The Amazon Molly

     

The Amazon Molly is an all-female freshwater fish species found in southern Texas and Mexico. The Amazon Molly resulted from a cross between the Atlantic Molly and the Sailfin Molly. When Amazon mollies reproduce, their offspring are clones of the parents’ DNA. Typically, asexual species do not survive long because there is no sexual recombination through mating. However, this species uses gene conversion, a DNA repair mechanism, to stay healthy and produce viable offspring. How does this work? The fish use a “copy and paste” method, taking specific stretches of genetic code from their own chromosomes and using them on others. This method works because it allows the fish to pass on beneficial traits, erase harmful mutations, and fix errors from its two parent species. Without the ability to purge harmful mutations through sexual reproduction, the Amazon Molly “avoids accumulating harmful mutations by shuffling its own genome around” (Schartl, 2026).

Picture/Article: https://www.sciencenews.org/article/sex-skipping-fish-hacks-evolution-gene 

Second Article: https://www.lmu.de/en/newsroom/news-overview/news/how-a-clonal-fish-avoids-genetic-decay-752cd04a.html 

Genetics Decides Your Lifespan

 

Oftentimes you are told that your environment and lifestyle choices are the determining factor in how long you live.  However, recent research suggests that there is something else that impacts life expectancy more than lifestyle: genetics.  As reported by U.S. News, a landmark study published in the journal Science revealed how genetics makes up 55% of a person’s life.  Previous studies estimated 6% to 33%.   This study focused on the lifespan of twins.  Twins were the study subjects of choice in order to isolate heritability.  The study also separated deaths by external factors and internal aging.  External deaths were classified as accidents, cars, natural disasters, etc, and infections.  Internal aging factors were categorized as chronic diseases and natural decline due to age.  This research found that if you remove external death from the equation, then your life expectancy is dictated more by DNA than lifestyle choices.  While DNA can account for 55% of life expectancy, 45% is still dependent on diet, exercise, and healthy habits.  Overall, the 55% dictates your life expectancy, and the 45% helps you reach that expected age.

https://www.usnews.com/news/health-news/articles/2026-02-02/study-finds-genetics-may-shape-up-to-55-of-how-long-you-live 

https://pubmed.ncbi.nlm.nih.gov/41610249/ 

Picture: https://fastercapital.com/topics/the-impact-of-genetics-on-life-expectancy.html/1 

Sick Baby Now Thriving After Experimental Gene Therapy

 

This article details advancements in personalized medicine.  Specifically, how this experimental therapy helped a once-sick baby now prosper.  KJ Muldoon, the ill baby, was born with a rare and life-threatening condition called Carbamoyl phosphate synthetase I deficiency, or CPS1 Deficiency.  The mortality rate for infants born with this deficiency is about 50% because CPS1 keeps the body from removing ammonia in the blood, which can lead to toxic buildup that can be fatal for ½ of the cases.  Researchers at CHOP and Penn Medicine thought that a base editing technique could fix the mutation.  They used precise technology known as CRISPR methods.  This involved “cutting” DNA to change one letter, and therefore, fix the mutation.  How did this work out for KJ Muldoon?  According to the article, he is growing, and he can eat a more regular diet.  His body is also fighting common illnesses off better.

Picture & Article: https://www.pbs.org/newshour/science/experimental-gene-editing-helped-a-desperately-ill-baby-thrive-scientists-say-it-could-someday-treat-millions 

Second Article: https://almanac.upenn.edu/articles/medical-miracles-at-penn-medicine-breakthrough-with-customized-crispr-treatment-for-patient-with-cps1 

Genome Editing

 

Columbia University and Broad Institute have been researching a new tool, designed for gene alterations.  Unlike the CRISPR, which is designed to fix DNA sequences through cutting, the evoCAST is designed to insert entire genes that are healthy into precise locations.  With the evoCAST, diseases like cystic fibrosis and hemophilia could be treated more smoothly and reliably.  So, how does it work?  The evoCAST is based off of the CRISPR, so the genes are able to “jump” to new locations in the genome.  “Jumping” genes are also referred to as transposons.  Genetic diversity can also be a byproduct of  genes moving from place to place in the genome.  In order to make this usable for medicine, researchers used the PACE technique, or the Phage-assisted continuous development, where enzymes had to go through rounds and rounds of fast paced evolution.  This technique raised the efficiency levels in human cells to a place where it could potentially be used for real world gene-therapy.  Treatments like this could be revolutionary to those afflicted with diseases like cystic fibrosis and hemophilia, which are caused by many different gene mutations.  Back before the evoCAST, the CRISPR had to be used, and to use it for treatment, a custom drug had to be designed for every mutation.  With the evoCAST, one therapy could be used to insert an entire healthy copy of a gene into the genome.

Picture/article: https://www.cuimc.columbia.edu/news/sternberg-evocast-gene-editor 

Second article: https://www.broadinstitute.org/news/technology-brings-new-precision-to-genome-editing 

DNA Picks Favorites

 

Research from Kyoto University claims that cells can recognize inefficient genetic instructions and basically silence them.  The protein DHX29 plays a fundamental part in this research.  DHX29 identifies and silences inefficient messages.  The research from scientists at Kyoto University showed that the protein recognizes weaker messages when it is physically interacting with the 80S ribosome.  Once it notices the weak message, it uses another protein called GIGYF2•4EHP to specifically suppress that mRNA, and therefore, halting that gene's output.  This research suggests that our DNA does not simply control which genes go on and off, but how the particular makeup of those genes affect their endpoint overall.  This could lead to the understanding of how “silent” mutations disrupt expression and contribute to diseases.  

Photo/Article: https://www.sciencedaily.com/releases/2026/04/260408225946.htm 

Second Article: https://www.kyoto-u.ac.jp/en/research-news/2026-03-23 

Allergies Evolved from a Cleaner Lifestyle

 

Scientists have hypothesized that modern allergies are the result of a cleaner and simpler way of life.  They believe our immune systems evolved for a dirtier, germ-filled past, and the idea is that in the world’s cleaner environment humans immune systems overreact to simple things causing allergies.  The research done for this hypothesis included the study of over 15,000 humans’ genomes from 18,000 to 200 years ago.  With the start of farming, research suggests that in the denser societies natural selection favored genes that fought off bigger issues like influenza and tuberculosis.  These changes caused an increase in autoimmune diseases risks, but they also lowered the signals linked to allergy inflammation.  Will Barie, a geneticist, offered the perspective that modern immune systems work on a “patchwork” immune system.  The patchwork system works through different eras.  For instance, the hunter-gather phase favored a fast immune system to fight off continual infection.  As well as the agricultural phase where the immune system worked on a trade off: tempering harmful inflammation and fighting off new infections.

Picture: https://drathavale.com/nose-sinus/allergy/types-of-allergies/ 

Article: https://www.sciencenews.org/article/ancient-dna-allergies-dirtier-past 

Second Article: https://hms.harvard.edu/news/massive-ancient-dna-study-reveals-natural-selection-has-accelerated-recent-human-evolution 

Genetic Links to Hereditary Blindness Shared by People and Monkeys

 

https://www.ucdavis.edu/news/identifying-genetic-causes-blindness-people-and-macaques 

https://www.nei.nih.gov/research-and-training/research-news/discovery-monkeys-could-lead-treatment-blindness-causing-syndrome 

Researchers at UC Davis have located a genetic mutation in rhesus macaques, a species of monkey primarily found in Asia, that is identical to a form of blindness found in humans.  The condition found in humans is called Autosomal Dominant Optic Atrophy pr ADOA for short.  Researchers discovered that the OPA1 gene in some macaques had mutated.  This mutation causes these monkeys to suffer from progressive vision loss and eye abnormalities that mirror ADOA symptoms.  Due to primates close relation to humans, these macaques can be used as a biological model to test treatments and therapies.  Finding a cure for these monkeys could lead humanity to a permanent cure for blindness through gene therapies and other medical treatments.  

A Mutation That Makes Horses Athletic

     Horses are known to be very fast animals. Johns Hopkins Medicine researched and discovered how horses are so quick. Horses override a genetic "stop" sign which allows them to generate high energy to provide them with oxygen during exercise.  This method has only ever been seen before in viruses.

    The researchers discovered a mutation in the KEAP1 gene in horses, donkeys, and zebras. This mutation introduced a stop codon. However, if the codon appears early in a gene, the protein produced may not function correctly. Horses are able to recode the stop codon and allow their KEAP1 protein to be fully functional.

    Horses have an adaptation in their KEAP1 gene that makes the protein more reactive to oxygen which makes their NRF2 protein more active. The researchers concluded that this adaptation and mutation are the reason horses are able to fuel their body with enough oxygen when performing intense exercise.

Figure 1. Horse Running 

    This research does not only prove why horses are able to run so fast for so long, but it allows scientists to better understand chronic diseases, age related diseases, and exercise physiology.  Premature stop codons, like the stop codons seen in horses, account for 11% of inherited diseases such as cystic fibrosis and muscular dystrophy.  

    Overall, this study provided insight on the genetic make up of horses and how they are athletic but it also helps the future of inherited and age related diseases. I learned a lot about how horses function when exercising and how stop codons and be bypassed because of mutations from this article. I did not expect that this information on horses can be helpful in understanding chronic diseases. Hopefully this research allows scientists and doctors to better know their patients functions of genes to help treat their diseases.