomes,” holds the ability to help advance medicine, specifically gene editing, so long as the kinks in this specific method are worked out. One of these problems is the DNA damage caused by CRISPR “activates the protein p53,” which tries to protect the damaged DNA. This raises not one, but two concerns as present p53 can diminish the effectiveness of this technique, however when there is no p53 at all cells grow rapidly and become cancerous. As we learned in AP Biology class, typical cells communicate through chemical signals sent by cyclins that ensure the cell is dividing the right amount. Cancer cells, however, contain genetic mutations that prevent them from being able to receive these signals and stop growing when they should. “Researchers at Karolinska Institute” have discovered that “cells with inactivating mutations of the p53 gene” have a higher survival rate when contingent on CRISPR. To further their research, they discovered genes with mutations similar to those of the p53, and also “transient inhibition” of the gene could help prevent “the enrichment of cells” that are similar. Although seeming antithetical, these researchers proved that inhibiting p53 actually makes CRISPR work better and prevent enrichment of mutated p53 and other similar genes. 

CRISPR logoDNA animation

           These results give crucial information, helping advance CRISPR and make it more usable in current medicine. Additionally, the researchers have uncovered the possibility that the damage CRISPR causes to DNA might be key in creating a better RNA sequence (the RNA sequence tells us the “total cellular content of RNAs”) guide, showing where DNA should be changed. In future tests, these researchers want to try and get a better idea of when the enhancement of mutated p53 cells from CRISPR becomes a problem.    

Migraines Are Just in my DNA

           While over a billion people suffer from migraines, there is not much knowledge about what causes them or how they can be treated. This uncertainty led to a study in which researchers from Europe, Australia, and America all worked together to find how genetics might play a role in migraines. In this study data from over 800,000 individuals, around 100,000 of which had migraines, was collected, which led to the discovery of tons of new genetic risk factors. While it is understood that the recurrence of migraines in certain individuals is very likely due to genetics, it is unclear if the different types of migraines have the same genetic background such as migraines with aura vs. without aura. To test this, the International Headache Genetics Consortium acquired data on genetics in order to hold a “Genome-wide association study” to find specific genetic mutations commonly in migraines with aura and/or migraines without aura. The results found suggested that there are both genetic risk factors shared by the two main types of migraines, as well as some specific to each. The results also backed the belief that migraines are a neurovascular disorder by showing that neuronal and vascular genetic factors contribute to them. 

DNA orbit animated         

           As we are learning in AP Biology class, the genome is a person’s complete set of DNA. A person’s genetic risk factors are passed down from their parents through their genes, and while all humans have genes, everyone has slightly different variations of them inherited from their parents.  Humans typically receive 23 of their 46 chromosomes from each parent, as the two haploid sets of chromosomes join to make a diploid set.  This diploid set is the human’s genome, and holds the coding for genetic risk factors, such as the ones that contribute to migraines in some individuals.

               So many people are living susceptible to migraines with little ways to treat them, however with the new discoveries about what genetic causes may lead to migraines there is more hope for treatments in the future. One specific medication that has recently been developed is a CGRP inhibitor which prevents “calcitonin gene-related peptide”, which is a molecule playing a large role in the occurrence of migraines. Dr. Matti Pirinen from the Institute for Molecular Medicine Finland, University of Helsinki, commented on his optimism for finding “other potential drug targets among the new genomic regions” as well as the ability to learn even more about the issue through larger studies. Despite little known information about migraines causes and treatments in the past, recent studies offer a brighter future to finding out why some people are so susceptible to them, as well as new ways to provide relief for those who suffer from migraines.  

New Studies Uncover Truth About Vesicle Formation

Eating is one of the most simple tasks humans need to preform to maintain survival, and our bodies have numerous complex mechanisms to gather the nutrients from the diverse foods we eat. Eating starches for glucose to fuel our cells or vegetables to acquire the necessary vitamins and minerals to ensure a smoothly functioning body; eating provides us with the essential nutrients to survive. But what about the building blocks of life, our cells? So far in our biology class, we’ve learned that cells possess the capability to engulf food particles and microorganisms through a process known as phagocytosis, a subcategory of endocytosis. Endocytosis types

This process involves our cell’s plasma membrane, a highly complex cellular component that can undergo shape transformations. For a cell to perform phagocytosis, the cell membrane must alter its shape to create vesicles, tiny structures within a cell that consist of fluids and food particles enclosed by a lipid bilayer, which transfer food particles and microorganisms into the intracellular matrix. 

On the surface, phagocytosis seems like a relatively not intriguing and straightforward process, yet there is much more to uncover. Scientists at the Ohio State University state that “the question of how those pockets formed from membranes that were previously believed to be flat had stymied researchers for nearly 40 years,” which opens up an entirely new idea to be pursued (Ohio State University). To tackle this preliminary issue, the scientists experimented with highly powerful cameras to take a deeper view into the cell membrane’s ability to carry out phagocytosis. Using super-resolution fluorescence imaging, they watched the cell membrane form pockets within itself in live time. Now, the question of how these pockets form is answerable. 

Cell membrane detailed diagram en

According to the scientists, their studies revealed that ‘protein scaffolds’ deform the cellular membrane once designated to the site of vesicle formation. This discovery contrasts with the previous hypothesis, which states that protein scaffolds had to undergo an energy-required reorganization to create membrane curvature. Lead scientist Kural states that “Understanding the origin and dynamics of membrane-bound vesicles is important — they can be utilized for delivering drugs for medicinal purposes but, at the same time, hijacked by pathogens such as viruses to enter and infect cells”(Ohio State University).  Hopefully, with a better understanding of the shape transformation undergone by the cellular membrane, along with the fundamentals of life, we will be able to produce more effective therapeutic strategies.


COVID-19 May Induces Cell That Produce Antibodies for Life

Once in our body, SARS-CoV-2, the virus that causes COVID-19, forces the body’s innate immune system to activate. However, the innate immune system response typically is deemed unsuccessful due to the complexities of the virus’s structural components, which then paves way for the body’s adaptive immune response to initiate. As we learned in Biology, adaptive immune response begins with a macrophage engulfing SARS-CoV-2 through phagocytosis. Then, the MHC proteins present on the macrophages, white blood cells that surround and kills microorganisms, remove dead cells, and stimulates the action of other immune system cells,” display the antigen on the surface, creating a ‘wanted’ poster for the immune system (Cancer.Gov). We also learned that eventually, a T-Helped cell comes along and binds to the displayed antigen, which activates the T-Helper cell which fosters the secretion of interleukin, a cytokine. Finally, both B and T cells are stimulated, which then begin the process of fighting off the virus, along with preventing reinfection. One of the cells that assists in the preventing reinfection are B-Plasma Cells, which are, “antibody-producing immune cells [that] rapidly multiply and circulate in the blood, driving antibody levels sky-high”(WashU School of Medicine).

Tingible body macrophageOne crucial step in determining a person’s ability to fight reinfection is testing to see if antibody secretion has either occurred or is currently occurring. While typical blood samples will suffice, “the key to figuring out whether COVID-19 leads to long-lasting antibody protection, Ellebedy [ PhD, and associate professor of pathology & immunology] realized, lies in the bone marrow”(WashU School of Medicine). The B Lymphocytes, which initiate a humoral response, mature in the bone marrow, and so, to determine the prevalence of antibody secreting cells, bone marrow samples must be received from past COVID-19 patients. To determine if antibody production increases after the body completes its fight against, Ellebedy collected blood samples and “As expected, antibody levels in the blood of the COVID-19 participants dropped quickly in the first few months after infection and then mostly leveled off, with some antibodies detectable even 11 months after infection” (WashU School of Medicine). However, people who exhibited mild cases of COVID-19, meaning that their body removed the virus after two to three weeks, antibodies continue to secrete antibodies, and will continue for an indefinite time period.

Covid-19 San Salvatore 09One problem introduced was rooted in the mainstream media, which spread a misinterpretation of data, being that “antibodies wane quickly after infection with the virus that causes COVID-19” (WashU School of Medicine). Ellebedy believes that this is a major misinterpretation of data, and actually means that antibody production is continuing inside of the bone marrow. Typically, antibody production plateaus after a certain period of time preceding infection, yet these numbers don’t go to zero.

Ellebedy concludes that this result is highly promising, especially for people who experienced a more severe infection from SARS-CoV-2, because an increased amount of circulating virus cells typically leads to a stronger immune response due to the body being required to secrete more antibody cells. Although she believes that more studies need to undergo in people who experienced moderate to severe infections, and show if they also have the same everlasting antibody production.







Can Humans use Photosynthesis to “Breathe”?

Throughout our lives we learn that photosynthesis is a way plants “breathe”.  As learned in AP Biology class, plant cells use photosynthesis to make glucose, which is how they “eat”, and a byproduct of this is oxygen.  We also learned that photosynthesis takes place in the chloroplasts and the thylakoid disks, which have a large surface area, making them very productive for the cell.  The process of photosynthesis takes carbon dioxide and uses energy from the sun to produce oxygen and sugar.  While this process has been primarily used in plant cells, what if animal  cells could also use photosynthesis as a way to “breathe”?

German scientists have explored this question and found a way to “introduce algae into [tadpoles] bloodstream to supply oxygen”.  This idea began with a researcher who thought that frog nerve cells could be stimulated using photosynthesis. His hypothesis was tested by putting green algae into the hearts of tadpoles, turning their veins green as it was pumped to their brains.  The researches did this by temporarily pausing the firing of the nerves in their brains before adding the algae.  Only 15-20 minuets later the nerves regained functionality which was “about two times faster than…without the algae”.  The experiment proved that photosynthesis was a “quick, efficient, and reliable” to revive neural activity in tadpoles.


While algae use in tadpoles was proved effective, this does not mean it is a dependable for other animal species yet.  Work is still being conducted to implement this technology for the benefit of humans.  Scientists believe that the use of photosynthesis could potentially be used as a treatment for strokes or other medical situations where oxygen in the body is limited.  First, they need to understand if the use of photosynthesis works for prolonged periods of time, or just momentarily.  The side effects of a process like this also need to be explored.

While the research required is not complete to help humans “breathe” using photosynthesis, scientists are headed in the right direction of a scientific breakthrough that could potentially save lives and help change modern medicine.

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