BioQuakes

AP Biology class blog for discussing current research in Biology

Dire wolves are back?

Recently, we covered evolution and, by extension extinction. When a species or population lack individuals with traits suited for their environment, the given group may very well die out. We learned how if a species loses its ecological niche they may go extinct. This trend can be seen with dire wolves–who went extinct a few million years ago. These wolves were bigger and had sharper teeth than the typical grey wolf of the modern age. They hunted horse, bison, and possibly mammoths. Unfortunately, their prey began to dwindle. Some of which–like the mammoth–even went extinct. As a result, the dire wolves went extinct as they lost their primary food sources and were not well adapted to hunt other animals.

Miraculously, dire wolves have once again be born to this earth. Colossal Biosciences has finally been able to successfully perform de-extinction. Using fossils found in 2021–they were previously thought to be of little use–the company was first able to map the history of the dire wolf. Leading to the conclusion that dire wolves and grey wolves are 99% identical. Only 8 genes are notably different between the two. Next, the scientists altered a wolf egg with the dire wolf DNA that could be implanted into large dogs–who would serve as surrogate mothers. Most of the embryos failed to develop, but four developed–and thus four pups were born.

It is exciting to see extinct animals once again roam the earth. Nonetheless; the question is asked: will they, as a collective species, survive? Without human aid, I would argue they would not. The dire wolfs were adapted to a past age; there are other species better suited for the modern day. Regardless of my viewpoint, do you believe the dire wolves can thrive?

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CRISPR: Revolutionizing Cancer Research and Treatment

CRISPR is a groundbreaking gene-editing tool that allows scientists to make highly specific changes to DNA. The system was originally discovered as a bacterial defense mechanism against viruses, where bacteria store fragments of viral DNA in special regions of their genome called CRISPR sequences. These fragments are used to create guide RNAs (gRNAs) that pair with a DNA-cutting enzyme called Cas9. When the same virus tries to attack again, the guide RNA matches with the viral DNA, and Cas9 cuts it, disabling the virus.CRISPR illustration gif animation 1

Scientists realized that this natural system could be repurposed in the lab to edit any gene by designing a custom guide RNA that leads Cas9 toa specific DNA sequence. Once the Cas9 enzyme cuts the DNA, the cell tries to repair the break. This repair process can introduce mutations that deactivate the gene, or scientists can insert a new piece of DNA to replace the original sequence. This makes CRISPR much faster, cheaper, and more precise than earlier gene-editing technologies like ZFNs and TALENs.

CRISPR is transforming cancer research by allowing scientists to study the function of individual genes involved in cancer. By using CRISPR to “knock out” or edit specific genes in cancer cells, researchers can see which genes are essential for tumor growth, metastasis, and drug resistance. For example, in the Cancer Dependency Map project, scientists used CRISPR to disable thousands of genes across hundreds of cancer cell lines. They identified over 600 genes that tumors depend on for survival—potential new targets for cancer drugs.

CRISPR is also used to create precise cancer models in cell cultures and animals by introducing mutations in oncogenes (genes that cause cancer when mutated) or disabling tumor suppressor genes (which normally prevent cancer). These models help researchers study how tumors develop and test potential treatments in a more controlled and accurate way.

In cancer treatment, CRISPR is being used experimentally to engineer patients’ immune cells to fight cancer more effectively. For instance, in clinical trials, scientists use CRISPR to modify T cells so they can better recognize and attack cancer cells. This includes deleting genes that suppress T cell function and inserting new genes that help them target tumor-specific antigens. One study modified T cells to recognize a protein called WT1, which is found in many tumors. These edited cells were then infused back into patients, showing early signs of safety and effectiveness.

This connects directly to what we learned in AP Biology, especially in our molecular genetics unit. We studied how DNA is transcribed into RNA and translated into proteins, and how mutations can affect gene expression. CRISPR works by directly targeting DNA to create those mutations or introduce new sequences, changing how genes are expressed. We also learned about bacterial immune responses and plasmid-based gene transfer—CRISPR was originally discovered as a prokaryotic immune system that captures viral DNA, and that same system is now one of the most powerful tools in modern medicine.

This topic is especially exciting to me because I want to go into cancer research and oncology. It’s incredible to see how a molecular system that bacteria use to fight viruses is now being used to fight cancer in humans. CRISPR allows researchers to explore the genetic roots of cancer and develop therapies that are personalized, precise, and potentially curative. Learning about how CRISPR works not just in theory but in actual clinical settings motivates me to be part of the next wave of scientists and doctors using genetics to save lives.

How Enzymes Could Finally Beat Plastic Pollution

Imagine tossing a plastic bottle into the trash and knowing that tiny microbes down the line are already ready to eat it. In October 2024, scientists found an enzyme in the wastewater microbe Comamonas testosteroni that chops up PET— the same plastic in water bottles—into its building blocks, terephthalate and ethylene glycol. When they moved the gene for that enzyme into a different microbe, it suddenly gained the power to break down PET on its own, proving the enzyme is all you need to kick-start the process (American Chemical Society).

If you think that’s cool, engineers have tweaked PET-eating enzymes to consume 90% of a bottle in just ten hours after a quick mechanical chop-up step. By recovering the monomers and feeding them back into plastic production, this trick could mean less new oil-based plastic and way less waste (Novonesis).

And it’s not just wastewater. A March 2025 survey scoured landfill samples from six countries and used machine learning to spot nearly 32,000 possible plastic-eating enzymes—then focused in on 712 that seem especially good at breaking down plastics like PET, PLA, PBS, and more. These landfills are like natural enzyme factories, and every new enzyme is another tool (Phys.org).

In our AP Bio class, we learned that enzymes work because their unique 3D shapes let them grab onto specific molecules and speed up reactions. These plastic-eaters have special active sites shaped to fit polymer chains, holding them in place so they can cut them into smaller pieces—just like how lysozyme in your body breaks down bacterial cell walls. By studying and tweaking those active sites, scientists are making enzymes that work faster and under tougher conditions.

Ideonella Sakaiensis Eating Plastics

Imagine wastewater plants with bioreactors full of these super-enzymes, or landfill digs that mine and deploy them on the spot. With a bit more research and some creative engineering, we could turn our world’s plastic mountains into feedstock for new bottles, clothes, or even building materials. Could enzyme-powered recycling be the breakthrough we need to beat plastic pollution? Let me know what you think!

The Hidden Pathways to Modifying Cell Functions

Organelles, proteins, and other intracellular structures can resemble a labyrinth within already complex cells. For scientists, cell function has been a similar mystery to crack, as modifying cell functions has long been challenging.

Eukaryotic Cell (animal)

Diagram of an eukaryotic animal cell.

However, new pathways to altering these functions have recently been discovered within cell membranes, allowing scientists to use laboratory-developed drugs to edit and change cell functions.

In a recent study by the Hospital del Mar Medical Research Institute, researchers utilized highly detailed computer simulations to find hidden “gateways” that could be used to modify the G protein-coupled receptors (GPCRs) suspended in the cell membrane.

According to the research team, “GPCRs are important because a significant portion of existing drugs target them to act on cells. In fact, 34% of FDA-approved drugs are based on these receptors,” highlighting the significance of this new discovery and its possible implications on new technologies and medicines!

G protein-coupled receptor (Seven-transmembrane receptors)

Simplified diagram of a G protein-coupled receptor (GPCR) suspended in a cellular membrane.

More specifically, the cell membrane is composed of phospholipids, proteins, lipids, and other molecules, including GPCRs. As we have learned in AP Biology, the cell membrane is often referred to as a “phospholipid bilayer” due to the multilayer structure the phospholipid molecules form to create the membrane that surrounds the cell’s cytoplasm. In the first units of the course, our class learned about the hydrophilic heads and hydrophobic tails that form phospholipids as well as the types of proteins that plasma membranes contain.

We discussed the roles and functions of membrane proteins, especially the significance of integral membrane proteins — the family of membrane proteins that GPCRs are a part of. Best explained by LibreTexts Biology, “Integral membrane proteins are permanently embedded within the plasma membrane. They have a range of important functions. Such functions include channeling or transporting molecules across the membrane. Other integral proteins act as cell receptors.”

Detailed diagram of lipid bilayer cell membrane

Detailed diagram of the phospholipid bilayer cell membrane.

As shown by the researchers’ discoveries and understood in our class, GPCRs play an important role in cell signaling and physiological system functions, as the proteins have direct linkages to crucial cell functions and operations.” GPCRs are involved in sight, taste, smell, behavior, mood, and immune system regulation. Even though the signaling molecules, types of GPCR, and mechanisms of action may differ for all these roles, they all involve certain extracellular signals that are converted into a cellular response,” states the National Library of Medicine.

In fact, GPCRs make up the largest group of membrane-bound protein receptors! In this way, their abundance in eukaryotic cells is what truly makes their presence so powerful, and the researchers’ work even more important to discovering new therapies for modulating GPCR-related cell functions.

Ultimately, the team’s work has opened the door to more precise drug targeting and could even lead to developing new therapies focused on targeting specific receptor pathways.

While this research is still ongoing, it still serves as a revolutionary step in understanding how GPCRs regulate cellular functions and how that knowledge can be used to create unique medical treatments in the future. The possibilities could be endless!

 

Reviving Dire Wolf Traits Through Targeted Gene Editing

Reconstruction of Canis dirus (dire wolf) (Pleistocene, North America) 2 (32194767411)

Colossal Biosciences’ recent discovery sparked both fascination and skepticism: three genetically engineered wolf pups—Romulus, Remus, and Khaleesi—have been introduced as the first step toward dire wolf “de-extinction”. These animals, which went extinct more than 10,000 years ago, have become famous in both science and popular culture. However, many scholars believe the story is more complex.. The pups are not exact genetic replicas of Aenocyon dirus (the original dire wolf species), but rather gray wolves whose genomes were edited to resemble certain physical traits of dire wolves.

Instead of reconstructing the full dire wolf genome, Colossal scientists retrieved fragmented DNA from 13,000- and 72,000-year-old fossils and compared those fragments to the complete genome of the gray wolf. They identified key differences and made 20 specific edits to gray wolf cells. For example, modifications to the CORIN gene contributed to the pups’ light-colored fur. After editing, nuclei from these cells were inserted into denucleated dog egg cells via a cloning technique known as somatic cell nuclear transfer. The resulting embryos were implanted into surrogate dogs and delivered via C-section.

Canis lupus & Aenocyon dirus

While these pups exhibit dire wolf-like traits, they are not genetically identical to true dire wolves. This has sparked criticism within the scientific community. Paleoecologist Jacquelyn Gill argues that the absence of a full dire wolf genome disqualifies these animals from being considered de-extinct. Others, like Colossal’s chief science officer Beth Shapiro, defend the work as a legitimate revival of extinct characteristics, even if the animals themselves are not exact replicas.

Still, the technology involved holds real promise for conservation. Colossal is also working with endangered red wolves (Canis rufus), using similar genetic techniques to introduce lost ancestral traits and increase genetic diversity. These efforts may offer long-term solutions to preserving critically endangered species by equipping them with greater resilience to disease.

This article connects to what we’ve learned in AP Biology about how mutations in DNA affect protein function and influence phenotype. In Colossal’s study, scientists analyzed ancient DNA fragments from dire wolf fossils and compared them to the gray wolf genome to identify genetic differences at specific loci—locations of genes on chromosomes. Using this information, they edited 20 genes in gray wolf cells to match the sequences found in dire wolves. We learned a mutation is a change in the DNA sequence that can affect the structure or function of a resulting protein, and phenotype is the observable trait determined by genotype. When a gene’s nucleotide sequence is changed, it can lead to the production of a different protein during translation, altering the organism’s traits. In this study, those changes were inherited in the cells used for cloning, demonstrating how scientists can directly manipulate the genetic code to produce specific phenotypes by targeting mutations.

I think it is interesting how small changes to DNA sequences can lead to major differences in physical traits. This research shows how much information about an organism’s traits is stored at the molecular level. Do you think using gene editing to recreate traits from extinct species is a valuable scientific goal? Share your thoughts in the comments!

“Walk It Off”: How Your Coach’s Most Annoying Phrase Might Just Save Your Brain

We all know that regular exercise keeps our bodies strong, but what if it could help keep our memories sharp, too? According to a new study published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, researchers at UC San Diego and Wake Forest University found that both low and moderate-high intensity exercise can slow cognitive decline in older adults at risk for Alzheimer’s disease. 

Brain Exercising

The study, called EXERT, tracked nearly 300 sedentary older adults with amnestic mild cognitive impairment (aMCI), a condition marked by memory problems that don’t yet interfere severely with daily life, but often lead to Alzheimer’s. About 16% of people with aMCI progress to Alzheimer’s each year. Participants were assigned to either a moderate-to-high intensity aerobic group or a low-intensity stretching and balance group. Each person exercised three to four times per week at a local YMCA, under supervision, for 12 months. What’s remarkable is that cognitive function remained stable in both exercise groups over the year, whereas cognitive decline is usually expected in this population. Additionally, participants showed less brain volume loss, especially in the prefrontal cortex, a key region involved in decision-making, attention, and memory, compared to individuals who only received standard care like regular check-ups and medications.

What makes this study stand out is its accessibility. The team partnered with local YMCAs to bring the interventions into community settings, showing that effective brain health treatments don’t have to involve fancy equipment or extreme intensity. Other researchers have come to many similar conclusions. Researchers at Harvard Medical School tackled the question: Which exercise is best for your brain? This article concluded, “forms of aerobic exercise that get your heart pumping might likely yield the best benefits,” says Dr. Scott McGinnis, assistant professor of neurology at Harvard Medical School.

So, how does this connect to what we’ve learned in AP Biology? This connects to neural networks, which are incredibly complex webs of interconnected neurons that process and transmit information through electrical and chemical signals. When a neuron receives a stimulus, like a signal from another neuron or the environment, it fires an action potential, an electrical impulse that travels down its axon. This triggers the release of neurotransmitters like glutamate or acetylcholine into the synapse, which then bind to receptors on the next neuron, continuing the message. These transmissions are what allow you to think, remember, and even move. Exercise helps maintain the health of this communication system in several ways. First, regular movement increases blood flow to the brain, delivering more oxygen and glucose, which neurons need for aerobic respiration, and more ATP means more power for the sodium-potassium pumps that reset the neuron after firing. Without that pump, your neurons can’t keep firing signals. We’ve talked in class about how stimuli are detected and translated into neural responses, and how neurons relay messages using action potentials and neurotransmitters. This study is a real-world example of that biology in action. Exercise acts as both a stimulus and a support system for the neural pathways that keep our brains functioning. It doesn’t just make you feel better, it keeps your neurons alive and talking.

I chose this topic because the science behind memory and cognition fascinates me, especially knowing that there’s something we can do to protect our minds. It’s hopeful. With Alzheimer’s affecting so many families, the idea that something as accessible as regular walking or stretching could delay or prevent decline is powerful.

Here’s a question for you: Would you commit to 30 minutes of light exercise a day if it meant possibly protecting your brain health? Why or why not? Let me know in the comments—I’d love to hear your thoughts.



Warty Birch Caterpillars: Using Vibration as a Survival Tactic

Flight or fight mode? How about vibrating to escape your predator? In Rohini Subrahmanyam’s article, she explains how many species of small caterpillars, like warty birch caterpillars, use vibrations to mark their territory on the tips of leaves. These tiny vibrations aren’t just random movements, they’re part of a highly specialized defense mechanism. When another insect comes too close, the caterpillar rhythmically shakes its head and body against the leaf surface, producing pulses that act as a warning. To other insects, this signal is telling them that the leaf is taken. 

These little caterpillars are extremely vulnerable after they hatch, so this form of “vibrational shouting” is crucial to their survival. If the intruder doesn’t back off, the caterpillar doesn’t hesitate to escalate. In a last-ditch effort to stay safe, it springs off the tip of the leaf like Spider-Man to escape danger.

To us, these vibrations are tiny, but for small insects, the scale of these movements is massive. For a caterpillar, generating such strong signals with their body is a big feat, showing how evolution has fine-tuned even the smallest creatures to communicate and defend themselves in surprisingly sophisticated ways.

Caterpillar on birch leaf - Flickr - S. Rae

In our AP Biology class, we have recently learned about evolution. Mutations that allow these caterpillars to perform this act have become more apparent in the species due to natural selection. Individuals with these genes are able to survive for longer and reproduce more, ultimately spreading the trait.

I hope you enjoyed learning about this fun survival technique! Are we underestimating the abilities of tiny organisms like the warty birch caterpillars? What other small organisms have you heard of that have similar survival tactics to these caterpillars that go unnoticed?

How Parental Metabolism Influences a Child’s Long-Term Health

A new study published in Diabetologia by researchers at Lund University and the King Edward Memorial Hospital and Research Centre in Pune, India, highlights how a child’s long-term risk of developing type 2 diabetes and cardiovascular disease can be influenced by the metabolic traits of their parents. Using data from over 2,400 participants in the Pune Maternal Nutrition Study, researchers analyzed parent and offspring relationships related to cardiometabolic traits such as body mass index (BMI), blood glucose levels, cholesterol, and insulin function at three different developmental stages: 6, 12, and 24 years of age.

The study found that maternal genes had the strongest influence on a child’s blood sugar and cholesterol levels throughout their early life and into adulthood. This influence was seen even at birth, where the mother’s genes had affected the baby’s birth weight. These findings suggest that maternal contributions, through both genetic inheritance and the prenatal environment, play a dominant role in shaping how a child regulates glucose and lipids. On the other hand, paternal genes had a larger impact on insulin-related functions over time, showing a stronger paternal influence on the child’s insulin sensitivity and secretion as they aged.

Participants in the study underwent tests measuring insulin sensitivity and the function of insulin-producing cells. The results showed that if the father had impaired insulin secretion or insulin resistance, these traits were more likely to appear in the child later in life. Researchers noted that this type of information could be valuable for early interventions, such as promoting physical activity, which is known to improve insulin sensitivity and lower the risk of developing type 2 diabetes.

This research provides insight into parent-of-origin effects, where the influence of a trait differs depending on whether the gene is inherited from the mother or the father. These findings have implications for developing preventive strategies targeted at parents, particularly mothers during pregnancy, to help reduce their children’s risk of cardiometabolic diseases.

This connects to what we learned in AP Biology because this study shows the concept of parent-of-origin effects and their connection to epigenetics and genomic imprinting. While classical Mendelian inheritance assumes equal contribution from both parents, this study shows that gene expression can be modified depending on the parent from whom the gene is inherited. Furthermore, the maternal effect observed in this research connects to the role of the prenatal environment in influencing phenotypic outcomes. This reinforces the idea that both genetic and environmental factors inherited from parents can significantly shape an individual’s physiological traits and disease risk over time.

On a more personal note, this topic stood out to me because I’ve seen how family health traits can run deep. What are some ways that schools and communities could help families better understand and manage their health risks across generations?

A family walking through a meadow at Gwynns Falls-Leakin Park

The Caterpillar That Dances for Its Life

Researchers observing the silver-spotted skipper caterpillar (Epargyreus clarus) have recently uncovered a fascinating behavior that may redefine how we think about animal responses to danger. While most animals rely on the typical “fight, flight, or freeze” strategy when faced with a threat, this tiny caterpillar appears to have developed a fourth option—rhythmic thrashing, or what scientists are informally calling a “defensive dance.”

Silver-spotted Skipper - Hodges-3870 (Epargyreus clarus)

This movement is unlike anything seen before in similar species. When disturbed, the caterpillar vigorously swings its rear end side to side in a consistent, patterned motion. Scientists suspect this strange, repetitive thrashing may confuse predators or make the caterpillar harder to track. The behavior was so unique that it challenged researchers’ expectations and encouraged them to rethink how defensive strategies in prey species are categorized.

The study, published in Scientific American, highlights how these caterpillars do not respond with the common freeze-and-hide tactic typical of many insects. Nor do they try to flee. Instead, they display a coordinated series of movements that seem to serve as a proactive defense mechanism. This rhythmic display isn’t random—it’s controlled and repeatable, suggesting it may be hardwired into the caterpillar’s nervous system.

Intrigued by this behavior, researchers began to test different predator interactions and environmental triggers. What they found was that the caterpillar’s thrashing typically began before a predator made physical contact—implying it is an anticipatory response to threat. In short, this caterpillar doesn’t wait to be touched—it senses danger and starts “dancing” immediately, likely increasing its chances of survival by catching the predator off guard.

While this behavior might seem like a quirky exception, it has major implications for how we define animal responses. Most biology textbooks list “fight, flight, or freeze” as the three standard reactions to threat. But now, researchers are asking whether this rhythmic movement should be recognized as a legitimate fourth category of defensive behavior—one that is active, deliberate, and possibly more common in the animal kingdom than previously thought.

This discovery ties directly into AP Biology’s exploration of innate behavior and nervous system responses. In Unit 8, we learn about how organisms react to external stimuli through genetically programmed behaviors. This caterpillar’s rhythmic thrashing seems to be an innate response—one that evolved over time to increase its chances of surviving predation. It also ties into evolutionary biology concepts, such as natural selection and adaptation. If this behavior helps the caterpillar avoid being eaten, it would likely be passed on to future generations, showing how even unusual traits can become beneficial adaptations.

I came across this study on the silver-spotted skipper caterpillar and was immediately hooked—who would have thought that a caterpillar could “dance” its way out of danger? I’ve always thought of animal defenses as kind of predictable, but this breaks the mold. It’s such a cool reminder that biology is constantly evolving (literally) and that even the smallest creatures can rewrite the rules.

This makes me wonder: should we start teaching “thrash” as a legitimate addition to the “fight, flight, or freeze” model? Could there be other animals with similar secret strategies that we just haven’t observed yet? What do you think this tells us about the diversity of behavioral adaptations in nature?

CRISPR-Cas12a: The Next-Level Gene Editing Breakthrough

Did you ever wonder if gene editing was something from a science fiction film when you heard about CRISPR-Cas9? So grab a seat, because scientists at Yale are making fresh discoveries that will revolutionize gene editing technology! For many years, CRISPR-Cas9 allowed scientists to use a “guide” RNA to target and alter a single gene. That was amazing in and of itself, but now they have created a new set of mice models that can manage several genetic changes simultaneously. This means that researchers can continue to examine complex interactions in conditions like cancer and autoimmune diseases. 

File:CRISPR-Cas.svg
By Mariuswalter, translation by TheBartgry – GRNA-Cas9.svg, CC BY-SA 4.0, Link

The Yale team’s introduction of a next-generation technology called CRISPR-Cas12a, which can simultaneously target several genomic sites. This isn’t just advanced lab work; it’s a game-changer since it allows researchers to simultaneously fine-tune genes in different directions, similar to pressing several piano keys to produce a powerful chord. In simple terms, the project’s main researchers, Sidi Chen, Matthew B. Dong, and Xiaoyu Zhou, are promoting gene editing to investigate a variety of immune system responses. Now, we can acquire information on how particular changes affect immune cells in diseases including liver problems, skin cancer, and lung cancer. Furthermore, they can quickly create new disease models, which accelerates the development of treatments for a wide range of diseases.

Wait till you learn about the potential for the future if you think that’s incredible. These novel CRISPR-Cas12a mouse lines allow scientists to further studies on autoimmune illnesses, cancer, metabolic diseases, and even neurological conditions. With the help of the “molecular scissors” Cas9 and Cas12a, we can precisely cut, replace, or alter DNA, revealing details about how our bodies react to illness. These new discoveries are being used by Yale’s Systems Biology Institute and its Centers for Cancer, Stem Cell, and Biomedical Data Science to help develop medicines of the future. And it’s obvious that the world is keeping an eye on these innovative studies because they are supported by important organizations like the U.S. Department of Defense and the National Institutes of Health. Everyone is excited with the expectation that discoveries may occur quicker than in the past.

File:CRISPR-Cas9 mode of action.png
By ViktoriaAnselmOwn work, CC BY-SA 4.0, Link

A guide RNA follows the same base‑pairing rules learned in AP Bio: adenine pairs with thymine in DNA and with uracil in RNA, while cytosine pairs with guanine. Once the guide RNA locks onto its matching DNA sequence, the Cas enzyme acts like molecular scissors that let researchers remove, change, or swap genes, demonstrating how complementary strands are read and cut just as seen during DNA replication. After the cut, the cell’s transcription machinery copies the edited DNA into mRNA, and translation at the ribosome uses codons and tRNA anticodons to assemble new proteins, revealing in real time how a single nucleotide change can cause a point mutation, trigger a repair pathway, or alter gene regulation.

New Approach to Gene Editing

Recently, we learned about gene mutations during DNA replication. Firstly, we broadly covered what a gene mutation is: a change in the DNA sequence of a gene. Moreover, we gained an understanding of the various kinds of mutations. One of which was substitution: One nitrogenous base is replaced by another.

This kind of mutation can have disastrous effects. Take alpha-1 antitrustypsin deficiency (AATD) for instance. This condition is caused by a substitution mutation and can lead to emphysema or chronic obstructive pulmonary disease in unprotected lungs.

Recently, a cure may have been found in the form of a new approach to gene therapy. Typically gene therapy involves added new genes with the intention of counteracting present ones or splicing DNA to spliced genes. This new method involves altering current DNA. The therapy will change an incorrect nitrogenous base for the correct one.

Specifically, the procedure entails infusing lipid nanoparticles into the bloodstream via an inoculation of some kind. Encased within the nanoparticles are microscopic gene editors. These editors are CRISPR molecules that function as a guide for the genome and enzymes to fix the mutation. After the lipid casing of the nanoparticles has been peeled off, the gene editors will begin the process of replacing DNA bases.

These findings are extraordinary. Perhaps they will also mark the beginning of a something great. As Dr. Kiran Musunuru, of the University of Pennsylvania has stated, “this is the beginning of a new era of medicine.” With this sentiment I leave you the question of should the American government allocate more funding to CRISPR gene editing research?

Unlocking the Future: How CRISPR’s New Upgrade is Supercharging Gene Editing

Researchers at Yale University have developed a new approach using CRISPR-Cas12a technology to create advanced mouse models for studying genetic interactions that influence immune responses to diseases like cancer. This method allows scientists to simultaneously analyze multiple genes in a single experiment, making genetic research more efficient and insightful. 

File:CRISPR CAS9 technology.png - Wikimedia Commons

Over the past 15 years, advancements in the gene-editing technology CRISPR-Cas9 have provided significant insights into the roles specific genes play in various diseases. However, this technology, which uses a “guide” RNA, a small piece of RNA used in CRISPR gene editing to help scientists find the exact spot on the DNA they want to change, to modify DNA sequences and assess the outcomes, is currently limited to targeting, deleting, replacing, or modifying only single gene sequences at a time. 

 

However, the scientists have now created advanced mouse models using CRISPR  technology that enables them to simultaneously evaluate genetic interactions across various immunological responses to multiple diseases like cancer. Gene editing technologies enable scientists to use enzymes, such as Cas9, as molecular scissors to precisely cut or modify specific segments of DNA or RNA, providing valuable insights into the role of these genes in various disorders. The new tool, CRISPR-Cas12a, allows researchers to simultaneously evaluate the effects of multiple genetic changes that influence different immune system responses, according to the researchers.

 

The research noted this advancement could be valuable in the future to combat a host of pathologies, including cancer, metabolic disease, autoimmune disease, and neurological disorders.

 

This connects to AP Bio in multiple ways. For example, modifying genes can affect cellular functions and processes like cell division and apoptosis. This new technology is used to understand how changes in specific genes can influence cell behavior, which is essential in studying diseases like cancer. In addition, the new developments in CRISPR can be used to study impacts gene editing has on the immune system, and its various responses and functions throughout the body. Lastly, genetic mutation can be better understood through CRISPR editing as it effectively is creating its own “mutation”, changing sequences of codons to form different amino acids after DNA Replication, Transcription, and Translation. What are your thoughts on this research? How can it impact how we know genetics as we understand it today?

Revolutionizing Cancer Treatment: CRISPR’s Role in Classifying BRCA2 Mutations

Advancements in gene-editing technologies have significantly enhanced our understanding of genetic mutations associated with cancer risk. A notable study published in Nature (Huang et al. 2025) utilized CRISPR–Cas9-based saturation genome editing to evaluate the functional consequences of all possible single-nucleotide variants in BRCA2 exons 15–26, which encode the DNA-binding domain known for pathogenic missense variants. The researchers introduced nearly all possible single-nucleotide variants into human haploid HAP1 cells and assessed their impact on BRCA2 function. This comprehensive analysis enabled the classification of 6,959 out of 6,960 evaluated variants into seven pathogenicity categories, providing crucial insights for clinical assessments and patient management.

BRCA Genes

BRACA Gene locations by Tessssa13

Similarly, another study published in The American Journal of Human Genetics (Hu et al. 2024) conducted a functional analysis of 462 germline BRCA2 missense variants affecting the DNA-binding domain. This research employed a validated homology-directed DNA repair functional assay to assess the impact of these variants on BRCA2 activity. The findings contributed to the clinical classification of these variants, aiding in the interpretation of genetic test results and informing patient care decisions.

These studies exemplify the transformative potential of CRISPR–Cas9 in functional genomics. By facilitating precise editing and evaluation of genetic variants, CRISPR–Cas9 allows for a deeper understanding of gene function and the consequences of mutations. Such insights are invaluable for developing targeted therapies and personalized medicine approaches. For instance, accurately classifying BRCA2 variants can inform decisions regarding the use of PARP inhibitors, which are particularly effective in patients with specific BRCA mutations.

In our AP Biology curriculum, we’ve explored the mechanisms of DNA repair, including homologous recombination—a process in which BRCA2 plays a pivotal role. Mutations in BRCA2 can disrupt this repair pathway, leading to genomic instability and increased cancer risk. Understanding these molecular mechanisms underscores the significance of precise gene-editing tools like CRISPR–Cas9 in both research and therapeutic contexts.

The application of CRISPR–Cas9 in classifying BRCA2 variants enhances our comprehension of cancer genetics and paves the way for more accurate risk assessments and personalized treatment plans. As research progresses, addressing ethical considerations and ensuring equitable access to these advanced technologies will be crucial.

I chose this topic because someone in my family carries a BRCA1 mutation. When I learned that researchers could now clarify similar variants in BRCA2 using CRISPR, it made me hopeful that one day everyone could know their genuine risk. That kind of clarity can save lives. It also shows how what we learn in class—like transcription, translation, and gene regulation—applies directly to the frontlines of medicine.

I invite anyone who wants to learn more to leave a comment, and I’ll get back to you!

Building Better Brains: Gene Editing the Fetal Mind with Nanoparticles

Imagine if we could fix a brain disorder before a baby even takes its first breath. Sounds like something straight out of a sci‑fi movie, right? But thanks to some cutting‑edge CRISPR advancements, this idea is closer to reality.

A recent breakthrough described by CRISPR Medicine News showcases a fascinating new approach: using densely packed nanoparticles for in utero gene editing aimed at the brain. Researchers have developed a delivery system that uses these ultra‑tiny particles to safely transport CRISPR components to specific cells in the developing fetal brain. The idea is to correct genetic errors at their source, potentially preventing debilitating neurological conditions before symptoms even emerge.

This research isn’t just a headline grabber– it’s rooted in detailed science. A study published in ACS Nano delves into the intricacies of nanoparticle design for gene editing. The scientists behind the work engineered nanoparticles that are not only effective in targeting the brain but are also designed to minimize toxicity and ensure long‑lasting results. This smart engineering is a critical step because safely delivering CRISPR components in utero poses unique challenges: the fetal environment is incredibly delicate, and precision is key when you’re tinkering with the blueprint of life.

Adding another layer, Neuroscience News reports on how these innovative gene‑editing strategies during early development could influence overall brain and neurological development. These approaches are not only aiming to prevent disorders but might also provide insights into how our brains are wired during critical stages of early growth. The idea is to harness the body’s natural developmental processes while subtly guiding them with CRISPR—a sort of gentle nudge toward a healthier genetic future.

In our AP Biology course, we learned how DNA is transcribed into RNA and then translated into proteins, and we studied how mutations in the genetic code can alter these processes. This foundation helped us understand how CRISPR-Cas9 gene editing works: by accurately targeting and cutting the DNA at a precise location, it allows the cell’s natural repair machinery—like homologous recombination—to correct a faulty genetic sequence. We see a direct connection here, as in utero gene editing leverages these same principles to repair harmful mutations before they disrupt the gene expression that ultimately determines an organism’s traits, offering a real-world application of the central dogma we explored in class.

CRISPR-Cas

When we break it down, this technique isn’t just about editing genes. It’s about merging advanced nanotechnology with the precise cutting power of CRISPR to intervene at the cellular level when it might matter most. Think of it as delivering a repair crew directly to the construction site of your brain, fixing potential issues before the building even rises.

What do you think? Could this nano-delivered in utero gene editing be the key to preventing neurological disorders from ever forming? Imagine a future where a difficult genetic condition is corrected while the fetus is still nestled in the womb. Let me know what you think!

CRISPR Reveals How mRNA Vaccines Work

Dr. KIM V. Narry led an important study on mRNA vaccines, like COVID-19, and how cells take them up and respond, as described in the article “Cellular regulator of mRNA vaccine revealed… offering new therapeutic options” from the Institute for Basic Science. This research explains how these vaccines enter cells, carry out their functions, and eventually get degraded. These new insights could lead to the development of better mRNA vaccines and treatments for diseases like cancer and genetic disorders.

In the study, over 19,000 genes were analyzed using a CRISPR-based screen, which led to the discovery of three key factors that affect mRNA vaccine effectiveness. First, the cell surface molecule heparan sulfate (HSPG) was found to help mRNA enter the cell. Second, a protein called V-ATPase was shown to release mRNA inside the cell by creating an acidic environment. Third, the protein TRIM25 acts like a security guard, detecting and destroying foreign mRNA.

The scientists found that proton ions, tiny charged particles, act as signals that tell the cell to launch a defense. When mRNA enters the cytosol, these ions alert TRIM25 to take action. This is the first evidence showing that proton ions can function as immune signals.

Cas9 in complex with sgRNA and target DNA

This article relates to what we’ve learned in AP Biology about protein synthesis and how mRNA is used by ribosomes to make proteins. The study shows that foreign mRNA must avoid being destroyed for this process to happen. TRIM25, part of the innate immune system (which we also studied this year), works to break down foreign RNA, but mRNA vaccines use a modified base (m1Ψ) to protect it and allow translation. This ties into what we’ve just learned about gene mutations. The discovery of proton ions also connects to our unit on cell communication, as it shows how cells respond to threats through chemical signaling.

I found this article fascinating as it included content from almost every unit we have learned this year! Let me know your thoughts in the comments. Did you know a single chemical change in mRNA could make or break a vaccine’s success? Do you think understanding our cells better be the key to curing diseases like cancer?

CRISPR: Bringing back the Woolly Mammoth

You may have heard that the gene-editing tool CRISPR has provided hope for treating genetic diseases. Did you know that it is being used to bring back the woolly mammoth?

A company called Colossal Biosciences has been working to revive the species by using genetic modification. They started off by editing five genes in mice, with hopes of one day genetically modifying Asian elephants into woolly mammoths.

The results were cute, fluffy, mice with coats that resemble woolly mammoths. So what steps did they take to create the “mammoth” mice? They first identified mutations in mice that affect fur characteristics, such as curliness, color, and length. They found eight genes linked to these traits, one of which is also disabled in mammoths. Additionally, they identified a mutation in the mammoth genome related to hair pattern and another affecting fat metabolism. Using CRISPR, they disabled five of these genes in fertilized mouse eggs, resulting in 11 pups from 134 edited eggs.

However, much more progress needs to be made. Performing the work on Asian elephants will involve much more effort, and the results may differ significantly. With the size and slow reproduction rate of elephants the experiment will take more time and incur higher costs, but this doesn’t mean it is impossible.

Woolly mammoth (Mammuthus primigenius) - Mauricio Antón

In our AP biology class, we have recently learned about gene expression. Gene expression is accomplished through transcription and translation to create a protein so a trait or phenotype can be expressed. Transcription is the synthesis of RNA using information from DNA, and translation is the synthesis of a protein using information in mRNA. This flow of genetic information from DNA, to RNA, to a protein is known as “Central Dogma”. CRISPR relates to this because it can stop or alter how the gene is expressed, affecting the production of proteins.

It is so interesting to see the advances of CRISPR. I wonder, will it be used to potentially bring back other extinct species? In addition, what are the ethics behind this study? Is it necessary? What else do you think we will see in our future as CRISPR advances?

How far is too far?

Colossal Biosciences is working to bring back woolly mammoths by genetically modifying Asian elephants, but progress is slow. They have successfully created mice with mammoth-like fur using CRISPR gene editing, but replicating these changes in elephants will be much harder due to their size, slow reproduction, and complex genetics. So far, only one of the genetic changes in the mice exactly matches the mammoth genome, meaning much more research is needed. Scientists warn that modifying too many genes could cause unintended CAS 4qyzproblems, and some experts argue that creating a furry elephant is not the same as bringing back a true mammoth. Ethical concerns and practical challenges also raise doubts about whether this project will succeed.

The idea of bringing back woolly mammoths with the help of gene editing has caused controversy since everyone has a different perspective on this.  Colossal Biosciences, is a company that is interested in doing do with woolly mammoths as they successfully created mice with fur similar to that of a mammoth. It is hard to succeed in this mission due to over 1.5 million differences within genes of a mammoth compared to an Asian elephant.

A recent study performed by Colossal showed that eight genes affected characteristics associated with fur such as color, length, etc. Scientists used CRISPR gene editing to turn off five specific genes in mice, which ultimately led to fur that is similar to that of a mammoth. Although this is progress, it is hard to also find similarities in elephants to show cross over. Mice are very small and more simple, whereas elephants are very large and have long reproducing cycles.

Additionally, many researchers recognize that extensive genetic modifications can be very complicated and come with some risks. If you change too many genes it can result in problems with their metabolism and lead to problems within the organism’s body.

Another question and complexity within gene editing is if it is ethical. Many people, specifically researchers believe that it is very invasive especially in certain situations regarding the eggs of an organism.  Another argument that is made is that even if an elephant is successfully modified to have fur, it would still be an elephant, not a mammoth.

This raises curiosity if you can make a species not extinct which seems impossible, or if you can just use gene editing to make modern hybrids. This data and research portrays that scientists can attempt and succeed in replicating specific traits, but overall it is extremely difficult and complicated to just bring a species back. This shows that while science can replicate certain traits, bringing back a long-extinct species is far more complex than just altering a few genes. Advancements and new studies  in genetic engineering raise many questions if it is moral as humans.

This connects to what we have learned in AP Biology since it connects to DNA. DNA is shown in all living things since it provides a set of instructions from the parents. In regards to the woolly mammoth, scientists studied the DNA of the mammoth to find genes such as fur. They then used CRISPR gene editing and they changed the DNA of mice by turning off or just modifying certain genes to make their fur  look like a mammoth. Changing the DNA led to a different appearance since it changed their features. So, ultimately the DNA is changed to make the mice have a similar appearance to the woolly mammoth. I wonder if majority of people think this is ethical or unethical to the organism, and if so, how far will CRISPR go?

Self Vaccinating Bacteria?

In an interesting article written by John Hopkins Medicine on March 21, 2025, it becomes apparent to John Hopkins Medicine scientists that bacteria protect themselves from certain phage invaders (viral invaders that replicate themselves within bacteria) by seizing the genetic material from the weakened phages, using it to vaccinate themselves, allowing them to protect themselves from the more intense invaders. In the scientists experiments, they note that the bacteria take advantage of weaker phages known as temperate phages, by stealing genetic material from these phages when they are dormant and form a “memory” of the invader and their offspring as the phage multiplies. Then, the bacteria is able to recognize the invaders and fight them off.

After recognizing the unique response, John’s Hopkins investigators concluded that bacteria used CRISPR-Cas systems to break down phage DNA. These CRISPR systems can only break down DNA that matches a memory, captured from a previous invader. The scientists stated that the CRISPR systems acts as a “recording device” that documents all past invaders the bacteria encounters, and when one returns, the bacteria is ample and able to swiftly rid of it.

To try and understand more about this complex process, the scientists performed an experiment and concluded that the bacteria’s CRISPR system works best against naturally dormant phages as it was during the dormant phase where the bacteria created the memories of the phages.

This study from John Hopkins relates the the immune system unit we learned in AP Bio. The Bacteria’s process of making a homemade “vaccine” is naturally very similar to vaccines humans get like Flu shots. When we get a vaccine the weakened antigen enters the system and the cell-mediated and humoral responses kill the antigen, B memory and T memory cells are created, ensuring that if the same, or a similar antigen enters the body, it is swiftly dealt with. In the instance of the bacteria, the dormant phage is the weakened antigen, which allows the bacteria to create a memory of the phage and therefore be ready to eliminate it next time it enters the bacteria.

There are many implications to this study, one being an advancing in phage therapy an alternative process tp antibiotics that uses phages to target bacterial infections. If scientists make phages that bypass the CRISPR defense, phage therapy will be a lot more effective. As someone who hates to get sick, advancements in treatments to stop bacteria and disease in general always interests me. What do you think the future implications of this study will be?T4 Bacteriophage

(picture of phage)

CRISPR: Zebrafish and gRNA

CRISPR-Cas9 is a revolutionary gene-editing technology, first invented by biochemist Jennifer Doudna and microbiologist Emmanuelle Charpentier. This method, aptly dubbed “genetic scissors,” enables scientists to cut DNA through precise removals and alterations of DNA sequences, which allows for the correction of genetic errors and the manipulation of gene expression. This technology has extreme potential to correct mistakes in DNA that cause conditions ranging from congenital birth defects and cancer. Additionally, CRISPR utilizes gRNAs (guide RNAs) to target specific sections of DNA/RNA in a cell. These gRNAs enable scientists to use CRISPR technology to cut genetic information with high precision.

Last month, researchers from Spain and the USA worked together to test how well modified CRISPR-RfxCas13d gRNAs could improve gene targeting in zebrafish embryos. They wanted to see how they could further improve CRISPR technology to target specific sequences in living organisms. They used chemically-modified gRNAs along with a protein called RfxCas13d to turn off genes active during the developmental stages in zebrafish embryos. They then modified the protein to be particularly efficient in zebrafish cells, and compared their various results of the CRISPR targeting.

Zebrafish (26436913602)

The scientists found that chemically-modified gRNAs do in fact improve the process of cutting out genetic information in living embryos. They further proposed that this process could be replicated to enhance the effectiveness of CRISPR editing in other organisms, too.

In this past AP Biology unit, we have learned about how harmful mutations can be, and what kinds of disorders can arise from those mutations. In class, we learned the different types of mutations (substitution, deletion, etc) and how even one seemingly small change in genetic code could have devastating effects on the affected organism; CRISPR might eventually be used to correct these harmful mutations in humans. Although there is still much more research to be done on CRISPR technology to reach the point at which we can begin to resolve genetic problems in humans, the possible uses of CRISPR are vast.

Whenever I think of CRISPR, I’m always reminded of the novel Brave New World, by Aldous Huxley. The book is set in a dystopian world where embryos are genetically modified to create people that “perfectly” fit their specific hierarchical positions and roles in society. As a result of gene editing, people in the depicted society lack true emotions and individuality. Although Huxley’s novel was written decades before CRISPR was invented, its warning about the dangers of manipulating genes rings true, especially now. What do you think of the ethical dilemma that CRISPR gene editing poses? How far is too far when it comes to scientific and technological progress, and who gets to decide those limitations?

Using CRISPR and AAV gene insertion to cure disease

What is CRISPR?

CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) are genes that quickly repeat DNA base sequences that are mechanically edited using a protein called Cas9. This system is based on the Cas9 protein’s ability to splice a given DNA sequence by being given a matching RNA code.  This is incredibly similar to how alternative RNA splicing works in gene regulation for eukaryotic organisms.  In the same way that alternative RNA splicing removes sequences of RNA code during the RNA processing stage of gene expression to create a variety of different proteins, the Cas9 protein removes sequences of code from DNA to synthesize unique proteins. When given a specific RNA sequence, the Cas9 protein will match that RNA sequence to a sequence of DNA, commencing the splicing of the DNA at that location. This process was discovered by Emmanuel Charpentier et al. in bacteria that use the Cas9 protein to target harmful DNA code inserted into the bacterial cytoplasm by viral organisms. Using the Cas9 protein, genetic engineers are able to remove DNA sequences in organisms to cause them to create different proteins and show a wanted phenotypic trait.

DNA alternative splicing

What is AAV?

AAV is a method of inserting DNA into a non-embryonic organism through structures similar to that of viruses.  However, instead of containing harmful virus DNA, these vessels contain modified DNA using CRISPR to force a desired gene expression at a given location in the human body.  AAV-based delivery systems are able to change a person’s genome during their lifetimes, potentially reducing the harm of/eliminating genetic diseases.

Experimentation

Dr. Peace Chinonyerem Ike et al. ran an experiment this year on pediatric males to test the effectiveness of using CRISPR editing through AAV to alter the genomes of certain cells. The diseases they chose are those that have been linked to the X-linked chromosome, meaning that men are more likely to get these diseases such as hemophilia and DMD. This is because X-linked traits in men come exclusively from the mother making it statistically more likely that they will express the phenotype of that gene. After experimentation over five years with treating patients, they saw that using CRISPR was significantly more effective than previous methods for reducing symptoms in these x-linked traits (such experiments include ZFNS).

What Does This Mean

After concluding that CRISPR can be used to treat genetic diseases on the X chromosome we may be able to expand its capabilities to more genetic illnesses such as Cystic Fibrosis that are autosomal. Using CRISPR, we can move medicine away from preventing side effects to outright curing illnesses at the level of the genome. This is a huge feat in the field of medicine and may predict a wave of new treatment strategies involving DNA modification in the future. I believe that, although this possible form of treatment is monumental, we must be incredibly cautious about using AAV-based systems as they may cause harmful mutations in the person’s genome. If we do not make sure that this treatment is safe we may cause multiple people to undergo harmful gene mutations and, for example, develop cancer. So you think that we will see the application of this treatment form in practice? If so, what do you think the ethical and moral ramifications are when using gene editing on a developed person?

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