avalution – BioQuakes

Author: avalution

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.

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!

CRISPR Gene Editing Disables Key Herpes Virus Genes

By avalution

On April 7, 2025

In Student Post

A new study, has introduced a promising new application for gene drives—this time, targeting viruses instead of insects. The researchers developed a CRISPR-based gene drive system that spreads through herpes simplex virus type 1 (HSV-1), potentially opening the door to a future treatment or even a cure, researchers report in Nature Communications.

Herpes Simplex Virus Type 1: Procapsid and Mature Capsid

3D model of herpes simplex virus type 1 (HSV-1)

Gene drives are designed to copy and spread specific genetic information through a population. In this case, scientists engineered a gene drive virus that could insert itself into the genome of other herpes viruses during co-infection. They tested this in mice by introducing a standard HSV-1 virus that glows yellow and a gene drive virus marked with red fluorescence. Within four days, nearly 90% of the viruses in certain tissues were replaced by the gene drive version, confirming that it had successfully spread between viruses inside the body.

Most notably, the gene drive spread to latent HSV-1 already hiding in the neurons of previously infected mice. This is a major breakthrough since herpes viruses are known for their ability to become dormant and evade treatment. Existing antiviral medications can only suppress symptoms—they can’t eliminate the virus. A gene drive that targets latent infections could change that.

The system works by using CRISPR to cut the virus’s genome and insert its own DNA, essentially rewriting it. In this study, the gene drive targeted UL23, a gene that helps HSV evade the host immune system. Disabling UL23 and replacing it with a red fluorescent marker made the virus easier to track and less virulent.

Cas9, guided by a complementary RNA strand (sgRNA), binds to the target DNA sequence and makes a precise double-stranded cut, disabling the viral gene.

While this technology is still in early stages, the results show that viral gene drives can work in mammals and may one day be used to treat chronic infections. However, safety concerns remain—researchers must prevent resistance, off-target effects, and unintended spread to others. Future versions will need to be made safer and more controlled before clinical testing.

This article connects to what we’ve learned in AP Biology about transcription, complementary base pairing, and CRISPR gene editing mechanisms. Researchers created guide RNAs (gRNAs) that are complementary to essential HSV genes, UL8 and UL29. These gRNAs were made through in vitro transcription, in which RNA polymerase reads a DNA template strand 3’ to 5’ and builds an RNA strand 5’ to 3’ with matching bases. The gRNAs were then packaged into lipid nanoparticles and delivered into infected neurons. Once inside, each gRNA binds to a Cas9 protein, forming a CRISPR-Cas9 complex that searches for matching viral DNA sequences via base pairing—similar to how tRNA anticodons pair with mRNA codons during translation.

When the gRNA finds a matching sequence in the viral DNA, the Cas9 enzyme makes a double-stranded cut at that site. The host cell attempts to repair the break using non-homologous end joining (NHEJ), an error-prone mechanism that often results in insertions or deletions—leading to frameshift mutations that disrupt the gene’s reading frame. These mutations render the targeted viral genes nonfunctional. Since UL8 and UL29 are essential for HSV replication and reactivation, the virus is effectively disabled. This demonstrates how scientists can use complementary RNAs to target and silence specific genes by inducing disruptive mutations, showing that gene expression can be permanently shut down through physical edits to the DNA itself.

I find it fascinating how genes can be edited to serve a specific purpose, especially in targeting and disabling viruses. I think CRISPR technology has the potential to completely transform the way we approach treatment for persistent infections like HSV-1. What do you think about this mechanism? Do you believe CRISPR is an ethical tool with the potential to benefit human health? Leave a comment sharing your thoughts!

Kidney Cells Can Remember: A New Twist on Cellular Memory

By avalution

On March 7, 2025

In Student Post

New research shows that kidney cells, like neurons, can retain information and recognize patterns at the molecular level. New York University researchers discovered that human embryonic kidney cells exhibit a memory-related phenomenon known as the “massed-spaced effect,” which is commonly observed in the brain.

Researchers used an artificial gene that replicated memory-associated DNA to test kidney cells’ responses to chemical inputs. They specifically studied the function of CREB (cAMP response element-binding protein), a protein that is known to play a part in the way neurons form memories. Chemical signals cause CREB to become active in neurons, which helps to regulate the production of memory-related genes. The scientists aimed to determine whether kidney cells used a similar process.

They tested this by inserting a synthetic gene that resembled the DNA sequence that CREB normally binds to and contained instructions on how to produce a glowing protein after the activation of the memory gene. The amount of the glowing protein produced was used to measure CREB activation when kidney cells were exposed to chemical pulses that mimicked signals related to memory. They discovered that cells stored information more effectively when exposed to multiple short signals rather than a single long signal, just as neurons do. This shows that memory-related processes may not be limited to the brain.

While kidney cell “memory” will not help you learn math, this discovery could have a major impact on medicine. Scientists believe that understanding how non-neural cells receive information may lead to better treatments for disorders such as cancer and memory loss.

This discovery challenges standard ideas of memory and opens up possibilities for thinking about learning at the cellular level.

This study connects to what we have learned in AP Biology about cell communication and signaling. The researchers focused on the protein CREB (cAMP response element-binding protein), which is important in neuron memory formation. This is related to signal transduction pathways, in which an external signaling molecule (ligand) binds to a receptor, triggering a cascade of reactions inside the cell. When neurons receive a chemical signal (such as a neurotransmitter), secondary messengers such as cAMP are activated, which then activates protein kinases that phosphorylate CREB. As a transcription factor, CREB then binds to DNA and initiates gene expression changes that allow the cell to “remember” the signal. This method is a great example of how cells process and respond to external signals, which is an important concept in cell communication.

What do you think about the idea that memory might not be limited to the brain? Could this discovery change how we think about learning and disease treatments?

Plants’ Photosynthetic Machinery Functions inside Hamster Cells

By avalution

On January 20, 2025

In Student Post

Scientists have achieved a fascinating breakthrough by transplanting chloroplasts from algae into hamster cells, allowing them to photosynthesize and produce energy for up to two days. This experiment, recently published in Proceedings of the Japan Academy, Series B, could open new doors in biotechnology and cellular engineering.

Researchers from the University of Tokyo sought to replicate the mechanism in mammalian cells after being inspired by sacoglossan sea slugs, which naturally use chloroplasts from their algae diet to produce energy. The scientists used robust chloroplasts from red algae, which flourish in harsh conditions, to successfully transplant chloroplasts into fungal cells, although earlier attempts to do so quickly destroyed the cells.

After carefully separating the chloroplasts, the researchers changed the growth media to allow the hamster ovary cells to naturally absorb the organelles rather than putting them in using force. After entering, the chloroplasts remained structurally sound and carried out electron transport, which is an essential part of photosynthesis, for 48 hours before breaking down.

There are still difficulties in spite of this progress. Animal cells lack the genes necessary to support chloroplasts long term, and thus depend on protein assistance to function. By inserting genes linked to photosynthesis into animal cells, researchers hope to fix this issue and possibly extend the survival and utility of the cells.

Looking ahead, these findings could lead to groundbreaking applications such as photosynthetic materials that capture carbon dioxide or boost oxygen production in lab-grown tissues. However, as it would require an unfeasible quantity of surface area covered in chloroplasts, the idea of solar-powered humans is still unattainable.

In our AP Biology class, we have learned about the endosymbiotic theory, which explains how organelles like mitochondria and chloroplasts originated from symbiotic relationships between primitive cells. According to this theory, a larger host cell engulfed smaller prokaryotic cells capable of energy production, and instead of digesting them, they formed a mutually beneficial relationship. Over time, these engulfed cells evolved into organelles, such as mitochondria for ATP production and chloroplasts for photosynthesis in plant cells. This theory is supported by evidence such as the presence of their own DNA and double membranes.

The recent experiment connects to the endosymbiotic theory by demonstrating how animal cells can temporarily host chloroplasts and perform photosynthesis. It provides a modern-day parallel to the evolutionary process that occurred billions of years ago, suggesting that under the right conditions, symbiotic relationships could potentially be engineered in the lab. This research could deepen our understanding of cellular evolution and pave the way for innovative applications in synthetic biology.

Personally, I find this research incredibly exciting because it highlights how science can push the boundaries of what’s possible. Could we one day engineer cells to create their own energy from sunlight? What other possibilities might arise from blending plant and animal biology? I’d love to hear your thoughts—leave a comment!

Rogue Antibodies May Cause Some Long COVID Symptoms

By avalution

On January 9, 2025

In Student Post

According to recent research, rogue autoantibodies may be the source of several chronic COVID symptoms, such as pain and neurological problems including lightheadedness. Long-term COVID has been linked to autoantibodies, which target an individual’s own tissues. Researchers have produced concrete proof by transferring these antibodies from long-term COVID patients to healthy mice. The mice’s symptoms, which mirrored those of the humans, included heightened sensitivity to pain and issues with balance. These results imply that autoantibodies actively contribute to the illness rather than being passive spectators.

According to the findings, autoantibodies may damage nerve tissues, resulting in neurological impairment and chronic pain. Mice given these antibodies, for instance, had enhanced heat sensitivity and damage to their skin’s nerve fibers. Additionally, researchers noticed that mice that received antibodies from dizziness sufferers had trouble balancing. These findings point to a mechanism through which chronic COVID symptoms, including pain and neurological impairment, may manifest separately from other residual viral effects.

These results may pave the way for focused COVID-19 therapies. Treatments to lower the levels of pain-linked autoantibodies may greatly improve symptoms if physicians are able to identify people who have them. Larger, longer-term studies are required to confirm these findings and investigate how they can enhance patient care, according to experts. However, the study offers patients hope and a way ahead for the development of treatments by advancing our understanding of the intricate mechanisms behind long-lasting COVID.

In AP Biology, we learned about the immune system’s role in defending the body against pathogens, with antibodies playing a crucial part in this defense. Antibodies are specialized proteins produced by plasma cells, which are derived from activated B cells. They are Y-shaped molecules that bind specifically to antigens—unique markers found on the surface of pathogens like viruses or bacteria. This binding neutralizes the pathogen by preventing it from infecting cells or marking it for destruction by other immune cells, such as macrophages and natural killer cells. However, autoantibodies, like those implicated in long-term COVID symptoms, represent a malfunction in this system. Instead of targeting harmful pathogens, these rogue antibodies mistakenly bind to the body’s own tissues, causing inflammation and damage. This immune dysfunction can lead to the chronic pain and neurological issues seen in long COVID, as the autoantibodies attack nerve tissues and disrupt their normal function.

I think it’s fascinating to see how antibodies, which are meant to protect us from pathogens, can also hurt us. What do you think? Feel free to comment!

Scientists Have Traced all 54.5 Million Connections in a Fruit Fly’s Brain

By avalution

On October 24, 2024

In Student Post

Scientists have accomplished a remarkable feat by creating the first comprehensive map of a fruit fly’s brain, or “connectome,” containing information on all 139,255 neurons and their 54.5 million connections. The brain of Drosophila melanogaster, a creature small enough to fit its brain into the size of a poppy seed yet complex enough to provide new insights into brain function, is shown in this map as it transmits neuronal information throughout the brain. More than 149 meters of brain wiring are shown on the map.

This enormous study, which took almost 20 years to complete, used machine learning to map the complex neuronal pathways and complicated electron microscopy to examine over 7,000 thin slices of a female fruit fly’s brain. Nevertheless, human skill was still required to guarantee accuracy and fix mistakes.

The map was proofread by hundreds of people and more than fifty laboratories. Given the intricacy of neuronal connections, the experiment, which was led by researchers at Princeton University and the Allen Institute for Brain Science, required meticulous attention to detail.

Significant discoveries have already resulted from the project. For example, the entire fly’s eye is covered by just two CT1 neurons, each of which makes about 148,000 synapses and is involved in motion and light detection. Another discovery revealed that certain neurons function as “integrators,” taking in information from a large number of other neurons, while other neurons work as “broadcasters,” dispersing messages across the brain. These patterns shed more light on the information dispersion process in neural networks.

The connectome also makes it possible to build computer models that, using these connections as a foundation, mimic brain activity. To show how this map can imitate and anticipate brain processes, scientists have already started modeling the effects of taste neurons on other brain regions.

In addition to being a significant accomplishment for insect neuroscience, the mapping of the fruit fly’s brain provides a preview of what lies ahead for more sophisticated creatures like mice and humans. By building more thorough connectomes, scientists expect to provide important insights into how brain wiring affects behavior, if individual differences exist in connectomes, and how these connections might change over time.

This study is related to AP Biology, as it revealed that certain neurons function as “integrators” or “broadcasters,” taking in or dispersing messages across the brain. We learned that neurons communicate with one another through the flow of chemicals(ions) in and out of the plasma membrane of the cell. When an impulse is received, Na+ channels open and Na+ flows in by facilitated diffusion. However, this causes a more positive charge on the inside of the neuron, so K+ flows out through channels, so it is once again more positive on the outside. This process is a vital part of the discovery, as it explains the ways neurons communicate with each other to integrate or broadcast information.

This study is particularly fascinating to me, as I am intrigued by neuroscience and hope to study it in college! I think this connectome will lead to excellent scientific development! What do you think? Comment and share!

BioQuakes

AP Biology class blog for discussing current research in Biology

Author: avalution

Reviving Dire Wolf Traits Through Targeted Gene Editing

CRISPR Gene Editing Disables Key Herpes Virus Genes

Kidney Cells Can Remember: A New Twist on Cellular Memory

Plants’ Photosynthetic Machinery Functions inside Hamster Cells

Rogue Antibodies May Cause Some Long COVID Symptoms

Scientists Have Traced all 54.5 Million Connections in a Fruit Fly’s Brain

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