AP Biology class blog for discussing current research in Biology

Author: elendometrium

Harnessing the Power of Photosynthesis for Environmental Gain

Human use of fossil fuel as a form of energy to sustain industry and modern lifestyle has had a detrimental effect on environmental efficiency. Nature’s ecosystems are dying and the atmosphere is polluted, causing climate change that further negatively impacts the ecosystems. With fossil fuel sources being depleted, humans must find new energy sources to sustain their current way of living while minimizing the potential harmful effects on the environment. Perhaps, surprisingly, a solution to these problems may be found in the untapped power of plants to sustain themselves through use of sunlight and water in a process called photosynthesis.

Sun shining

Photosynthesis is the process by which photons of light (coming from the rays of the sun) and water molecules are converted, through a complex, multi-step process, into glucose, a form of stored energy. Today, scientists are working on various ways to mimic the natural process of photosynthesis through artificial photosynthesis. Their goal is to find clean, affordable, efficient and sustainable ways to create energy that would allow humans to subsist as they do. 


Harnessing the power of the sun is full of potential because the sun’s energy is so great that the amount of sunlight hitting the earth in one hour can satisfy the energy needs of all humans for one year. 


Currently, the process most similar to artificial photosynthesis is photovoltaic technology which allows a solar cell to convert the sun’s energy into electricity. A small PV cell usually produces between 1 and 2 watts of power when sandwiched between protective materials like glass and plastics. In order to harness maximum energy, these PV cells, which are composed of semiconductor materials, are often chained into arrays that have the capacity to be bound to a larger electrical grid.  However, this process is inefficient because it harnesses only 20% of the sun’s energy, in part because the semiconductors in solar panels have limited ability to absorb and store sunlight energy.


By contrast, photosynthesis can store 60% of sunlight as chemical energy in biomolecules. In her research, Yulia Pukshar, a biophysicist at Purdue University, has been replicating the photosynthesis process by creating an analog that collects sunlight then splits water molecules to create hydrogen. Hydrogen is useful as a fuel to be used in fuel cells or as a fuel to be combined with other fuels (like natural gas) to provide power to homes, cars, electronic devices, etc. Much of Pushkar’s research has focused on determining which combinations of catalysts and photosystem II proteins work best to generate hydrogen from water molecules. She seeks to use chemicals and compounds that are abundant, easily accessible, inexpensive and non-toxic. Artificial photosynthesis is being developed with “nontoxic, easily available elements” which sets it apart from preexisting forms of “clean” energy. 


Currently, researchers have determined that the most durable oxygen evolving complexes (the portion of photosystem II that promotes photo-oxidation of water during photosynthesis) are those composed of cobalt-oxide based water oxidation catalysts. The use of such catalysts, that most closely resemble the true catalyst present in photosystem II, is highly costly and impractical when applied at a large scale. What seems to be a breakthrough in man-made, photosynthetic technology is merely in its infancy. If human civilization is to ever make a dent in this environmental crisis, new sources of sustainable energy must be implemented globally.  


Ever since I moved to Brookville from New York City, I developed a greater appreciation for the beauty and peacefulness of nature in my surroundings. My understanding of the process of photosynthesis has reinforced my sentiments as I now fully comprehend the value of plants to human life. As my family plants more trees on our property, I recognize that such plantings are helping the environment by absorbing CO2 and providing vital oxygen to the atmosphere. For this reason, among others, I support reforestation initiatives around the world as well as the Forest Program at FA.

Cell Cycle Regulation in Revolutionary Gene Editing Technique (a.k.a. CRISPR)

There are more than 500 different types of human cancers. Wouldn’t it be wonderful if scientists could develop cures for all of them? Scientists believe that CRISPR gene-editing can be used to cure some cancers. CRISPR (an acronym for clustered regularly interspaced short palindromic repeats) is a way of targeting a specific bit of DNA inside a cell which can then be gene-edited to change such bit of DNA. CRISPR has also been used for other purposes, such as turning genes on or off without changing their DNA sequence.


Recent research has found a link between CRISPR gene-editing and mutated cancer cells. Scientists believe that a further understanding of this link can identify a group of genes which should be monitored for mutations when cells are subjected to the CRISPR gene-editing method. Although CRISPR gene-editing holds promise for cell repair, the application of CRISPR gene-editing, which is meant to identify and correct damage in cells, can also cause damage to cells in a controlled manner. Such damage activates a protein, p53 (“also known as the guardian of the genome”), which helps repair damaged DNA. 

CRISPR-Cas9 mode of action

P53 is a transcription factor, which is a protein that regulates the rate at which DNA is transcribed into RNA. These transcription factors bind to regulatory sequences in proteins, thus changing the shape of DNA, ultimately making them the most vital form of gene regulation. Transcription factors include many proteins but exclude RNA polymerase, which pries two strands of DNA apart and joins two strands of DNA together (Campbell, 280). P53 works by sliding along the damaged DNA, seeking a critical site to which it attaches and then sends a message to halt cell division until the DNA is repaired. In other words, p53 acts as a checkpoint in the cell cycle, preventing cell from proceeding though the G1 and G2 phases of the cell division cycle. In mice, the same exact transcription factor exists; those that lacked the Trp53 gene developed tumors at a far faster rate than those with the functioning gene.


By using CRISPR technology to damage DNA at the same cite at which DNA damage occurs, scientists are able to identify the protein responsible for cellular proliferation. If damage to the cell is too severe then p53 triggers apoptosis (the death of cells which occurs as a normal and controlled part of an organism’s growth or development) so that the damaged cell is destroyed. However, sometimes p53 is itself damaged which prevents such protein from binding to the damaged DNA in order to repair it or otherwise signaling destruction of the cell. When this occurs, the damaged cells multiply and grow, resulting in tumors. Scientists have found alterations in p53 in more than half of all cancers and thus, consider p53 the most common event in developing cancer.


New studies show that p53 inhibition can make CRISPR more effective thus, counteracting “enrichment” (the process of purifying cells for downstream applications such as qRT-PCR, cell polarizations ex vivo, or to enrich cells for use in a flow cytometry experiment) of cells with p53 mutations which has been observed to occur in cell cultures when such cells have been subjected to CRISPR. In other words, there is in vitro evidence that CRISPR technology causes harmful p53 mutations to be more prevalent in the population that has been subjected to the CRISPR technique. These findings suggest that there is a group of genes that should be monitored for mutations when the CRISPR gene-editing method is applied to cells. 


Cancer is a devastating disease that has taken the lives of many people. Members of my family have suffered and lost their battle to cancer (most recently my dear aunt this past weekend). CRISPR presents the possibility of finding cures to cancer which are specifically designed to target the particular genetic mutations that are unique to each individual. Perhaps, the cure to cancer will be achieved sooner than we realize,  although clearly not soon enough. 


Works Cited:

Reece, Jane B, and Neil A. Campbell. Campbell Biology. Boston: Benjamin Cummings / Pearson, 2011. Print.

The Compound with the Potential to Decimate COVID-19 Morbidity  

Severe cases of COVID-19 result in respiratory problems and blood clots. Scientists are currently looking for a molecular solution to enhance therapeutic treatment. According to the authors, immunometabolic suppression seems to be the the main contributor to the shut down of the immune system, leading to a more severe response from SARS-CoV-2. In severe cases of COVID-19, it seems that a certain family of phospholipases has been associated with determining the outcome of symptoms in patients. Higher levels of the molecule secreted phospholipase A2 and its 12 other variants have been prevalent in cases of cancer, sepsis, bacterial infections and atherosclerosis. Similarly, high levels of sPLA2 were found in 127 blood plasma samples from severely affected COVID-19 patients. 


These new findings provide a potential path towards effective treatment for Coronavirus. In new research led by the University of Arizona, the overabundance of the active enzyme, secreted phospholipase A2 group IIA, in the human immune system has been associated with increased severity of COVID-19 symptoms faced by infected individuals. 


Maintaining host resistance and disease tolerance is an important part of successfully fighting Coronavirus related infections. Secreted phospholipase A2 group IIA (sPLA2-IIA) is naturally circulated by the human body in order to defend against bacterial invaders. The average healthy individual typically circulates around half a nanogram per milliliter of sPLA2-IIA. Researchers found that 63% of COVID-19 infected individuals being monitored at Stony Brook Medical Hospital who circulated amounts greater than or equal to 10 nanograms per milliliter of sPLA2-IIA died from the symptoms of COVID-19. 


Why would certain infected individuals circulate 20 times the healthy amount of sPLA2-IIA? 


When the human body encounters bacterial pathogens, the secretion of the enzyme sPLA2-IIA protects the body against the pathogens in an innate defense. Therefore, in an attempt to combat Coronavirus, the human body secretes a greater amount of sPLA2-IIA. This increased amount of sPLA2 can be considered a double-edged sword. On the one hand, the enzyme aids in attacking the virus. On the other hand, the enzyme acts as a “shredder,” tearing apart the membranes of vital human organs. The attack on the host’s cell membranes leads to organ failure and death. Interestingly, the active enzyme sPLA2-IIA resembles an isotopic enzyme found in snake venom, which similarly destroys microbial cell membranes. Much like the active enzyme found in rattlesnake venom, sPLA2-IIA has “the capacity to bind to receptors at neuromuscular junctions and potentially disable the function of…muscles.”

Several vaccines (2021)

By looking at the lipid metabolite levels in blood samples of Coronavirus patients, researchers were able to corroborate severe Coronavirus symptoms with an overproduction of sPLA2. It seemed that individuals whose circulatory systems contained elevated levels of lysophospholipids (lyso-PLs), unesterified unsaturated fatty acids (UFAs), acylcarnitines, and mitochondrial DNA as well as a decrease in plasma levels of phospholipids experienced higher mortality rates. Expectedly, there was cell energy dysfunction and unexpectedly high levels of sPLA2-IIA enzyme. 


In the future, it is highly plausible that an sPLA2-IIA inhibitor may become a standard component of treatments distributed amongst patients with severe symptoms. Hopefully, such a treatment could help to diminish the ever rising mortality rate of Coronavirus and furthermore alleviate the suffering of thousands of patients. 


Ultimately, our vast knowledge of molecular biology has an application beyond the mere observations of a published study. It is discoveries like this one that have the capacity to positively affect the course of a person’s life. My mother, for example, contracted COVID-19 a few weeks ago and had to endure days of intense fevers and coughing fits while she was confined to her bed. Although he never tested positive, my father too was bed-ridden with the same symptoms. In the meantime, I, a high school student, found myself taking care them as well as their household duties: cleaning the house, cooking three meals a day, doing laundry, etc. As a high school senior who has completed the college application process, I fortunately had the time to manage the extra workload. However, it is important to realize that many citizens around the world do not have the same privilege; some people are displaced from work while others catch the virus and never make a full recovery. With the robust power of anatomical science, we have the capacity to change people’s lives for the better.

Can Obesity Be Cured Through Thermogenesis by Brown and Beige Fat Cells?

In an attempt to find methods for treating obesity and diabetes, researchers recently discovered a new cellular pathway that triggers thermogenesis, the process by which fat cells (called adipocytes) create heat by burning energy. 

The human body has white adipocytes in which energy is stored in the shape of a single, large oily droplet. It also has brown adipocytes which contain a mixture of many, small oily droplets and dark-colored mitochondria (which create the brown color of these fat cells). The mitochondria in the brown adipocytes act as engines that turn the oily droplets into heat and energy. Some people also have “beige” adipocytes consisting of brown-like cells found within white adipocytes which can be triggered to burn energy. 

Brown fat cell

Adipose tissue, otherwise known as fat tissue, can be composed of either white adipocytes or brown adipocytes. The white tissue is primarily used for triglyceride storage while brown tissue functions to expend energy, potentially counteracting obesity. BMP7 is the protein that causes the adipogenesis (formation) of brown fat cells. It was found in a study that mice lacking the gene BMP7 did not have any brown fat and subsequently had a more difficult time losing weight. The protein BMP7 causes an increase in energy expenditure and reduction in weight gain. 

In order to create energy, the human body converts carbohydrates into glucose (much like the mice described above), a type of sugar used as fuel for cells. Excess glucose is stored in the white adipocytes of muscles and the liver for later use by the body to stabilize blood sugar levels and create energy as needed. By contrast, in adipocytes, glycogen not only stores energy but also sends a signal to the uncoupling protein to “uncouple” ATP, the molecule providing energy for fueling cellular processes. This process, which is completed using Uncoupling Protein 1 (UCP1), ensures that only the adipocytes with sufficient energy to provide fuel for heat are triggered to generate heat and balance energy needed by the body. 

The uncoupling protein, formally known as Uncoupling Protein 1 (UCP1), is a unique protein, located in the inner membrane of mitochondria. UCP1 is devoted to adaptive thermogenesis, a special function performed by brown adipocytes. The protein itself is located near the multi-enzymatic complex called the respiratory chain where, by reducing coenzymes, electrons are driven towards oxygen in a process called oxido-reduction. Through oxido-reduction, an electrochemical gradient of protons is generated across the inner membrane of the mitochondria.

This electrochemical gradient is normally consumed by ATP-synthase, which occurs from the phosphorylation of ADP. UCP1 simultaneously transports proteins passively, in what is known as a futile cycle. Named after its lack of perceived utility, the futile cycle was thought to be a quirk of metabolism when initially discovered. In reality, the futile cycle generates heat by dissipating energy through two separate metabolic pathways. Playing an integral role in regulating metabolism, the futile cycle maintains thermal homeostasis within brown adipocytes.

In the future, it is possible that the injection of brown fat cells into white fat cells will become a common method of inducing fat burn in individuals struggling with obesity.

Throughout my life, I’ve personally struggled to maintain an appropriate weight. It always seemed to me that even though I didn’t eat as much as others, I somehow seemed to gain weight more easily than many people who ate more than I did and yet remained skinny. This new understanding by researchers of how glycogen works in fat cells to promote fat burning and better metabolism has implications for obese people who may someday be injected with more brown fat cells to help increase their metabolism and thus decrease their weight gain. Hurray!!

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