AP Biology class blog for discussing current research in Biology

Tag: DNA (Page 1 of 7)

CRISPR-Cas9 – The Human Editor

What is CRISPR-Cas9? CRISPR-Cas9 (Clustered, Regularly Interspaced Short Palindromic Repeats) is a powerful technology that allows geneticists to modify or “edit” parts of the target genome by adding or removing whole sections of the DNA sequence. Currently, CRISPR is the most versatile and accurate DNA modification tool globally. This tool allows scientists to fix flaws in most organisms’ DNA and has minimal risk of off-target damage.

Cas9 cleavage position

CRISPR-Cas9 has two main molecules that carry out the change in DNA, an enzyme called Cas9, and a piece of RNA called guide RNA (gRNA). The Cas9 enzyme locates the target area and can cut the DNA in a specific location in the genome so that small pieces of DNA can either be added or removed. The gRNA is made of a small piece of a lab-designed RNA sequence, roughly 20 bases long, located within the RNA scaffold. To ensure that the Cas9 enzyme cuts at the right point in the genome, the scaffold binds to the DNA, and the lab-designed sequence pilots the Cas9 enzyme to the correct location. The gRNA has RNA bases that match those of the target DNA sequence in the genome. The Cas9 enzyme follows the gRNA to the specific area and makes a precise cut across both strands of the DNA. During this stage, the cell recognizes that the DNA has been damaged and will try to repair itself. Scientists use this DNA repair system to add or remove changes in one or multiple genes. This technology is consistent with our most recent AP Biology Unit, DNA Replication, and Gene Expression/Replication.

In my opinion, CRISPR-Cas9 is an incredible technology as it has so many practical applications. The future of this technology has potential in many diverse fields such as genetic engineering, bioengineering, and molecular biology, among other areas of study.

The technology has been tested on dogs with Duchenne Muscular Dystrophy, a gene mutation adversely affecting muscle proteins. In this case, a CRISPR gene-editing treatment demonstrated promising signs of permanently fixing the genetic mutation responsible for this disease, which in humans, affects approximately 1 in 3,500 male births worldwide. The mutation prevents an organism from producing an appropriate level of functioning dystrophin which causes muscles to be weak and not respond efficiently. Researchers at the University of Texas Southwestern found that gene editing restored the functioning dystrophin levels in the dog’s muscles and heart tissue. The increase in the dystrophin levels would need to be more significant for it to work in humans, but researchers have been making substantial progress in advancing this developing CRISPR-Cas9 technology.

Have you ever been caught with a viral disease and been misdiagnosed by your doctor? New CRISPR technology may eliminate this from happening.

So first, what even are viral diseases and how can they affect your health?  Well, some common viral diseases include HIV, herpesvirus, COVID-19, or even the common cold. Any disease classified under viral can enter your body through breathing air, touching something with viruses on it, intercourse, close contact, or getting bitten by a bug “such as a mosquito or tick”. Viruses typically infect one type of cell in your body and this is why the “common cold typically infects only cells in your nose, mouth, and throat”

In a study by PubMed Central (PMC) their goal was to identify the most common errors in diagnosing infectious diseases and their causes using physicians’ reports. In their concluding results, “the most common infectious diseases affected by diagnostic errors were upper respiratory tract infections (URTIs) (n = 69, 14.8%), tuberculosis (TB) (n = 66, 14.1%), pleuro-pulmonary infections (n = 54, 11.6%)”. This data was taken from a sample of 465 patient cases and the researchers concluded that, “a substantial proportion of errors in diagnosing infectious diseases moderately or seriously affect patients’ outcomes”. So when diagnosing viral infectious diseases, steps need to be taken to improve our testing process.

Researchers from the American Chemical Society are looking at using “glow in the dark” proteins to help diagnose viral diseases. Fireflies, anglerfish, and phytoplankton all create a glowing effect using bioluminescence, which is caused by a chemical reaction involving luciferase protein. This protein has been used in sensors for point-of-care testing, but lacks the high sensitivity needed for clinical diagnostic tests. Researchers wanted to combine CRISPR-related proteins with a bioluminescence technique to improve sensitivity. They developed a new technique called LUNAS, which uses recombinase polymerase amplification (RPA) to amplify RNA or DNA samples. Two CRISPR/Cas9 proteins bind to targeted nucleic acid sequences and form the complete luciferase protein, causing blue light to shine in the presence of a chemical substrate. This new technique successfully detected SARS-CoV-2 RNA in clinical samples within “20 minutes, even at low concentrations“. The researchers believe this technique could be used to detect many other viruses effectively and easily.

In relation to AP Biology, we have learned about the process of gene expression where RNA and proteins are produced due to a specific gene being activated. The regulation of gene expression conserves energy and allows organisms to turn on and off genes only when they are required. The CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) gene which are found in prokaryotes cut DNA phages and plasmids to prevent damage to the prokaryote itself. It is used as a rudimentary immune response system. The CRISPR can be associated with other proteins to create an associated complex which allows for the excision and insertion of genes along the length of the genome. Using this process, viral diseases can be identified when combined with the bioluminescence mentioned above.

Looking into the future, researchers are searching for ways to apply CRISPR proteins to detect a greater range of viral diseases so that all patients can get the proper care that they need.

Can Gene Editing Prevent Disease in the future?

There is very exciting news in the world of biology right now. For the first time ever, according to the University of California San Francisco‘s chancellor,  Sam Hawgood, CRISPR gene editing will be delivered to a human in an attempt to study how gene editing can help with asthma.

CRISPR-Cas9 Editing of the Genome (26453307604)

CRISPR-Cas 9 was adapted from a naturally occurring genome that allows bacteria to fight off viruses. When a bacteria was infected with a virus, it would use this genome to take pieces of the DNA from the virus and add them to its own DNA to create a pattern known as a ‘CRISPR array.’ The ‘CRISPR array’ allows the bacteria to remember the virus and cut the DNA of the virus apart.

In 2021, Peter Turnbaugh administered CRISPR into mice in order to target a specific gene and edit it out of the mouses gut. It was this work that inspired the scientists at UCSF to experiment with adding the CRISPR to a human microbiome.

Asthma is the perfect place to start because there is a clear microbial target to attack. There is a molecule that is produced by bacteria in the human gut that can trigger asthma in childhood. The scientists goal is to stop the microbes from producing that molecule, rather than remove the microbe altogether, as that microbe plays other beneficial roles in the human body. By taking a small piece of sgRNA, the scientists would be able to attach that to the target sequence in the DNA of the bacteria that produces that molecule, and ultimately stop the bacteria from producing the molecule that causes asthma.

This can be related to the topic of DNA and Genes that I learned about in AP bio. While reading the UCSF article, I couldn’t help but think about DNA replication, and what implications gene editing would have on DNA replication.

As we learned in AP bio, DNA replication is the process by which a cell copies its DNA before cell division, ensuring that each daughter cell receives a complete set of genetic instructions. During replication, the double-stranded DNA molecule is unwound and separated into two strands, each of which serves as a template for the synthesis of a new complementary strand. The result is two identical copies of the original DNA molecule.

If the scientists at UCSF were able to edit the genes to properly stop the microbes from producing the molecule that causes asthma, would that trait now be passed on to the new complementary strands? Would this gene editing get passed on through DNA replication, and even further would it be passed on to gametes? If both parents were to get this gene edited, would their zygotes now also be immune to asthma, and if so it is almost as if this gene editing is affecting natural selection and evolution.

All of this was very interesting to me and it seems that if/when this becomes a regular part of society, it will have major implications on the way our species sees diseases in the future.

CRISPR May Be the Cure!

There are still many disorders and diseases in this world that cannot be cured, and Huntington’s disease (HD) is one of them.

HD is a neurological disorder that causes individuals to lose control of movement, coordination, and cognitive function. HD occurs because of a mutation in the Huntingtin (HTT) gene where a specific codon sequence repeats, creating a long, repetitive sequence that turns into a toxic, expanded protein clump. These clumps form in a part of the brain that regulates movement called the striatum and prevent the neurons in the striatum from functioning properly. As of now, HD still has no cure, but CRISPR gene editing (Clustered Regularly Interspaced Short Palindromic Repeats) might just be the solution.

Dr. Gene Yeo of UC San Diego School of Medicine, along with his team and colleagues from UC Irvine and Johns Hopkins University, researched RNA-targeting CRISPR/Cas13d technology as a way to possibly eliminate HD and its negative effects on the brain. CRISPR gene editing, as its name suggests, enables scientists to “edit” – add, remove, or alter – existing genetic material. The group desired to see if RNA-targeting CRISPR would be able to prevent the creation of the protein clumps that damage the function of the striatum. As we learned in AP Biology, the addition, removal, or substitution of a base of a codon can drastically change the structure and function of a protein. Each codon codes for a specific amino acid, and if multiple codons have changed due to a mutation, it is likely that the protein will fold differently than it is supposed to and will lose its function.

Yeo and his team desired to develop an effective therapy for HD, hoping to stop the formation of toxic protein clumps and alter the course of the disease. However, they did not want to create permanent changes in the human genome as a precaution. The team instead engineered a therapy that alters the RNA that turns into the protein clumps.  They conducted testing on mice and found that RNA-targeting CRISPR therapy reduced toxic protein levels in a mouse with HD, improving motor coordination. In connection with the molecular genetics unit in AP Biology, since the RNA that causes HD is altered, the protein that is translated will change since different amino acids correspond to different codons.

Transcription and Translation

Further testing will be necessary to confirm the benefits of this therapeutic strategy, but CRISPR does look like a promising medical treatment for HD and many other diseases in the future.

CRISPR Tool PASTEs in New Genes

Researchers at Massachusetts Institute of Technology developed a revolutionary new gene editing tool. The tool is called PASTE, and it is a new CRISPR-Cas9 based genome editing tool. It combines traditional CRISPR and integrases, enzymes that can insert or remove DNA sequences, to cut out certain DNA segments and “paste” in other DNA segments. This new method removes the necessity for double-stranded DNA breaks, which can lead to mutations in the DNA sequence. CRISPR logo

PASTE combines CRISPR-Cas9 nickase, which cuts out a singular DNA strand, with serine integrase, an enzyme that can insert a lot of DNA, and reverse transcriptase, an enzyme that allows PASTE to add a single strand of DNA each time while preventing double-stranded DNA breaks. PASTE produces less indels than CRISPR-Cas9 alone. Indels(insertions or deletions are genetic mutations that often occur when a gene is edited. They can alter the function of genes, thus affecting the organism’s overall health or specific traits (New Atlas).

Additionally, PASTE researchers believe that PASTE could possibly treat genetic diseases by replacing “bad” genes with “good” genes. This is because PASTE is great at “pasting” genes into various parts of an organism’s genome. PASTE researchers tested PASTE against homology-independent targeted insertion and homology-directed repair, discovering that paste had higher insertion effectiveness than homology-independent target insertion, but lower insertion effectiveness than homology-directed repair. PASTE, however, produced less “inaccuracies” than homology-directed repair. These inaccuracies occur when the tool inserts DNA into the wrong part of an organism’s genome, effectively risking unwanted effects (Genome Web).

While PASTE is still in its infancy, it is already revolutionizing the gene editing industry. It not only reduces the risk of undesired mutations, but also increases the efficiency of gene insertion. It is pioneering treatment of genetic diseases. 

AP Bio Side Note 🙂

This technology relates to AP Bio because of its use of introns and exons. PASTE can remove or replace introns and exons, depending on what causes the genetic mutation. This is interesting because although introns are noncoding sequences of DNA, mutations in them can still cause negative effects in people. Additionally, while more intuitive, it is also revolutionary that technology is able to replace exons. I am excited to see what the future for Crispr tools holds. Please leave a comment if you found this post interesting!

Medicine of the Future

According to researchers at Karolinska Institutet in Sweden, there are many challenges when it comes to using CRISPR gene editing as a part of medicine of the future. One challenge is how cells behave when subjected to DNA damage. 

TopBP1 Activation of ATR in DNA Damage ResponseDamage to cells activates the protein p53. The technique is less effective when p53 is activated, but a lack of p53 allows cells to grow rapidly and become cancerous. The p53 protein gene is a tumor suppressor gene. If a person inherits only one copy of the p53 gene from their parents, they are predisposed to cancer and usually develop numerous tumors, Other linked genes with mutations can have a similar effect to p53 mutations. The transient inhibition of p53 is a strategy for preventing the advancement of mutated cells. The DNA damage response can potentially be a marker in development of more precise guide RNA sequences. 


We have learned thus far in AP Biology that mutations are changes that occur in the DNA sequence of an organism or a change in a genetic sequence. Mutations can be caused by mistakes during cell division. They can be harmful, beneficial or have no effect. 

The researchers plan to further conduct clinic-centered tests in order to understand how pertinent these mechanisms are. This study is largely focused on CRISPR screening experiments on isolated cells and analysis of the DepMap database. 

CAST is in the past, it’s time for HELIX

CRISPR stands for clustered regularly interspaced short palindromic repeats.’ The term references a series of repetitive patterns in the DNA of bacteria discovered in the 90s. 20 years later, Jennifer Doudna and Emmanuelle Charpentier discovered that CRISPR-Cas9 could be used to cut any desired DNA sequence by just providing it with the right template, meaning it could be used as a gene-editing tool. To add a desired DNA sequence, one needs an upgraded version of CRISPR editing called CAST, CRISPR-associated transposases. Unfortunately,  CASTs suboptimally insert more DNA sequences than wanted and have a relatively high rate of unwanted off-target integration at unintended sites in the genome. This leads to mutations, the three being, silent mutations, missense mutations, and nonsense mutations. A silent mutation is an insertion or deletion of a nucleotide that doesn’t change the amino acid sequence. A missense mutation is an insertion or deletion of a nucleotide that changes one or more of the amino acids. Lastly, a nonsense mutation leads to an early stop signal.

4.2. The CRISPR Cas 9 system II

Luckily, new research published in Nature Biotechnology tells the reader that an improved CAST system called HELIX now exists. Helix stands for Homing Endonuclease-assisted Large-sequence Integrating CAST-compleX. This mouthful dramatically increased the efficiency of correct DNA insertions, reducing insertions at unwanted off-target sites. HELIX has over a 46% increase in on-target integration compared to that of the CAST system. This discovery is one of many that will continue to help us understand the complexity of our genes.

If You Give A Mouse…Sight!

In a recent study published in the Journal Of Experimental Medicine, researchers in China successfully used CRISPR Gene-Editing technology to restore sight to mice with retinitis pigmentosa.

That’s a lot of vocabulary all at once, so let’s establish some definitions first and foremost.  According to the National Eye Institute, retinitis pigmentosa is a “genetic disease that people [and animals] are born with…that [affects] the retina (the light-sensitive layer of tissue in the back of the eye)”. As for CRISPR Gene-Editing technology, YG Topics defines it as, “a unique technology that enables geneticists and medical researchers to edit parts of the genome by removing, adding or altering sections of the DNA sequence”.

Most inherent forms of blindness and loss-of-vision stem from genetic mutations, and thus retinitis pigmentosa is one of many forms of genetically caused blindness.  However, through CRISPR technology, the researchers in the study successfully edited the DNA of mice who had the mutation to eliminate retinitis pigmentosa and give them the ability to see.  The results of the study are very promising, as not only does retinitis pigmentosa affect mice, but human beings.  Thus, there is evidence that CRISPR could be used to cure blindness among everyday people.  Kai Yao, a professor from the Wuhan University of Science and Technology who contributed to the study said, “The ability to edit the genome of neural retinal cells, particularly unhealthy or dying photoreceptors, would provide much more convincing evidence for the potential applications of these genome-editing tools in treating diseases such as retinitis pigmentosa”.

In AP Biology, we discussed how DNA factors into the traits of a living being.  DNA is made up of 3 base codons that form up to 20 different amino acids.  These amino acids code for specific proteins.  Through a process of DNA transcription and translation, the DNA uses various forms of RNA to code for proteins, which help tell the cell what to do.  Thus, the way the cell acts is largely determined by its DNA.  Essentially, DNA codes certain traits through various amino acid sequences.  Mutations and alternations to amino acid sequences cause different traits, such as red hair, blue eyes, or blindness.

Thus, successfully altering the DNA of mice has huge implications for the human race.  CRISPR could potentially be used to edit the DNA of humans, and thus help limit and prevent certain genetic conditions.  Many diseases are based on genetic mutations, and if CRISPR Gene Editing technology is proven successful, we could potentially eliminate genetic diseases in a few decades.  While “much work still needs to be done to establish both the safety and efficacy” of CRISPR technology, some groundbreaking scientific treatments could be coming sooner than you think (Neuroscience News).

Мышь 2

The “Most Complicated” Cancer Treatment EVER

There are many approaches to treating cancer, ranging from invasive surgeries to extremely damaging radiation and chemotherapy.  The teeny-tiniest clinical trial ever began at UCLA in yet another attempt to find another way to eradicate cancer.  With only 16 participants, this trial combined two areas of research: gene editing and T-cell engineering.   The reason for the miniscule sample size is the intensely customized nature of the treatment.  Each patient’s tumor had completely unique mutations, so each patient needed equally unique T-cell engineering through gene editing.  

One reason cancer is so hard to treat is because they have adapted to be resistant to the body’s own immune response.  The patients that have cancers, especially ones in the later stages, have lost the battle against their cancer with their own immune system, so a new super-immune system must now be built.  This army of new T-cells (white blood cells, which identify and kill bad cells, seen below) will need “training” for its difficult battle ahead.  First, however, the researchers must determine how to train these cells so they will actually be successful.  They used algorithms to find identifiable mutations in the tumor, something that the T-cell can seek out to differentiate the cancerous cells from the normal cells.  Healthy Human T Cell

After testing to make sure that the T-cells can actually identify these mutations, T-cell receptors are designed specifically to their tumor.  Then, each patient’s blood is taken so that the DNA code for the new receptors can be inserted using CRISPR,  a genome editing technology at the cutting edge of genetic medical research.  The DNA code is transcribed to mRNA, which is then used in the ribosome to build polypeptides, in this case, the receptor proteins for the T-cells.  In order to ensure that these new T-cells (with the special receptors) are received, the patients had to take medication that suppressed the number of immune cells, so that the ones they are given can take hold.  

One month into treatment, 5 of the patients’ tumors stopped growing, and only 2 of the participants had associated side effects.  Although only 5 patients had the desired results, Dr. Ribas, one of the researchers, says that they “need to hit it stronger the next time” because they were limited to a small dosage of T-cells to start in order to establish safety.  Additionally, the technology will only get better and better as the research progresses and the T-cells can have more and more mutation targets to look for in a tumor.  

We Live In a Time Where We Can Hack and Edit The DNA In Diseases, and We Have Only Just Begun…

CRISPR gene editing, (Clustered Regularly Interspaced Short Palindromic Repeats), is a relatively new biological technology that allows scientists to fix unimaginable flaws with an unprecedented minimal risk of off-target effects. This advanced technology aligns perfectly with our current unit of DNA replication and Gene expression/replication, so it should be a good review to keep reading.

CRISPR gene editing has two main components; the Cas9 protein and a guide RNA (gRNA). The Cas9 protein acts as the Helicase, cutting and unzipping the DNA strand. The gRNA is designed to recognize a specific sequence in the DNA of a cell. Once the DNA is cut, the cell uses a homologous DNA template to repair the break in the DNA molecule. The template DNA, Homology Directed Repair (HDR), is designed to carry the desired genetic modification and incorporate it into the DNA through the natural DNA repair mechanisms. This process alters or even adds new genetic information to the organism. For example, researchers from UT Southwestern Medical Center used CRISPR to treat Duchenne muscular dystrophy (DMD). A genetic disease that causes muscle degeneration and weakness. The team used CRISPR to delete the gene responsible for producing a toxic protein that causes DMD. They then replaced the missing gene with a shorter, functional version, which allowed the muscles to regenerate and become stronger.

CRISPR illustration gif animation 1

This advanced technology has been used to increase crop yield from various crops. In California it was used to create more drought resistant rice. In another state, it was used to eliminate browning of red apples. This process is becoming increasingly useful and popular because of its safety. The gRNA can be designed to target a very specific sequence of DNA, which means that scientists can modify genes with precision and accuracy. This specificity also reduces unintended genes, which remains to be a large concern for other gene-editing processes. This technology has enormous potential in the science world and can safely guide us into disease treatments, agricultural efficiency, and advanced biological research.

DCas SAM system

Is Nobel Prize-Winning CRISPR Technology as Sound as Scientists Say?

CRISPR—short for ‘clustered regularly interspaced short palindromic repeats’—is a nobel-prize winning scientific advancement in genetic modification technology. It was initially developed by Dr. Jennifer Doudna of Harvard University, and is based on the naturally occurring gene-editing system found in bacteria. Researchers now use this new method to modify the DNA of various organisms, potentially being able to make advancements in disease treatment, improving resilience of crops, correcting genetic defects, and more. 

CRISPR-Cas9 Editing of the Genome (26453307604)

To make an understatement, the introduction of CRISPR into the scientific community has been nothing short of groundbreaking, but researchers from Rice University have raised their own doubts about this seemingly miraculous technology, and whether or not it is as fool-proof as it’s presented to be. In response to this question, they have begun to lead an effort with a goal “to reveal potential threats to the efficacy and safety of therapies based on CRISPR-Cas9…even when it seems to be working as planned.” 

CRISPR-Cas9 was designed to treat sickle-cell anemia. In order to combat this disease, the technology works to edit large sequences in a patient’s DNA, therefore aiming to change their DNA and erase the aspect of it that makes them suffer from the illness. However, researchers have begun to fear that taking such a large step as this (erasing large portions of one’s DNA) is presumptuous, and could possibly yield dangerous, long-term effects, since this genetic modification CRISPR allows will only further spread throughout the patient’s body through stem cell division/differentiation. 

These fears mainly stem from the fact that scientists are not sure how DNA strands are able to rejoin after so many of their sequences have been cut out, and therefore, separated. However, bioengineer Gang Bao of Rice University has other concerns, as well: “large deletions (LDs) can reach to nearby genes and disrupt the expression of both the target gene and nearby genes.’”

Gene expression is a very complex process that occurs in the cells of all organisms, but which can be broken down into two major steps: transcription—”synthesis of RNA using information from DNA”—and translation—”synthesis of a polypeptide or protein using information in the mRNA.”  This process running smoothly is extremely important, as the ‘information from the DNA,’ or amino acid bases, need to be copied exactly without any mistakes, duplicates of bases, etc.. 

Bao also expresses another concern about CRISPR-Cas9: “‘you could also have proteins that misfold, or or proteins with an extra domain because of large insertions. All kinds of things could happen, and the cells could die or have abnormal functions.’”

With so many hypotheses at play, Bao and his research team knew they had to somehow figure out answers: they developed a technique called SMRT—’single molecule, real time’—that utilizes molecular identifiers to seek out and find accidental LDs, long insertions, and chromosomal rearrangements that are located at a Cas9 cutting site. To do this, a machine was used called the ‘LongAmp-seq’ (long-amplicon sequencing) to emphasize the presence of particular DNA molecules. This allows for the quantification of LDs and large insertions on a DNA strand. 

Researchers used streptococcus pyogenes as a medium. With this bacteria, they edited enhancers such as beta-globin (HBB), gamma-globin (HBG), and B-cell lymphoma/leukemia 11A (BCL11A), and genes such as PD-1 gene in T-cells of sickle-cell anemia patients. 

In testing these, they found incredible results: across the 3 enhancers and 1 T-cell gene, the average frequency of several thousand large DNA deletions averaged a whopping 20.025%. 

While it is unclear at this time whether Bao’s team’s discoveries will unveil consequences of genes modification by CRISPR technology, they state that they will work to “determine the biological consequences of gene modifications due to Cas9-induced double-strand breaks,” and look forward to testing if “‘these large deletions and insertions persist after the gene-edited HSPCs are [transplanted] into mice and patients.’

New CRISPR Technique can Potentially be a Treatment for Leukemia

An article published on December 11, 2022 on newscientist, shares fascinating information on a 13 year old patient with leukemia, having no detectable cancer cells after being the first person to receive a new type of CRISPR treatment, to attack cancer.  

The 13-year-old leukemia patient, Alyssa, has had many treatments that have been unsuccessful in helping her condition. Leukemia is caused by immune cells in the bone marrow dividing and growing rapidly. This relates to what we learned about in Biology class in how cancer cells become cancerous by cells dividing uncontrollably. It is also related to how cancer is caused by changes to the DNA (mutations) that alter important genes and change the behavior of them. Leukemia is also caused by the mutations in DNA.

Normal and cancer cells structure

The most common treatments for leukemia are known as killing all bone marrow cells with chemotherapy and then replacing it with a transplant. If this treatment is unsuccessful, an approach known as CAR-T therapy is used. This involves adding a gene to a type of immune cell known as a T cell that causes it to destroy cancerous cells. This also relates back to how in biology class we learned about the functions of T- cells being vital because they protect us from infection. The modified cells are called CAR-T cells. Alyssa’s leukemia was caused by T cells so if they used this technique to modify CAR-T cells to attack other T cells, it would lead to these cells killing each other. Wasseem Quasim at the University College London Great Ormond Street Institute of Child Health, has discovered many drawbacks with this treatment. Due to the many problems conventional gene editing can cause, Qasim and his team used a modified form of the CRISPR gene-editing protein, and Alyssa is the first person ever to be treated with. Alyssa received a dose of immune cells from a donor that had been altered to attack the cancer, and tests revealed 28 days later she had no signs of cancer cells. CRISPR is technology that can be used to edit genes. It finds specific DNA inside a cell and then changes that piece of DNA. It has also been discovered that CRISPR can be an effective tool for cancer  treatment. This new approach to CRISPR treatments could be hugely beneficial  to cancer patients and Many other treatments involving CRISPR base editing are being developed.  





New Generation of Coral!

As global warming continues to increase the temperature of the atmosphere and water column across our planet, the coral populations in our oceans are decreasing. Normally, to survive, coral hosts microscopic algae in its structure, which provides the coral with the energy it needs to grow. The algae produce glucose through photosynthesis, which the corals use to survive and to build their skeletons. This coral then releases oxygen that the algae takes back in. The stability of this symbiotic relationship is critical to corals’ survival. When a coral loses these symbiotic algae due to increases in water temperature, it causes the coral to turn white, as the coral struggles to meet its energy needs, which can often prove fatal. This phenomenon is called “bleaching.”

Bleached Staghorn Coral
Scientists studying coral bleaching have found evidence that some species of coral appear to be adapting to climate change and increasing their tolerance to warming ocean waters by changing the symbiotic algae communities they host. This allows the photosynthetic process to continue and provides them with the energy they need to live. This more resilient species of coral have been found in eastern tropical Pacific places such as Costa Rica, Mexico, and Colombia. These locations are projected to have higher coral cover through 2060. Pocillopora is one such species of coral and is an important genus found within the shallow coral reefs in the eastern tropical Pacific Ocean and the Indian Ocean.
I selected this article for my blog as it embodies several key biological concepts that we have studied and discussed in detail in class this year. These include the photosynthetic process and its important energy-producing biochemical reactions, the various types of successful symbiotic relationships between different organisms, and the role that DNA and genetics play in the evolutionary process of advancing successful biological adaptation.

Consistent with Darwin’s theory of evolution, it appears that Mother Nature, once again, may have found a way to overcome climate change, at least in this specific instance, and we may be witnessing it firsthand!

Researchers Discover Hacking Enzymes as New Cancer Treatment

We all know that mutations occurring in the synthesis of our cells lead to cancer, whether that be via ultraviolet light radiation, the inhalation of cigarette smoke over a long period of time, or otherwise. But how do these mutations actually occur, and if modern science knows that much, why can’t scientists step in before the mutation occurs in the cell and stop the creation of a cancerous one altogether? While the answer to this is evidently easier said than done, researchers such as Szymon Barcawz, Rahul Bhomick, Malgorzata Clausen, Marisa Dinis, Masato Kanemaki, Ying Liu, Katrine Lundgaard, and Wei Wu have found a way to limit the success of cancer-yielding cell mutations. 

In this study titled, ‘Mitotic DNA Synthesis in Response to Replication Stress Requires Sequential Action of DNA Polymerases Zeta and Delta in Human Cells,’ researchers studied the replication process of cells, also known as mitosis, in human body cells (all human cells except gametes, sex cells). In order to understand the study fully, a few biological concepts should be covered first; For starters, the activation of the oncogene in relation to developing cancer. ‘Oncogene’ is simply a term for a mutated cell which turns cancerous. The activation of such creates disorder to cells going through mitosis called DNA replication stress, the name of which essentially reveals its effect: when genetic material is being synthesized under these conditions, it is extremely difficult for the mitotic cell to correctly replicate, causing faulty, under-replicated DNA regions (UDRs) to be built. Since DNA replication is completed in the S phase of interphase, which technically is before the commencement of mitosis in a cell; enough genetic material needs to be available for the cell to split in order for it to be replicated. Therefore, if UDRs are going to occur in a cell, they are created during this time. 

However, our cells have developed clever adaptations to attempt to fight this type of cellular mistake. The strategy includes performing “‘unscheduled’ DNA synthesis in mitosis (termed MiDAS) that serves to rescue under-replicated” genetic material (Barcawz et al.). In studying this cellular defense mechanism, these researchers have discovered how exactly cells make up for a faulty S phase (the phase which copies DNA during mitosis) utilizing DNA gap-filling mechanisms (REV1 and Pol ζ) and DNA polymerases (group of enzymes) whose sole purpose is to replicate unfinished genomes (Pol δ). The study’s main goal, however, was to reveal which of these polymerases was the most crucial in the “rescuing” of under-developed genetic material, which were not, and which were not really necessary at all. 

The researchers were most interested in studying POLDI (a subunit of  Pol δ), REV 1, and REV 3 / REV 7 (both subunits of Pol ζ).  These are all different polymerases whose main job is to “[promote] the bypass of damaged DNA sites” (Barcawz et al.). Each one works to solve a different issue within DNA replication that could lead to a mutation. For example, a TLS polymerase called Pol ζ4 is better at “bypassing bulky regions” of genetic material than the others (Barcawz et al.); this can be defined as Pol ζ4’s ‘role.’  

A crucial realization in this study was that the polymerases Pol ζ and Pol δ may actually be switching roles at some point within the rescuing process by switching their subunits, which we defined earlier as POLDI, and REV3 / REV 7. But, this still doesn’t answer the question of whether or not all the aforementioned polymerases are essential in the process of fixing mutations in the copying of genetic material during mitosis. 

The study at hand was successful at answering this question. It found that POLDI, REV1, and REV 3 are crucial to MiDAS, while REV7 is not at all. Additionally, it was discovered that POLDI and REV1 colocalize with another substance (FANCD2) in mitosis, which reveals how they both indeed play a role in the ‘rescue’ of under-replicated regions” (Barcawz et al.).

However, something unexpected about REV1 was also discovered. While it was found to be useful in mending UDRs in conjunction with POLDI and FANCD2, it actually does more harm than good: When REV1 was removed from the rescuing process in a situation where all the cell’s defense mechanisms failed at stopping the synthesis of a cancer cell, cancer cells were much less likely to survive in the human body. This suggests that it is very possible for a new and effective way to treat cancer to be the inhibition of the presence of REV1 polymerase. 

In the coming years, if the inhibition of REV1 is found to be possible and turns out to be a promising way of preventing cancer cells from surviving in the body, we could be looking at a groundbreaking advancement to modern medicine and the world of cancer treatment as we know it changing forever.

Cancer cells

Real image of cancer cell under a microscope.

A View into Life Millions of Years Ago

In an obscure geological valley at the very northern tip of Greenland’s large ice sheet, investigators have uncovered scientifically derived evidence of the existence of a lush, ancient ecosystem that was functioning over 2 million years ago. The clues to this ecosystem come from the oldest DNA ever recovered, bits and pieces of genetic material, carefully and tediously extracted from buried sediments representing more than 100 kinds of animals and plants. The investigators painstakingly extracted and “sequenced” the DNA strands and compared them to libraries of existing DNA “reads” from living species today.

DNA double helix horizontal
This is an incredibly impressive example of the power of environmental DNA (eDNA), as it is genetic material collected from the ambient environment and not individual organisms. The investigative team aimed to collect hundreds of samples from different locations within the ancient valley and reconstruct what this ecosystem looked like before the ice age. They found many different types of conifers, including poplars, thujas, and species like black geese and horseshoe crabs, that are now common further south of Greenland, but most of which are no longer found in the Arctic at all.
There are many reasons that I believe this discovery is important, not the least of which is that it may give scientists clues as to how some species were able to adapt to climate change in the past and give us some insight into climate change and evolution as we advance. It may also turn the time-honored discipline of paleontology on its head by driving it from its almost all fieldwork mode into the molecular biology laboratory.

The DNA/RNA biochemical process plays a very important role within the nucleus of each cell which defines the existence and evolutionary success of living plants and animals on the planet. The article which I selected from “Nature” discussed above, really emphasizes importance of these chemical structures regardless of whether we are investigating the past, looking into possible future biological scenarios, or looking to “improve”, correct or modify existing biological systems. Understanding both the future and historic past of the biology of the planet is no longer simply relegated to the desktop microscope, but more appropriately is a function of understanding the complex biochemical reactions at the molecular level, not just the cellular level. The extraction of biological (environmental DNA) material from historic sediments thousands of years old underscores the important changes taking place in this exciting new field and emphasized to me that the study of DNA/RNA biochemistry is very relevant to understanding all living systems, past, present and likely into the future.


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



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.” (

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?

Shhhhhhh! Some Viruses Can Sneak into Cells and Cause Cancer

Viruses! We all hate the colds we get in the fall that come with a cough, a runny nose, and a sore throat.  These bugs have gone around since nursery school, so we were taught that viruses were transmitted through touching door knobs, getting coughed on, and touching someone who is sick.  While these are how viruses are spread from person to person, the infection that occurs on a cellular level is much more complex.  

For starters, only a handful of viruses are known to actually cause illness in humans, but the ones that do have adapted to do it very efficiently, and some are even known to cause cancer.  Viruses that cause cancer include human papillomavirus, Kaposi Sarcoma-associated Herpesvirus, and Epstein-Barr virus.  The way that these viruses get into the cells is very unique compared to the common cold virus, and a team at the University of Michigan Medical School decided to take a closer look at just how they invade to try and get a better grasp on how to prevent cancers caused by viruses in humans.

The virus they researched is called SV40 and it causes tumors in monkeys.  The way that SV40 infects monkey cells is by burrowing itself through the cell membrane and then into its nucleus in order to duplicate itself.  SV40 is used as a tool to understand how the cancer causing viruses work because of the biological similarities that monkeys and humans have.  An earlier team studied how SV40 travels through the cell.  It goes from the surface, through the endosome, the ER, and then enters the cytosol.  

The most recent study illuminates the rest of the virus’ passage through the cell. The way SV40 gets into the nucleus is through the nuclear pore complex.  This is how many viruses enter the nucleus, but the SV40 is too large to enter through this pore.   The virus must disassemble in order to gain access to the nucleus. This process partially disassembles the virus into a smaller package made of two proteins and genetic material (DNA).  As we have learned in class, the DNA is the macromolecule that codes for how to build the proteins that build the virus.  When the DNA for the virus is connected with the two proteins, it uses both the nuclear pore complex and another complex called LINC.  LINC connects the two membranes of the nucleus together.  Many other viruses grab onto the little fingers sticking out of the nuclear pore complex (seen below), while SV40 seeks out LINC in order to get into the nucleus.  

202012 Nuclear pore complex

The difference in entrances between more common viruses and SV40 could be what makes SV40 cancer-causing.  The next step is to research how SV40 exploits LINC in order to expand upon how other diseases could enter the nucleus, and hopefully find a way to trigger the immune system in order to expel or digest the viruses before it is too late.  

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.

Can extinct animals be resurrected?

Recently the CIA has been looking into “resurrecting” extinct animals, specifically Mammoths. Colossal Biosciences, a company based in Texas, believes they can genetically engineer the mammals’ DNA. Although it would be virtually impossible to bring Mammoths back from the dead, their goal is to insert their distinctive traits into present-day Elephants. For this process, scientists need to use “CRISPR,” a method used to replicate gene sequences. According to MedlinePlus, CRISPR “is a group of technologies that give scientists the ability to change an organism’s DNA…and allow genetic material to be added, removed, or altered at particular locations in the genome”. While some scientists are for this idea, others believe it is impossible and the time and money spent could be allocated elsewhere. Ben Shapiro, a professor of ecology and evolutionary biology at the University of California, stated “The biggest misconception about de-extinction is that it’s possible.” Even if scientists were able to collect preserved DNA from the animal, it is nearly impossible to replicate them using technology.

AP Biology Connection

All animal cells need oxygen, food, and water, so when they are deprived of it, they die. Cells consume these through a process called endocytosis. Endocytosis is a process in which cells pull substances from the outside and then engulf them in a vesicle. Without this process, not only would the cell die, but so would all of its contents. DNA is the cells “carrier of genetic information“. DNA itself is very fragile, and under no circumstances will it survive from the extinction of the Mammoths to the present day. Ancient DNA, such as the ones we have from Mammoths, has gone through many environmental issues. Elements such as sunlight, water, and heat can accelerate the DNA degrading process. Unless very well persevered by freezing and sealing it, the DNA will not be functional. The rupturing of cells, when dead, release nucleases causing damage to DNA. Although “bringing back” the Woolly Mammoth would be a great scientific revelation, it seems infeasible due to the inner workings and preservation of the cells.  Woolly mammoth (Mammuthus primigenius) - Mauricio Antón

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