"Trashfish" AKA the Ultimate ‘Living Fossils’ may Advance Human Medicine.

If you could hop into a time machine and travel back 150 million years, the world would have looked very different. The supercontinent Pangaea was just beginning to break up, stegosaurus roamed the Earth, and ichthyosaurs dominated the seas- but if you stuck your head into a stream, you might have spotted a familiar face from our modern age...Gars.






In 1859 Charles Darwin coined the term “living fossil” to describe lineages that have looked the same for tens of millions of years, such as the coelacanth, sturgeon, and horseshoe crab. The term captured the popular imagination, but scientists have struggled to understand whether such species just resemble their long-ago ancestors or have truly evolved little over the eons.

Gars, often dismissed as "trash fish," are toothy, torpedo-shaped fish that have remained relatively unchanged throughout time. These fish are 'living fossils' - among the most primitive animals on Earth for 150 million years. Over this whole time these fish have mostly stayed the same, a rare consistency not even seen in sharks. A new study says that at the molecular level, gars are the most living fossil-y out of all living fossils- and it’s not even close.

Of 481 vertebrate species, researchers—led by Chase Brownstein and Thomas Near of Yale University and Dan MacGuigan of the University of Buffalo—found that gars have the slowest rate of molecular evolution known to science. The team also proposes a mechanism to explain gars’ timelessness to be superb DNA repair machinery. They suggest gars are extremely efficient at repairing DNA after mutations or damage, keeping the animals from evolving even as the continents have shifted around them. This repairing ability has likely kept gar genomes so stable that species and even genera whose last common ancestor lived more than 100 million years ago have diverged very little, and some can still hybridize today to produce viable offspring.

A similar hypothesis has previously been proposed by other researchers for sturgeon, which had the second-lowest substitution rates among vertebrates in the study

The scientists believe this genetic quirk could lead to advances in human medicine- which I find fascinating.

“If we can isolate what that is—and we’ve got some ideas as to what gene that might be—we can then take it to the next step of thinking about implications for human medicine and disease,” says Solomon David, an aquatic ecologist at the University of Minnesota and co-author of the study.David believes that if whatever is correcting those mutations can be replicated in human bodies, it could potentially prevent or counteract diseases such as cancer, the result of shortcomings in DNA repair and cell growth run amok.




Sources:

https://www.nationalgeographic.com/animals/article/living-fossils-gars-fish-evolution

https://www.science.org/content/article/these-gars-are-ultimate-living-fossils

          Researchers from Switzerland has done a study on TORC1, which is an enzyme that controls the normal cell growth in the body. When this enzyme is too active it causes diseases such as cancer. The Target Of Rapamycin (TOR) was first discovered in yeast, and then in humans. TOR is found in two very different proteins, TORC1 and TORC2. Researchers from UNIGE, the University of Auckland, New Zealand, and the École Polytechnique Fédérale de Lausanne (EPFL) collaborated to understand how the nutrient regulates the activity of TROC1. The researchers were able to reveal the appearance of a new TORC1 structure in cells. When the cells lack glucose, the TORC1 assemble together forming a tubular structure. The tubular structure which is the TOROID, stores inactive TORC1 and stops cell growth. Another study done by National Centre of Competence in Research (NCCR) showed that the re-addition of glucose causes the TORIDS or the tubular structure to rapidly dissemble. NCCR has done the testing in yeast. The assembly and disassembly of the TOROIDS will make it possible to search for compounds that can stabilize and destabilize the cells. This article was very interesting to me  because it could lead to curing cancer. If the cancer cells could be stopped from growing, millions of lives would be saved. Its amazing to see how modern technology can change cells from being able to grow. This research could open up new approaches to treat many diseases and change the world for ever. 


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196627/

https://www.cancer.gov/publications/dictionaries/cancer-drug?cdrid=733685

Cell Repair or Death: The Protein That Decides

A recent study that appeared in Nature Structures & Molecular Biology served to examine a newly discovered protein that aids in the repair or death decision of a damaged cell. Genetic information is found in the DNA of each cell, nestled within the double helix. When a strand breaks, the cell has two options: to be repaired, or to be killed through a process called apoptosis. The purpose of apoptosis is to prevent the growth of cancer cells by stopping the issue before it can truly begin. The newly discovered protein, UFD-2, receives and sends off signals, deciding which of these two options are best.

The study was conducted by using two different strains of C. elegans (the wild type and a genetically modified form). The DNA was exposed to ionizing radiation in order to induce breakage. Once broken, the researchers observed the work of the UFD-2 protein and attempted to understand how and why a cell chooses to repair or chooses to die. They noticed that cells without UFD-2 did not undergo apoptosis, which allows damaged cells to stay alive. This work is important in the study of cancer cells because by allowing the damaged cells to live, there is a higher risk of cancer cells forming. Although more research needs to be conducted, the researchers pose the questions of how DNA damage leads to cancer, and how it affects the aging process. These observations are a preliminary step in further cancer and cell based research.

This article is important because it opens the doors for further research on cancer cells, something that is in huge demand these days. If we can understand how these cells form on a molecular basis and figure out a way to repair the cells instead of destroying them completely, there would be much better results for cancer patients. This data also serves to describe how the aging process works and data on this could lead to a whole new understanding of looking and feeling younger at an older age.

Link: https://www.sciencedaily.com/releases/2016/09/160927111446.htm