AP Biology class blog for discussing current research in Biology

Author: shaminoacid

The Fluorescent Frontier: Glow in the Dark Proteins in Disease Research

We all know that although science is improving rapidly on a global scale, diagnostic tests for diseases remain sensitive and require complicated techniques. One evident example is the tests for COVID-19. This complexity can range from their preparation to an interpretation of their results. However, recent research from the American Chemical Society has developed a method that is able to analyze viral or infected nucleic acids in less than 30 minutes and in just one step. This is all due to “glow in the dark” proteins.

Bioluminescence is a scientific phenomenon that powers many animals: a firefly’s flash, an anglerfish’s glowing head, and even phytoplankton’s blue color.  Here a chemical reaction occurs, involving the luciferase protein. This protein essentially causes the “glow in the dark” effect. The protein is incorporated into sensors which emit a light when a target is located. Although the simplicity of these sensors is idyllic for clinical diagnostic testing, they still lack the sensitivity

One solution to this problem is presented by a particular gene editing technique: CRISPR. The Broad Institute defines CRISPR as; Clustered Regularly Interspaced Short Palindromic Repeats. It is essentially an efficient and customizable alternative to other existing genome editing tools. With this new technique, Maarten Merkx and his coworkers wished to use CRISPR-connected proteins while combining them with a bioluminescence form whose glow could be seen by humans, through a digital camera for example.

CRISPR CAS9 technology

To ensure that there was an ample amount of DNA or RNA to analyze, they used a technique known as Recombinase Polymerase Amplification, or RPA. This is a simple method which works continuously at a temperature of 100 F. With this  two CRISPR proteins specific for different parts of a viral genome each have a different fragment of luciferase attached. In other words, the new treatment known as LUNAS (Luminescent Nucleic Acid Sensor), takes two CRISPR proteins for different parts of a viral genome and has a distinct fragment of luciferase added to each.

Moreover, if one specific viral genome that the researchers were testing was present, the two CRISPR proteins would bind to the targeted nucleic acid sequence. This would allow them to come together and promote the full luciferase protein to form and glow. Additionally, to account for the luciferase being depleted, the researchers used a control reaction which turned green. In the event of a positive viral detection the color would change from green to blue. To prove the validity of this method, the researchers tested LUNAS on clinical samples of nasal swabs testing COVID-19. The method successfully detected the virus in less than 20 minutes, even at low concentrations. With this, the LUNAS method holds great potential in detecting other viruses in a concise and efficient manner.


To connect to our AP Bio class, we learned about how specific proteins code for specific actions or results in our bodies. At their tertiary and quaternary structures, proteins have a myriad of functions ranging from acting as a receptor to interacting with an enzyme. This parallels with the luciferase’s specific function of creating a glow affect. Additionally we learned about cell communication and how interaction with a receptor would result, or cause a specific occurrence. This connects to luciferase’s binding to its sensor, causing the glow affect. This cell communication also connects to the two CRISPR proteins attaching to a specific nucleid acid sequence. If the nucleid acid holds the viral genome and the luciferase, it would connect and form a glow response – a direct example of intercellular communication. Continually, we learned about DNA manipulation and alteration and how segments can be added in, substituted, or even removed. This occurs in CRISPR gene editing’s nature as a genome editing tool. It exemplifies all these manipulations to both DNA and RNA. We also learned about ideal protein function at a variety of temperatures, pHs, and environmental settings. This idyllic setting in seen in RPA’s function at a continuous 100 F.

To close, I feel that the use of luciferase, or “glow in the dark” proteins fronts an entirely new way of combating diseases and supporting disease identification. It would provide a new way for doctors and scientists to diagnose patients in a time efficient manner. And frankly, the idea of being diagnosed by something “glow in the dark” is entirely lightening and provides some relief to the gravity of the situation. I invite any and all comments regarding this specific method of disease identification or any other relevant discussion points.

Can Your Lungs Work Against COVID-19?

Within the last two to three years there has been an immense focus in the field of science, COVID-19. This pandemic has sparked a myriad of research opportunities as well as brought up questions we didn’t even know we needed answered.

With this, recent research at the University of Sydney shows that our lungs contain a protein that blocks the COVID-19 infection and works to create a protective barrier within our body. The way it works is that a protein receptor found in our lungs sticks to the virus, and then pulls it away from the targeted cells. The protein is known as the Leucine-Rich Repeat-Containing Protein 15 or in short, LRRC15. For context, leucine is an essential amino acid for protein synthesis as well as many other biological functions. The protein is a built-in receptor inside of our bodies that binds to the COVID-19 virus and doesn’t pass on the infection.

Lungs diagram detailed

Initially, the research was published on February 9, 2023, in the PLOS Biology Journal. Led by Professor Greg Neely and his team members, the findings serve to open a new sect of immunology and COVID research, specifically around the protein, LRRC15. Moreover, it creates a path to develop new drugs and treatments to prevent infections such as COVID-19. Greely states that ” This new receptor acts by binding to the virus and sequestering it which reduces infection,” essentially the receptor is able to attach to the virus and “squish” it before it moves to infection. He also pushes the idea that the new receptor can be used to “design broad-acting drugs that can block viral infection or even suppress lung fibrosis.” Continually Dr. Lipin Loo, one of Greely’s team members, mentions, “We think it acts a bit like Velcro, molecular Velcro, in that it sticks to the spike of the virus and then pulls it away from the target cell types,” here he outlines the stickiness of both the receptor and the virus as well as the receptor’s nature to latch onto the virus and “hold” it. In addition, Loo states, “When we stain the lungs of healthy tissue, we don’t see much of LRRC15, but then in COVID-19 lungs, we see much more of the protein,” here he fronts the idea that COVID-19 lungs are far richer in the LRRC15 protein than normal lungs, this may be due to a result of the protein’s ability to immobilize the virus.

To outline COVID-19 infects us by using a spike protein to attach to a specific receptor in our cells. It mainly uses the ACE2 receptor to enter human cells. Moreover, our lung cells have high levels of ACE2 receptors, which is why being infected can often cause severe problems in our lungs. Similar to ACE2, LRRC15 is a receptor for COVID. But, LRRC15 does not support infection, instead, it sticks to the virus and immobilizes it. This prevents other cells from becoming infected. LRRC15 attaches to the spike of the virus and pulls it away from certain target cell types. The LRRC15 protein is widely present throughout our body, it is in the: lungs, skin, tongue, fibroblasts, placenta, and lymph nodes. However, the researchers observe that the lungs “light up” with LRRC15 after infection. They think the new protein is a part of our body’s natural response to combatting the COVID-19 infection. It creates a barrier that separates the virus from our lung cells most susceptible to COVID-19 infection


To connect to our AP Bio Class, we learned about adaptive immunity where we develop an acquired immunity after being exposed to pathogens, a specific response. I see some similarity here in that the LRRC15 protein is specific to immobilizing the COVID-19 infection. Additionally, in our Cell Signalling Chapter, we focused on signal transduction and its stages, reception, transduction, and response. Specifically in the reception stage, we focused on intracellular and transmembrane receptors. I think that LRRC15 would be transmembrane in order for it to efficiently bind to the COVID-19 Spike. With this, however, I would like to see more about the transduction component of the LRRC15 receptor. Lastly in our Enzyme Unit, we learned about how different factors can affect enzymatic activity; heat, pH, and even general surroundings. I wonder which factors work to hinder and work to stimulate the purpose of the LRRC15. I invite any and all comments with additional info relevant to the topics discussed.

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



Is Covid-19 Becoming Immune to Us?

The Coronavirus has been a focal point for each individual in the past three years. Regardless of your age, gender, ethnicity, or even location, COVID-19 has been the one commonality for everyone. Because of COVID-19’s immense reach and detriment, scientists have worked tirelessly to source treatments and provide them to the people. Although the initial treatments worked in the beginning, as the virus grew and adapted, scientists, doctors, and Coronavirus professionals were forced to follow suit. To this day professionals are still trying to keep up with the ever-changing nature of the virus.

New research shows that initial Coronavirus treatments are slowly becoming more and more ineffective as the virus continues to mutate. The initial treatments for COVID-19 mainly consisted of monoclonal antibodies. Simply put, these are antibodies targeted to a specific illness, Coronavirus in this case. Because the antibody is targeted to one specific disease, as the disease mutates the antibody can no longer be applied to the newly altered disease. For example, recently the US Food and Drug Administration issued information regarding one Coronavirus antibody, Evusheld. They essentially stated that there is an increased risk of COVID-19 as certain variants cannot be neutralized or treated by Evusheld, the current monoclonal antibody. These new changes are critical for those with weakened immune systems who are reliant on strong antibodies to protect them.

To continue, scientists are exploring new ways and attempting to find new treatments for mutated viruses. They do this by seeking out vulnerable parts of the virus and creating an antibody for it. A former Harvard Medical School Professor, William Halestine, hopes that these new treatments will soon be in clinical trials for research.

One example of these clinical trials is currently being administered in Brazil and South Africa by Immune Biosolutions, a biotechnology company. Here they have created a new mix of antibodies and administered them to patients with both mild and high-severity cases of COVID-19. Two of the antibodies in the mix aim at a region of a spike protein where the virus would attach to the human cell. They want these antibodies to block this region and prevent the virus from attaching.

This process can connect to multiple concepts and ideas learned in our AP Biology Class. First, we learned about ligands and receptors, where each ligand is shaped specifically to its own receptor. In this scenario, the virus and antibody are both specific ligands for the spike protein and can only attach to specific spike proteins. This can be compared to our understanding of ligands docking with shape-specific receptors. Second, our understanding of antibodies can be paralleled with the company’s antibody mix. We learned that cells have a certain adaptive immunity to respond to new viruses. This can connect to the company creating new antibodies to adapt to the new virus. Furthermore, we learned that cells can have humoral or antibody-mediated responses, Immune Biosolutions antibody mix is exactly this, a humoral response.

I personally believe that there will be a point where the efforts of scientists and professionals surpass that of the virus. Where we can take control of the virus rather than working for it.  Hopefully, we as humans will eventually stop having to create newer and newer antibodies as the virus slows its mutations.

SARS-CoV-2 without background


Can this Protein Cause Alzheimer’s?

What causes Alzheimer’s? Initially, one might think that it is a result of age-related changes in the brain or environmental and lifestyle changes. One may also think that it is caused by a genetic predisposition to the disease. Personally, I thought Alzheimer’s was a result of poor health as one got older. Although these all may be true, a new study has found that Alzheimer’s Disease can be caused by a certain protein, or rather, a protein mutation. These new findings provide scientists with a way to detect and treat the disease in the long run.  Using multiple methods to analyze mitochondrial DNA, researchers found a mitochondria microprotein that is associated with Alzheimer’s Disease. This protein, known as SHMOOSE is seen to have a role in the neurodegeneration of people, thus giving them an increased chance of Alzheimer’s Disease. Furthermore, the researchers found that the microprotein is found in over a quarter of Europeans. The researchers of The Cohen Laboratory at the University of Southern California published their findings in the journal of Molecular Psychiatry. The journal states that the microprotein, SHMOOSE was discovered through the use of neuroimaging, mass spectrometry, and transcriptomic. All of these are methods of looking into the mitochondrial DNA and locating the mutated protein. According to the study, a mutation of the SHMOOSE microprotein has a connection to a higher risk for Alzheimer’s Disease. They also discovered that 25% of individuals with European ancestry have the mutated version of the protein. Dr. Pinchas Cohen says that the SHMOOSE mutation is a result of a single nucleotide polymorphism or SNP. An SNP is essentially a change or alteration within a single nucleotide, in this case, the change resulted in the mutated SHMOOSE protein. Additionally, he states that the variant can guide ways to identify who is affected while also forming new medical treatments and preventative measures. In class, we learned about how proteins are created and coded for, and we also learned about how protein structure directly affects their function. Both of these concepts are directly seen in this study. Firstly, DNA is what codes for proteins, if the DNA or even the nucleotide is incorrect or altered, the protein would in turn also be incorrect or altered. This is seen directly through the SNP, the single change in the nucleotide entirely changed the protein creating the SHMOOSE protein. Next, the structure of the protein, the sequence of the amino acids, or just the overall composition of the protein entirely plays a role in the function and actions of the protein. For example, if the structure of a protein is compromised, so is the function. This is also directly seen in the study because the structure of the SHMOOSE protein was altered due to the SNP, its function was also altered. The altered function is that it would put people at a higher risk for Alzheimer’s Disease. Another article speaks on the silver lining of the SHMOOSE protein. Because the protein is the approximate size of an insulin peptide, it could easily be administered into the human body for a positive effect. This means that the mutated protein could be used for treating Alzheimer’s Disease and increasing its therapeutic value. This idea is just one of many that venture into the field of precision-based medicine. In the case of Alzheimer’s the mutated SHMOOSE would be focused upon as a target area rather than the disease as a whole. I think that the use of SHMOOSE in a medical or therapeutic way would be risky at first in that it would likely be difficult for scientists to specifically target the way to treat it. What may be a safer option for those with the mutation could be to continue with tried and tested Alzheimer’s Disease treatments rather than immediately opting for something new. The new precision-based medicine method should undergo severe trials, examinations, and successes before it is widely implemented.


Noun Alzheimer Nithinan 2452316


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