A genetic parasite may explain why humans and other apes lack tails

The interesting theory that a genetic parasite, more specifically, an Alu element, might have been a major factor in apes' tail loss about 25 million years ago is looked at in this article. Scientists believe that this DNA element's insertion into the Tbxt gene, which is important for tail development, changed the gene's function and caused apes to lose their tails while monkeys kept them. This genetic modification presents questions about the evolutionary importance of ape tail loss and could offer insights into spinal cord disorders such as spina bifida. 

These findings show the complex interactions between evolution and genetics, showing how even small changes in genetic makeup can have a huge impact on morphology and development. Also, the study challenges earlier theories that transposons are just genetic "junk," showing their significance in creating basic biological structures and functions.

In my opinion, this shows the complicated evolutionary processes are and how important genetic factors are in determining morphological adaptations. It shows the complex genetic systems that cause major evolutionary shifts, opening up new research directions for studying the evolutionary background of other mammals with similar physical adaptations in addition to apes.

Sources:

https://www.sciencenews.org/article/genetic-parasite-humans-apes-tail-loss-evolution

https://www.cdc.gov/ncbddd/spinabifida/facts.html 

Genetic Treatment to Malaria Growth in Mosquitoes

 

    Malaria is a parasitic disease, mainly transported into humans by over 30 species of mosquitoes. In 2019, 229 million people were infected with malaria and 409 thousand died. There are many antimalarial drugs on the market that can build up your immunity or fight the parasite itself. Children under 5 pose the greatest risk of dying to malaria, as 67% (274,000 deaths in 2019) of malaria deaths happen to them. Malaria has killed roughly 4-5% of anyone who has ever lived, making malaria one of the deadliest diseases ever. 

    Recently researchers from the Imperial College of London published a journal about their findings on genetically editing Anopheles gambiae mosquitoes' genes to inhibit the development of the malaria parasite within them. The researchers were able to make healthy mosquitoes that couldn't infect others with malaria. They then bred the mosquitoes and their spawn also were healthy without the malaria parasite developing within them. The researchers are currently looking to test the gene edited mosquitoes in the field as a way to prevent malaria, but that may be a long ways away. I think if we can conclude there are no dangers to the environment, mosquitoes or the people getting bit, this could be the end of malaria, and prevent millions of more deaths to malaria.

Links:

https://www.genengnews.com/news/curbing-malarias-spread-by-genetic-engineering/

https://elifesciences.org/articles/58791

https://www.who.int/news-room/fact-sheets/detail/malaria

New Genetic Blueprint Found in Parasitic Plants

Newfound research on the genetic instruction book of the Sapria genus reveals the lengths to which it has gone to become a specialized parasite. The new discovery illustrates the level of commitment S. Himalayana and its relatives have given to evolving a parasitic lifestyle and provides a comparison to other extreme plant parasites. 

Based on the findings published by Current Biology, most of the Sapria genus have lost half more than half of their genetic material. Not only that but plants like the Sapria Himalayana and their genomes were used for research. Findings showed they had completely removed the need for stems, roots, and even any photosynthetic tissue—and based on further research, even chloroplast genome have vanished

Charles Davis, an evolutionary biologist at Harvard University states that these genetic variations from such parasitic plants have left biologists confused by the sudden change. Such obvious plants recognize by their “rotting flesh” smell, are no longer producing flowers. He notes, “these plants have lost half of their genes, yet they still survive.” 

However, further investigation into this interesting genetic modification will allow researchers to determine some of biology’s limits, which I think will benefit us greatly. 

Links:

https://www.sciencenews.org/article/reeking-parasitic-sapria-plant-lost-body-much-genetic-code

https://www.cell.com/current-biology/fulltext/S0960-9822(20)31897-2?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0960982220318972%3Fshowall%3Dtrue

Marine Parasite with a Functional DNA-less Mitochondria

https://www.sciencenews.org/article/marine-parasite-mitochondria-no-dna-energy

Related Article:

https://advances.sciencemag.org/content/5/4/eaav1110

Amoebophyra ceratii is a parasitic plankton that seemed to have transferred all of its own mitochondrial DNA to its nucleus. This parasite infects algae that can cause toxic blooms (when algae grow out of control and produce toxic or harmful effect on people, fish, birds, etc). A. ceratti is the first discovery in which scientists have found an aerobic organism with fully functional mitochondria that do not have any mtDNA. This parasite has two mitochondria during the free-living stage of its life cycle and both organelles are able to produce energy. Researchers could not spot any DNA inside the mitochondria, but they found the genes for the mitochondrial function inside the organism's nucleus. They concluded that these genes made it possible for the tiny energy factories inside the mitochondria to keep producing energy after they lost their DNA.

I found this article to be interesting because I have never thought that transferring an organism's own mtDNA could be possible. Also, the fact that the parasite is still functioning surprises me. The thing is that the parasite is more dependent on its host because of its lack of mitochondrial genome in which I do not find advantageous.

Could this Be Malaria’s Achilles Heel?

Researchers at the Instituto de Medicina Molecular have discovered that the Plasmodium parasite, which is the cause of malaria, defends itself by replicating inside its host’s liver cells. Replicating inside the host’s liver allows the parasite to infect red blood cells and cause potentially deadly symptoms. Symptoms of malaria in humans include fever, chills, and a flu-like illness (cdc.gov).

Portuguese researchers have recently discovered that the Plasmodium parasite is resistant to autophagy, a cellular defense mechanism. However, the resistance to autophagy all hinges on the presence of UIS3, a protein which binds to another protein, LC3. When UIS3 is bound to LC3, a shield protects the Plasmodium parasite from autophagy, leaving the parasite free to replicate inside the liver of its host. However, parasites that lack the UIS3 protein do not have this protective shield, and can be eliminated by the host. Therefore, the UIS3 protein could potentially become a target for protection against the malaria parasite.

I think that this development in genetics could help so many people in the future. If a malaria vaccination or cure that renders the UIS3 protein inoperable could be developed, many lives will be saved. According to the CDC, 429,000 people died of malaria in 2015 alone. It would be amazing to see a combatant for malaria come out of this genetic discovery, especially now that drug resistance is becoming an issue.

Could This Be Malaria's Achilles Heel?

Information on Malaria from the CDC

Proving that You Are What You Eat

We often say, "you are what you eat," when it comes to a healthy diet. According to Samantha Heller, clinical nutritionist at NYU Medical Center, "everything you eat becomes a part of not only your inner being, but the outer fabric of your body as well." Healthier food promotes healthier skin and the opposite is true when you consume unhealthy foods. Eating junk food or unhealthy food can lead to sallow, dry and old skin overtime. In addition, other skin problems can occur such as acne, eczema, and psoriasis. However, scientists have found genetic evidence that proves "you are what you eat."

At the University of Oxford, researchers have proved that an organism's diet can affect the DNA sequences of their genes. By doing a study on two parasites, scientists have detected a difference in DNA sequences based on the organism's diet. Researchers hypothesized that the composition of an organism's diet can alter an organism's DNA.  The hypothesis was tested using two different groups of parasites: eukaryotic parasites (Kinetoplastida) and bacterial parasites (Mollicutes). According to Dr. Steven Kelly from Oxford's Department of Plant Sciences,  the parasites selected serves as an excellent model system because they share a common ancestor but have evolved to infect different hosts and eat very different foods.

Based on their results, researchers found that different levels of nitrogen in the parasites' diets contributed to the change in DNA sequences. Parasites that usually have a low nitrogen, high-sugar diet, had a different DNA comparison to parasites with nitrogen-rich, high-protein diets. Using mathematical models, researchers have been able to predict the diets of related organisms by analyzing the DNA sequence of the genes. 

While the hypothesis holds true for simple organisms, it is still unclear if the same will occur in complex organisms. While there are many factors that can affect the DNA structure of an organism, the study has proved that a high percentage of the differences in DNA sequences are due to diet composition. If results do end up proving to be true for complex organisms, it will be quite useful in encouraging public awareness for promoting a healthier lifestyle for everyone. It will serve essential in providing evidence how an individual's diet can certainly affect future generations and hopefully encourage everyone to maintain a healthy diet. 

The Path of Malaria Discovered by a Drop of Blood

 

 

In 1925, a Spanish doctor named, Ildefonso Canicio studied Malaria to find a cure. The same year that Malaria was eradicated from Spain in 1961, Canicio died. However, he left behind blood samples from patients he was working with in the 1940's. Each of these samples tell a chilling story.

 

 

Currently, scientists are trying to figure out how some strains of the malaria parasite arrived in Europe and the Americas. For more than half a century, malaria has not been an endemic in Europe. A large contribution to that is that fact that at one point, the European continent was a hot zone. As the continent cooled, malaria became less of a threat. This is because malaria is transmitted by mosquitos that live in tropical climates where water is plentiful. The European strains are now extinct, and therefore scientists have been struggling to figure out how this disease has spread and evolved across the world.

Remarkably, researchers were able to retrieve DNA from the malaria parasites in the old blood samples that Dr. Canicio left behind. In the DNA, scientists found Plasmodium vivax; which is found in Asia, the Middle East, South and Central America, and parts of Africa; and its cousin, Plasmodium falciparum, accounting for 90 percent of malaria deaths.

These findings suggest that the path of malaria followed the same path of human migration; from India to Europe and then Europe to the Americas after Christopher Columbus's arrival.
Dr. Fox, the scientists who analyzed the blood samples "was able to reconstruct the genomes of the European parasites, the full genome of P. falciparum and nearly 70 percent of the genome of P. vivax". With Dr. Conicio's samples and today's technology, Dr. Fox had more than enough information to make the historical and geographic connections.

Scientists hope to be able to identify the mutations that allowed the parasite to develop resistance over the years and even discover how the disease originated in the first place. 

Could having worms be beneficial for Crohn's patients?

A recent study suggest that parasitic worms could lead to new drug development for people with Crohn's disease and other bowel related diseases.  Mice with a mutation in the Nod2 gene were used in the experiment because its similar to the gene in humans that is associated with Crohn's.  The introduction of parasites caused the mice to have more mucus in their intestines than uninfected mice, as well as more bacteria from the Clostridiules family and less B. vulgatus bacteria.  This shift in the bacteria populations and increase of mucus in the intestines was shown to calm inflammation in the bowels.

Studies showed that chemicals from T helper cells, interleukin-4 and interleukin-13, are triggered by the worms which stimulate mucus production.  The Clostridiales bacteria feed on the mucus which allows them to outcompete the bacteria from the Bateriodales family.  When the interleukin-13 was blocked, mucus production was prevented and there was no shift in the bacteria populations.  Scientists believe that giving interleukin-4 and interleukin-13 to uninfected mice could alter the production of mucus and balance of bacteria without the introduction of parasites to the organism.

Although it seems like it could be a good idea, the article states that some individuals that took a deworming drug experienced negative consequences.  For these individuals, they had less Clostridiales and more Bacteriodales bacteria populations in their gut due to a significant drop in Trischuris trichiura whipworm eggs.  Evidently, more research needs to be done.