BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: DNA (Page 2 of 8)

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

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On April 23, 2023

In Student Post

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

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On April 23, 2023

In Student Post

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!

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On March 17, 2023

In Student Post

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.

DNA Structure+Key+Labelled.pn NoBB
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

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On March 15, 2023

In Student Post

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

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On January 19, 2023

In Student Post

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.

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On January 8, 2023

In Student Post

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?!?!

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On October 30, 2022

In Student Post

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

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

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

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

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

Shhhhhhh! Some Viruses Can Sneak into Cells and Cause Cancer

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On October 27, 2022

In Student Post

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

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On October 24, 2022

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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?

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On October 24, 2022

In Student Post

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

Are Skittles Toxic from Titanium Dioxide?

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On October 21, 2022

In Student Post

 

 

Skittles-Louisiana-2003

Link to Image

A lawsuit came out in recent months that made claims of the chemical titanium dioxide, a toxin known to scientists being found in a popular candy, Skittles. A consumer filed a suit against Skittles manufacturer, Mars, for titanium dioxide is now a banned chemical according to the European Union. However, in many countries, such as the United States and Canada, titanium dioxide is still considered to be safe to consume. There still needs to be regulations put about the amount of the chemical that can be found in food, but in limited amounts, many think it is relatively harmless in small doses. Toxicologists who are studying the chemical found research indicating that using chemicals. Agnes Oomen, a senior scientist at the Netherlands’ National Institute for Public Health and the Environment, told Scientific American that saying we’re not certain that it’s safe is very different from saying it’s unsafe.” When the European Union placed the ban on titanium dioxide, they were just being overly cautious.

What is Titanium dioxide? It is a white powder that is used as a pigment in many candies and other consumer items, such as makeup and paints. Titanium dioxide is good at scattering visible light. This causes products that contain the chemical a brighter and more vibrant color. What raised skepticism for consumers was the fact that Titanium dioxide is also used in many sunscreens because it is an efficient barrier to ultraviolet light.

DNA orbit animated

Link to Image

The United States Food and Drug Administration had deemed the chemical safe in food, but it still must be a regulated amount of not being able to be more than 1% by weight of the product. In contrast, Europe is going through a period of “great detox”, for the European Food Safety Authority (EFSA), an organization that researches the risks of foods, is banning many chemicals previously found in products. In 2021, EFSA found in a report that titanium dioxide can be genotoxic. That means the drug could alter genetic materials such as DNA. This possibility is what causes the EFSA to ban the use of titanium dioxide in products. Oomen participated in making the report about titanium dioxide saying the decision “is on the cautious side.” The European Union’s decision to ban the chemical was based on a slight possibility that titanium dioxide is harmful, for there has been no evidence so far that proves it could cause people any significant dangers.

Saji George, from McGill University, said researchers are “ missing other big parts of the picture. There are so many other things that could be happening with small, consistent amounts of titanium dioxide in a diet over a long period of time.” Along with his colleagues, they recently discovered that the chemical could amplify allergies to some proteins in foods, making titanium  dioxide still a concern. George also mentioned that the studies done on titanium dioxide were done mainly on rates, not humans. “We don’t know how titanium dioxide could enhance certain diseases—for example, inflammatory bowel disease in people with preexisting conditions,” he states. This just goes to show there is still a lot we don’t know about the drug.

Oomen agrees with the European Union’s decision to ban the use of titanium dioxide because researchers have not made any conclusive findings that confirm if the drug is safe or could be harmful. She feels there needs to be a more suitable method to study the chemical. Norb Kaminski, director of the Institute for Integrative Toxicology at Michigan State University said “I think that titanium dioxide in the amount that it’s used in Skittles and food products is of no toxicological concern or health concern to the public. There’s just not the evidence to support that currently.”

This topic relates to our most recent unit in Biology because one of the concerns regarding titanium dioxide involved the alteration of DNA. We learned about DNA in this unit when we learned about organic compounds. DNA is one of the nucleic acids we learned about when we studied different organic compounds. DNA functions to store all our hereditary information, and it plays an essential role in our cells. Also, that titanium dioxide had the potential to cause allergies to proteins found in certain foods. We learned about protein being another organic compound vital to the cell. We learned about all the different functions of proteins that are crucial for all cells to function properly.

 

Can this Protein Cause Alzheimer’s?

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On October 20, 2022

In Student Post

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

 

CRISPR Quits Coronavirus Replication

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On March 22, 2022

In Student Post

The gene-editing CRISPR has now been utilized by scientists to prevent the replication of Coronavirus in human cells, which can ultimately become a new treatment for the contagious virus. However, since these studies were performed on lab dishes, this treatment can be years away from now.

Firstly, CRISPR is a genome-editing tool that is faster, cheaper, and more accurate than past DNA editing techniques whilst having a much broader range of use. The system works by using two molecules: Cas9 and guide RNA (gRNA). Cas9 is an enzyme that acts as “molecular scissors” that cuts two strands of DNA at a specific location. gRNA binds to DNA and guides Cas9 to the right location of the genome and ultimately makes sure that Cas9 cuts at the right point.

 

CRISPR'S Cas9 enzyme in action

CRISPR’S Cas9 enzyme in action

In this instance, CRISPR is used to allow the microbes to target and destroy the genetic material of viruses. However, they target and destroy the RNA rather than the DNA. The specific enzyme they use for this is Cas13b, which cleaves the single strands of RNA, similar to those that are seen in SARS-CoV-2. Once the enzyme Cas13b binds to the RNA, it destroys the part of the RNA that the virus needs to replicate. This method has been found to even work on new mutations of the SARS-CoV-2 genome, including the alpha variant.

COVID-19 vaccines are being distributed around the world, but an effective and immediate treatment for the virus is necessary. There are many fears that the virus will be able to escape the vaccines and become a bigger threat. Although this treatment is a step in the right direction for effective treatment of COVID-19, this technique will ultimately take a long time for the treatment to be publicly available.

CRISPR is greatly relevant to AP Bio, as seen through its use of enzymes in DNA replication. CRISPR utilizes Cas9, an enzyme that is similar to helicase. In DNA replication, the helicase untwists the DNA at the replication fork, which after the DNA strands are replicated in both directions. 

This article is fairly outdated since there have now been immediate treatments created for COVID-19. But, what do you think about the use of CRISPR for future viruses and pandemics? Personally, I believe that CRISPR will ultimately become a historical achievement in science due to its various uses. Thank you for reading and let me know what you think in the comments! 

 

The Redesigning of CRISPR

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On March 20, 2022

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Cas9, a key component of a widely used CRISPR-based gene-editing tool has been redesigned by scientists at The University of Texas at Austin to be thousands of times less likely to target the wrong stretch of DNA while remaining just as efficient as the original version. This could potentially make gene replication safer and more abundant for medical use.

The CRISPR-Cas9 system consists of an enzyme that introduces a change or mutation into DNA. Cas9 enzymes can cut strands of DNA at a specific location in the genome so parts of the DNA can then be added or removed. CRISPR-based gene-editing tools are adapted from naturally occurring systems in bacteria. In nature, Cas9 proteins search for DNA with a very specific sequence of 20 letters. When most of the letters are correct, Cas9 could still change these DNA fragments. This is called a mismatch, and it can have disastrous consequences in gene editing.

The challenge with using CRISPR-based gene editing on humans is that the molecular machinery occasionally makes changes to the wrong section of a host’s genome. This could possibly repair a genetic mutation in one spot in the genome but may accidentallyDna, Analysis, Research, Genetic Material, Helix create a dangerous new mutation in another.

SuperFi-Cas9 is the name of the new version of Cas9 which has been studied and proven to be 4,000 times less likely to unnecessarily cut off-DNA sites but operates just as fast as naturally occurring Cas9. In the Sauer Structural Biology Lab, scientists were surprised to discover that when Cas9 encounters a type of mismatch, there is a “finger-like structure” that swoops in and holds on to the DNA, making it act like the correct sequence. Usually, a mismatch leaves the DNA unorganized since this “finger-like structure” is mainly used to stabilize the DNA. Based on this insight, scientists redesigned the extra “finger” on Cas9 so that instead of stabilizing the part of the DNA containing the mismatch, the finger is stored away which prevents Cas9 from continuing the process of cutting and editing the DNA. This result in SuperFi-Cas9, a protein that cuts the right target just as readily as naturally occurring Cas9, but is much less likely to cut the wrong target.

This applies to our unit on mitosis when cells are replicating DNA in the S-phase. When chromosomes are duplicated, gene replication occurs. Sometimes gene replication could result in mutations which could lead to a cell not functioning properly. A cancerous cell is an example of cell not performing normally since it rapidly performs mitosis causing the cell to duplicate uncontrollably. This results from an abnormality in gene replication where CRISPR technology can locate this mutation and restore the cell back to normalcy.

CRISPR Mini | New Territory Unlocked

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On March 20, 2022

In Student Post

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

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

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

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

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

CRISPR Causes Cancer, Sort Of

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On March 20, 2022

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

CRISPR logoDNA animation

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

Unnatural Selection: The Future of The Future?

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On March 20, 2022

In Student Post

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

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

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

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

CRISPR illustration gif animation 1

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

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

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

Megan Molteni / WIRED

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

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

 

Redesigned Cas9 protein provides safer gene editing than ever before!

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On March 20, 2022

In Student Post

Gene editing is a group of technologies that give scientists the ability to change an organism’s DNA. These technologies allow genetic material to be added, removed, or altered at particular locations in the genome. Several approaches to genome editing have been developed. A recent one is known as CRISPR-Cas9, which is short for clustered regularly interspaced short palindromic repeats and CRISPR-associated protein 9. The CRISPR-Cas9 system has generated a lot of excitement in the scientific community because it is faster, cheaper, more accurate, and more efficient than other existing genome editing methods.

File:CRISPR-Cas9 Editing of the Genome (26453307604).jpg

CRISPR-Cas9 Editing of the Genome

One of the challenges that come using CRISPR-based gene editing within humans is that the molecular machinery may sometimes make edits to the wrong section of a host’s genome. This is problematic because it creates the possibility that an attempt to repair a genetic mutation in one location in the genome could accidentally create a dangerous new mutation in another spot. Scientists at The University of Texas at Austin have redesigned a key component of a widely used CRISPR-based gene-editing tool, called Cas9, to be thousands of times less likely to target the wrong stretch of DNA while remaining just as efficient as the original version, making it potentially much safer.

File:CRISPR CAS9 technology.png

CRISPR CAS9 technology

The CRISPR-Cas9 system works similarly in the lab. Researchers create a small piece of RNA with a short ‘guide’ sequence that binds to a specific target sequence of DNA in a genome. The RNA also binds to the Cas9 enzyme. As in bacteria, the modified RNA is used to recognize the DNA sequence, and the Cas9 enzyme cuts the DNA at the targeted location. Although Cas9 is the enzyme that is used most often, other enzymes can also be used. Once the DNA is cut, researchers use the cell’s own DNA repair machinery to add or delete pieces of genetic material, or to make changes to the DNA by replacing an existing segment with a customized DNA sequence.

Other labs have redesigned Cas9 to reduce off-target interactions, but so far, all these versions improve accuracy by sacrificing speed. SuperFi-Cas9, as this new version has been named, is 4,000 times less likely to cut off-target sites but just as fast as naturally occurring Cas9. Scientists say you can think of the different lab-generated versions of Cas9 as different models of self-driving cars. Most models are really safe, but they have a top speed of 10 miles per hour.

In my opinion, setting aside any and all ethical concerns, genome editing is of great interest in the prevention and treatment of human diseases. Currently, most research on genome editing is done to understand diseases using cells and animal models. Scientists are still working to determine whether this approach is safe and effective for use in people. It is being explored in research on a wide variety of diseases, including single-gene disorders such as cystic fibrosis, hemophilia, and sickle cell disease. It also holds promise for the treatment and prevention of more complex diseases, such as cancer, heart disease, mental illness, and human immunodeficiency virus (HIV) infection.

Could Christmas Island rats make a comeback? Thanks to CRISPR gene editing, they might!

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On March 20, 2022

In Student Post

From climate change to overhunting by humans, there are many factors which contribute to the extinction of species in the animal kingdom. The Christmas Island rat, also known as Maclear’s rat, went extinct a century ago in what is believed to be the first and only case of extinction of a species due to disease. It has always been believed that once a species goes extinct, it is gone for good. That is until recently when scientists began experimenting with “de-extinction” efforts to bring back the Christmas Island rat.

Little does this rat know that his family reunions may be getting a whole lot bigger!

As published March 9 in the science journal, Current Biology, a team of paleo geneticists from the University of Copenhagen recently conducted a study into gene sequencing the Christmas Island rat, in order to estimate the possibilities of future gene editing experiments which could bring the species “back to life”. The process of genetic editing for de-extinction efforts, as explained by the research team in their abstract, consists of first identifying the genome of the species and then editing the genes of similar species to make it more similar to that of that extinct one. The team used frozen somatic cells of the extinct rats, cells with a 2n number of chromosomes which are made during the process of mitosis. The team was able to sequence the rats’ genome, aside from some small portions which remain missing. They then had to identify the modern species which they could gene edit. Their findings established that the Christmas Island rat shares around 95% of DNA with the modern Norway brown rat. At this point, it

Now that the rat’s genome has been sequenced to the best of the team’s ability and a similar species has been identified, the gene editing possibilities are endless, especially with CRISPR technologies and techniques. “CRISPR” stands for Clustered Regularly Interspaced Short Palindromic Repeats in DNA sequencing. This system was discovered by a group of scientists, led by Dr. Emmanuelle Charpentier. CRISPR uses Cas9, an enzyme which cuts DNA at specified sections as guided by RNA. There are three different types of edits drone with CRISPR technology: disruption, deletion, or correction/insertion. Disruption editing is when the DNA is cut at one point and base pairs are either added or removed to inactivate a gene. Deletion editing is when the DNA is cut at two points and a larger sequence of pairs is removed. Correction/insertion editing is when a new gene is added into a sequence using homology directed repair.

Thomas Gilbert, the lead scientist on the team, says that he would like to conduct CRISPR gene editing experiments on living species of rats before attempting to replicate the DNA of an extinct species. For example, attempting to mutate the DNA of the Norway brown rat into that of the common black rat. Once this experiment is conducted, the possibilities of reviving the Christmas Island rat will be more clear. Until then, we can only hope! Do you think it’s possible to see the Christmas Island rat revived anytime soon?

How Does Activation of p53 Effect the Use of CRISPR?

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On March 16, 2022

In Student Post

In a study conducted at Karolinska Institutet in Sweden, researchers looked into CRISPR gene editing and how that can play a critical role in mutated cancer cells as well as the medical field. CRISPR is “programmed to target specific stretches of genetic coding and to edit DNA at the precise location;” specifically, the CRISPR system binds to the DNA and cuts it, therefore, shutting the targeted gene off. Researchers can also permanently alter genes in living cells and organisms, and in the future, using this method they may even be used to treat genetic causes of diseases. Although CRISPR sounds amazing, will it really be as great as it seems?

CRISPR CAS9 technology

CRISPR

There are a few obstacles that need to be overcome before CRISPR can even become regularly administered in hospitals. The first is to understand how cells will behave once they are subjected to DNA damage which is caused by CRISPR in a controlled manner. When cells are damaged they activate a protein called p53 which has negative and positive effects on the procedure. The technique is less effective when p53 is activated, however, when p53 is not activated cells can grow uncontrollably and become cancerous. Cells, where p53 is not activated, have a higher survival rate when subjected to CRISPR and because of this can accumulate in mixed cell populations. Researchers have also found a network of linked genes that have a similar effect to p53 mutations, so inhibiting p53 also prevents these cells from mutating. 

Long Jiang, a doctoral student at the Department of Medicine at Karolinska Institutet, says that “it can be contrary to inhibit p53 in a CRISPR context. However, some literature supports the idea that p53 inhibition can make CRISPR more effective.” By doing this it can also counteract the replication of cells with mutations in p53 as well as genes that are associated with the mutations. This research established a network of possible genes that should be carefully controlled for mutations during CRISPR. This will hopefully allow for mutations to be regulated and contained more efficiently.

DNA, or deoxyribonucleic acid, is a long molecule that contains a genetic code; “like a recipe book it holds all the instructions for making the proteins in our bodies.” Most DNA is found in the nucleus of the cell, but a small amount can also be found in the mitochondria. DNA is a key part of reproduction because genetic heredity comes from the passing down of DNA from parents to offspring. Altering this DNA can have an impact on a number of someone’s physical characteristics. CRISPR does just that. It can be used to edit genes by finding a specific piece of DNA inside a cell and then modifying it. Since CRISPR is so new, it has its positives and negatives, but overall it is a groundbreaking discovery. 

DNA double helix horizontal

DNA

In conclusion, even though cells seem to gain p53 mutations from CRISPR, it has been discovered that most of the cell mutations were there from the start. Even though this is still an issue, we don’t know to what extent it can cause greater harm, so it will be exciting to see the new discoveries in the future!

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