Ancient Viruses can be useful to modern day research

    Researchers at Penn state have discovered that some bacteria can carry ancient dormant viruses called cryptic prophases in their genomes. These dormant viral sequences can become a part of bacteria's defense system. They found that recombinase can modify bacterial DNA in response to viral threats only if a prophage is already embedded in the genome. This specific recombinase is known as PinQ. When a virus goes near the bacterial ell, PinQ triggers DNA inversion flipping a section of genetic code inside the chromosome. 

    In experiments with E. coli the proteins were overexpressed, and viruses could not land on the bacterial surface. After repeated exposure the virus evolved a new attachment mechanism and overcame the barrier. Researchers suggest that this kind of ancient viral defense could be helpful for antiviral strategies especially those showing antibiotics resistance.

    Benefits to this research helps understand how antivirus systems operate. This can lead to a better understanding of how to effectively cultivate bacteria used to ferment foods like cheese and yogurt. This could also help improve how bacterial infections are managed in health care settings. 

Sources:  Ancient viruses hidden inside bacteria could help defeat modern infections. (2025, November 25). ScienceDaily. https://www.sciencedaily.com/releases/2025/11/251102205009.htm

Putol, R. (2025, November 1). Ancient viruses inside bacteria may help fight infections. Earth.com. https://www.earth.com/news/ancient-viruses-inside-bacteria-may-help-fight-infections/

Doug Whitney May Have the Key to Aiding Alzheimer's

    In this NYTimes article, Doug Whitney has been the focus of research for 14 years due to the fact he doesn’t have Alzheimer's Disease. This wouldn’t be anything special except for the fact that he was expected to show symptoms in his 50s, but now he is 76 with no signs. His family has the rarest mutation called Presenilin 2, which is shown to cause early-onset Alzheimer’s disease and has been seen in the family with memory problems starting to show between the ages of 44 and 53. After a while without seeing any issues, Mr. Whitney decided to go through with genetic testing and was confirmed to have the mutation, but no symptoms, which led to further research.

Alzheimer's is seen by the abnormal accumulation of two proteins in the brain: amyloid, followed by tau. Amyloid starts to clump together years before symptoms, and tau forms tangles after the accumulation of amyloid. It was found that Mr. Whitney’s brain was full of amyloids, but didn’t have nearly as many tau, which suggested that his brain is resistant to tau aggregation and spreading. Looking at his DNA, researchers have discovered that there are a couple of variations that his relatives didn’t have that could be helping with the prevention of Alzheimer’s. It was found that he has an excess of heat shock proteins that help keep proteins from folding incorrectly. This excess may be the reason why there aren’t as many misfolded proteins, especially tau, in his brain, since it can prevent them from spreading. There are many theories on why this has happened, but it is still being tested to find that piece of the puzzle.

Alzheimer’s disease is a disease that has no cure and affects many people and their families. This research could be a big breakthrough for those people and give hope for a cure or at least assistance for those who have it. I believe that this research is extremely important, since I know people whose family has a history of diseases that cause brain deterioration, and this could help ease their worries. Even if this doesn’t lead to a cure, it’ll help guide our understanding of these issues and get us one step closer.

A New Chapter in Gene Therapy

        Recent advances in gene editing are turning what once seemed like science fiction into real treatments. One striking example is a personalized therapy developed for a baby born with a rare metabolic disorder. Researchers at Children's Hospital of Philadelphia and Penn Medicine used a base-editing version of the CRISPR-Cas9 system to correct a mutation in the CPS1 gene of a child who suffered from carbamoyl phosphate synthetase 1 deficiency. Within months of receiving the therapy, the child was able to tolerate increased protein in his diet and required fewer nitrogen-scavenging medications.

        This breakthrough shows the feasibility of tailored gene-editing for ultra rare diseases, where traditional drug development isn't practical. However, as discussed in Innovative Genomics Institute's review, the case raises ethical questions about cost, accessibility, and equity in access to gene therapy.  

Lasting Cure Found for ADA-SCID Through Gene Therapy

 Lasting Cure Found for ADA-SCID Through Gene Therapy

    ADA deficiency inhibits the development and function of immune cells (due to a genetic mutation), usually combined with SCID, in which people lack all immune protection from bacteria, viruses, and fungi (Adenosine Deaminase Deficiency: MedlinePlus Genetics, 2013). A child named Eliana was born with this disorder since she was a baby and lived inside a "bubble" ever since, until researchers using experimental gene therapy cured the child's immune system when she was 10 months old, and she no longer lives in the bubble!

In the new gene therapy, the child's own blood stem cells were collected and treated with a modified virus that implanted a healthy copy of the ADA gene. These stem cells are now infused back into the child, where the healthy cells start producing immune cells to fight infections. For the immune system to reach normal levels, it takes about 6 months to a year.

This long-term research (2012-2019) included 62 patients, and only 59 were successfully treated with no complications! The gene therapy has not yet been FDA-approved, but researchers are preparing to apply!

A photo of Eliana Nachem

This is really important research because of the lives that could be saved with this gene therapy. Gene therapy is a great method because it targets the root of the problem instead of just treating symptoms. Gene therapy also gives hope to parents and families of those affected by ADA-SCID, just like Eliana's family. 

References

Adenosine deaminase deficiency: MedlinePlus Genetics. (2013, July 1). Medlineplus.gov. https://medlineplus.gov/genetics/condition/adenosine-deaminase-deficiency/

HealthDay. (2025). Gene Therapy Provides Lasting Cure For “Bubble Boy” Children. US News & World Report; U.S. News & World Report. https://www.usnews.com/news/health-news/articles/2025-10-16/gene-therapy-provides-lasting-cure-for-bubble-boy-children

 

The Genetic Adaptations for Heat Survival of Arizona Honeysweet in Death Valley

Benjamin Pruss
BIOL-2110-001 GENETICS
Professor Guy F. Barbato
November 7th, 2025

    Most plants don't survive very well in extreme heat, much less thrive. However, the Arizona honeysweet (Tidestromia oblongifolia) does just that— in Death Valley, no less. All because of a unique cellular ability it has.

    T. oblongifolia can change the shape of the chloroplasts within its cells, the organelles that convert light, water, and carbon dioxide into energy and oxygen. Chloroplasts are usually disc-shaped; however, the Arizona honeysweet plants' chloroplasts can change to a cup shape. Although not certain, scientists believe this shape helps the chloroplasts better trap carbon dioxide. This, combined with other plant responses to heat, such as smaller leaves, helps the plant thrive in Death Valley's extreme heat. 

    In an experiment conducted by Karine Prado and her associates, Arizona honeysweet growth was measured at 31°C and 47°C, the usual summer temperature in Death Valley. The seeds grown under Death Valley conditions grew significantly larger than the ones grown at 31°C. This suggests that the plant actually grows better under such harsh conditions. "These plants wait [for] the hottest month just to grow fast." said Prado about the plants. Some scientists believe that this plant's special adaptations could help future crops survive global warming. 

Sources:

https://www.sciencenews.org/article/death-valley-shrub-survival-heat

https://www.sciencedirect.com/science/article/abs/pii/S0960982225013120

A Genetic Finding Suggests Mutation to Make Horses More Rideable

        The modern domestication of horses can be dated back to over 4,200 years ago. A team of scientists, led by molecular archaeologist Ludovic Orlando, observed the genomes of ancient horses and compared them to ones of the domesticated horses humans are familiar with today. Whilst studying the genomes, nine specific genes stood out as selected and targeted by human breeders   

 

        One gene recorded was ZFPM1, a gene familiar to scientists as the marker for anxiety levels in mice and human well being. This was one of the first genes selected by breeders around 5,000 years ago, suggesting the original concern for domestication was keeping the horse tamer.

        Interestingly enough, around 300-800 years later, the breeders advanced their selection and the gene Gasdermin C (GSDMC) strongly started to appear. In humans, a mutation of this gene causes chronic back pain and disorders such as spinal stenosis. In horses, it is seen to be related to the body length to body height ratio. 

        Once Orlando and his team discovered horses with this gene mutation when first appearing had 20% more offspring than those without, they ran testing on mice and inactivated their GSDMC genes. This experiment found the mice's spines modified to become straighter and forelimbs to be stronger.

        Orlando concludes "people intended to put that variant more frequently into the population... when you see something like that, you know you're onto something that was a real game changer for horse biology".

        The research done by Orlando and his colleagues is impressive and presents the importance of to be able to fully understand the human selected genes of any animal, in this case horses, it must be compared to the original non-domesticated ancestor. Learning more about the genetic makeup of one of the first animals domesticated by humans can help us further learn about the scientific thought process of our ancestors. 

Sources:

https://www.sciencenews.org/article/tamed-horses-rideable-genetic-mutation 

https://www.ncbi.nlm.nih.gov/gene?Db=gene&Cmd=DetailsSearch&Term=56169 

                   

Is there a link between craving licorice and a specific gene?

https://link.springer.com/article/10.1186/2044-7248-1-22

Although not fully confirmed, there is a suspected link between cilantro tasting like soap and genetics. It is not necessarily linked to the taste of the cilantro itself but more so the way it smells. There are people out there who can not overcome the earthy smell of the cilantro, thus tasting like soap when eaten. This specific article is pointing out geographical location and the olfactory gene within people. More people from European countries can taste the earthy/soapy flavor whereas people from Central America/Latin countries taste the flavor less. Not only do the people taste it differently but the gene itself is more present in certain regions. Countries that have high coriander growth rates have a decreased OR6A2 gene, and countries that have a low cilantro growth rate have an increase in the soap taste gene. It was also revealed that people can overcome the smell and taste of the given herb with repetitions in trying it, does not eliminate the gene itself, but people can train themselves to like it. Dried cilantro has a completely different impact on people, probably because of the reduced scent of the herb it does not hit the neurons the same way as it would if it were fresh.

https://theconversation.com/the-science-of-liquorice-whether-you-love-the-dark-root-or-hate-it-74135

This specific thought process may be a reach but I wanted to try it out anyway. There was an already (semi) proven and thoroughly tested  study that has linked a specific gene OR6A2 to the taste and smell of cilantro/coriander, and why it tastes like soap, and there were studies that have linked the cravings of specific foods to various genes but there has never really been a specific study on licorice itself. Licorice has a very unique taste that some people love and some people hate, it is kind of hard to describe: kind of sweet, kind of medicinal, kind of salty. From a biochemical/neurological standpoint it is justifiable why people crave it, your body needs certain vitamins and minerals thus triggering a craving in the brain. But from a genetic viewpoint there is no link of the gene itself and the craving of licorice. That could be for many different reasons, whether there has not been enough scientific studies on it or there really is no actual gene for it. As a kid, I hated the stuff but I recently had a sudden need for it, i was just curious if it was similar to cilantro in it having a designated soap gene: or if my tastebuds have changed as I grew into adulthood. Either way- licorice is my new passion in life and I am excited to see what future geneticists have to say about it. 

https://archive.is/20240101045022/https://www.scientificamerican.com/article/your-genes-may-influence-what-you-like-to-eat/

https://pmc.ncbi.nlm.nih.gov/articles/PMC6930899/pdf/fgene-10-01272.pdf

A Medical First: Personalized Gene Therapy Saves Infant with Rare Disorder

    The University of Pennsylvania and The Children’s Hospital of Philadelphia (CHOP) have recently made a outstanding discovery that used ‘custom- built gene therapy’ to treat a baby with a rare and deadly condition called CPS1 deficiency. This is a genetic deficiency that creates a high amount of ammonia in your blood which can be toxic especially to the brain. With help from the National Institute of Health, the team used CRISPR gene-editing technology to fix this error in the baby’s liver cells. This marks the first CRISPR therapy treatment that can hopefully show a glimpse into the future about how other rare diseases can be treated.