GloFish: one step closer to Jurassic Park

 

    When I was in elementary school, my friends and I used to play this game on the computers called Duck Life. Duck Life was a franchise, plenty of games, but there was a continuous story throughout them all. I forget which game it was, but one of the Duck Life games had a story along the lines of: the previous game's duck was unbeatable, therefore, the only way to surpass it, is to genetically modify new ducks into freaks of nature that can swim, run, and climb faster than a normal duck. I always thought this one was the coolest, much to the disagreement of my friends. Growing up on Jurassic Park, specifically the book by Micheal Critchon, I always liked the idea of genetically modifying a creature into a new form, whether it was modifying my duck to have massive gorilla arms to climb Mount Fiji, or filling in the gaps of dinosaur DNA with that of modern reptiles to produce the featherless dinosaurs in Jurassic Park, something about the idea was just so neat to me.

     My little god complex aside; this happens everywhere! While not dinosaurs, genetic modification is a common technique nowadays in the pet industry. For many, many centuries, animals were bred for desirable traits, including pets like dogs and cats. This is different from genetic engineering, as where breeding focuses a lot more on the phenotypes, and breeding for desired traits, genetic engineering focuses on altering the DNA itself into a new form. The article focuses in on a new genetically engineered fish called GloFish, which were modified to express fluorescent proteins they do not typically express in nature. The first GloFish was actually made using Green Fluorescence Protein extracted from jellyfish; the same one used in this year's genetics lab. Since then, due to advances in technology and computers increasing in power significantly, many more colors are now available on the market. I think this also highlights a darker side of genetics, were, theoretically, organisms can be genetically modified into more dangerous versions of existing organisms. With increasing accessibility to genomic information due to massive online gene banks, it's only a matter of time before some sort of bioterrorism event happens where someone somewhere somehow gives a mantis x-ray vision and destroys the local Walmart supercenter. 

Sources:

https://247wallst.com/technology-3/2025/10/12/genetically-engineered-pets-are-here-and-you-can-buy-one-for-7/

https://petreader.net/the-origins-of-glofish-a-brief-history/

Similarities in Genetic Pathways Between Humans and Mice Regarding Disk Herniation

 

In a recent study examining the genetic factors and age regarding disk herniation in mouse models, researchers may have found similarities to the condition in humans.

“Disk herniation” is when the disks in between the vertebrae of the spine protrude, which often puts pressure on the nerve and can cause extreme pain and discomfort. While this is a well documented condition in human individuals over the age of 40, mice are also capable of experiencing disk herniation. When researchers analyzed genetic markers for the condition in mice, similarities were discovered to those in humans. Transcriptomic analysis confirmed that pathways for inflammation and the activation of immune cells were similar in mice and humans and this way.

This has very large implications for the medical industry, as the more genes that are discovered in mice that create similar pathways to those for humans, the better we are able to understand human diseases and treat them.

Sources:

https://www.science.org/doi/10.1126/sciadv.ado6847

https://pubmed.ncbi.nlm.nih.gov/15879573/

The Potential of Cardiac Gene Therapy

 

A recent article explains how gene therapy is rapidly transforming modern medicine by evolving from an experimental concept into a powerful tool with real world success in treating genetic disorders. Today, researchers are exploring how these same technologies could revolutionize the treatment of cardiovascular disease.

Although current treatments such as medications, medical devices, and lifestyle changes have improved patient outcomes, they fail to address the underlying molecular causes of heart disease. Gene therapy offers a new approach by targeting disease at the genetic and cellular levels, potentially providing long lasting or curative treatments for heart conditions, which include heart failure, cardiomyopathies, arrhythmias, and vascular disease.

One aspect of cardiac gene therapy is the development of advanced delivery systems, like viral vectors and lipid nanoparticles that can transport therapeutic genes directly into heart tissue. These technologies allow scientists to precisely control where and how genes are expressed. While challenges still remain, researchers are becoming increasingly optimistic about the future of molecular medicine in cardiology.

Link:
https://www.sciencedirect.com/science/article/pii/S0828282X26000644#sec14


Additional:

https://www.ahajournals.org/doi/full/10.1161/CIRCRESAHA.116.310039

Genetic test for the personalization of sport training

 The article explains that athletic performance is influenced by a combination of genetics, training, nutrition, and environment, rather than by a single “sports gene.” Researchers have identified certain genes, such as ACE and ACTN3, that may influence whether a person is naturally better suited for endurance activities or power-and-sprint-based sports. The paper also discusses how genetics can influence injury risk, recovery time, and response to different types of exercise. Although commercial DNA tests claim they can identify athletic talent and create personalized training programs, the authors argue that the science is still limited and cannot reliably predict elite performance. They emphasize that hard work, coaching, motivation, and lifestyle remain far more important than genetic testing alone, while also raising concerns about privacy, discrimination, and the ethical use of genetic information in sports.

#sports #dna #athletictalent #genes 

source: https://pmc.ncbi.nlm.nih.gov/articles/PMC8023127/

CRISPR Reprograms CAR T-Cells to Improve Cancer Treatments

Figure 1. A two-vector system is applied for in vivo CAR T-cell production, delivering CRISPR-Cas9 components that enable the engineered T-cells to target and destroy cancer cells.


     CRISPR, a gene-editing tool, has improved cancer immunotherapy by amplifying an immune cell’s ability to recognize tumors, effectively preventing them from further developing. With the use of CRISPR-Cas9 technology, T-cells (white blood cells produced in the thymus) were engineered to produce Chimeric Antigen Receptor (CAR) -T cells, which target cancer cells. Usually, CAR-T therapy is performed in a laboratory setting, requiring immune cells to be removed from a patient, genetically modified, and then reinfused. Consequently, the therapy is time-consuming and expensive. However, researchers have found a way to genetically reprogram T-cells in vivo, allowing for direct immune cell modification within the patient to be done.

     A two-vector system was developed to “deliver CRISPR-Cas9 ribonucleoproteins and a DNA donor template via enveloped delivery transporters and adeno-associated viruses” (Nyberg et al., 2026). By incorporating a CAR transgene into a particular locus receptive towards T cells, therapeutic levels of CAR T-cells were produced in vivo. This procedure was tested with humanized mouse models of B-cell aplasia, carrying blood and solid tumors. The engineered T-cells successfully attacked both the blood and solid tumors in the mouse models. Ultimately, the articles revealed the possibility of faster and more accessible CAR-T cancer treatments through CRISPR gene editing.



Links:

https://www.nature.com/articles/s41586-026-10235-x
https://pmc.ncbi.nlm.nih.gov/articles/PMC13096480/

Man studies the pond water; accidentally discovers protist that defies genetic law

   

In most cases, DNA replication stops at a stop codon, or an animo acid that codes for the stop codon. A team at Earlham Institute took samples of freshwater to collect a certain protist: Oligohymenophorea sp. The goal was simple: collect the samples, analyze the genome, and ultimately test a new DNA sequencing pipeline specialized in extremely small amounts of DNA. But for our brave scientists, fate had other plans: an undiscovered species that had a completely new take on DNA reading. The protist, somehow, reassigned the two codons typically associated with gene stopping signals had been changed to different amino acid sequences. In the specific protist, only TGA functions as a stop codon, and not TAG and TAA. Additionally, the protist had an elevated amount of TGA's, theorized to be a compensation for the repurposing of TAA and TAG. I find studies like this interesting for two reasons. One: It shows how our modern understanding of both biology and genetics is not a complete understanding, rather it is an explanation that BEST explains things. And two, it shows how science can be unpredictable, and new ideas can be found pretty much everywhere, even ponds.   

 Source:

 https://www.sciencedaily.com/releases/2026/05/260507024045.htm

https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1010913

https://ar.inspiredpencil.com/pictures-2023/protist-cell-microscope

Genetic Ties to Bone Density in the Younger Generation

Carmine Martino

BIOL-2110-001

Dr. Guy Barbato

May 7th, 2026 

        Researchers at Children’s Hospital of Philadelphia studied how genetics affect bone density in children and adolescents. Bone density during childhood is important because it can affect bone strength and fracture risk later in life. The article explains that things like chronic health conditions, dietary restrictions, and steroid use can affect bone health, but genetics also play a major role.

        Two recent studies looked at how genetic and genomic information can help scientists better understand bone development in young people. Most previous studies on bone density genetics focused more on adults, so these studies focused specifically on children and teenagers instead. The findings showed that genetics can strongly influence bone mineral density during childhood and adolescence. Bone density is kind of like building a foundation for a house. If the foundation is stronger early on, the structure has a better chance of holding up later in life. The same idea applies to bones during childhood and adolescence, since these years are important for bone development.

        Another thing that stood out was how genetic information may eventually help identify kids who are at greater risk for weaker bones or fractures earlier in life. It reminds me of how some people seem naturally more prone to injuries than others even if they live similar lifestyles. These findings show that genetics may help explain some of those differences.

Article:

https://www.news-medical.net/news/20251119/Scientists-uncover-genetic-components-linked-to-bone-density-in-young-people.aspx

Extra Source:

https://medlineplus.gov/bonedensity.html

Discovery of Mouse Genes Related to Heart Rate and Blood Pressure

In a recent study examining blood pressure and heart rate, researchers may have identified a genetic component.

It is a well known fact that both resting heart rate and blood pressure both have a significant effect on cardiovascular health. Unfortunately, while both factors have a relatively high heritability, the genes influencing their rates are difficult to locate. The key? ENU germline mutagenesis.

In this study, researchers utilized N-ethyl-N-nitrosurea (ENU) mutagenesis to create rapid mutations in the reproductive cells of mice. This was paired with meiotic mapping to find loci with genes that code for heart rate. After testing over 40,000 mice, 87 systolic blood pressure genes and 144 HR genes were found.

This research is important because of how deadly heart disease can be. By analyzing genes affecting heart rate and blood pressure in mice, medical researchers may get a better idea of preventative measures for human heart disease in the future.

Sources:

https://www.science.org/doi/10.1126/sciadv.adj9797

https://pubmed.ncbi.nlm.nih.gov/10221322/