AP Biology class blog for discussing current research in Biology

Author: henribosome

After 50 Years, Ancient Fish Finally Named

Tiktaalik roseae life restor

The Australian Outback is one of the most hostile environments on planet earth. Covering a land mass of nearly twenty two times the size of the United Kingdom, this dry landscape is a formidable and unforgiving adversary for the species that have adapted to inhabit it. But The Outback wasn’t always as dry as it is today. Millions of years ago, it was a lush, green biome that had rivers running in all directions. A recent archeological excavation has presented a team of scientists with a unique opportunity to name a fossil fish. Dr. Brian Choo of Findlers University and a team of researchers named the fish Harajicadectes zhumini after developing a more comprehensive understanding of the species. While fragments of Harajicadectes were discovered in 1973, a nearly complete specimen was unearthed by Flinders University in 2016, when they began constructing a comprehensive profile of the species.

By observing the skeletal remains, the team was able to reconstruct a hypothesized anatomy of the animal. One of its striking features was a series of large openings at the top of its head. “These spiracular structures are thought to facilitate surface air-breathing, with modern-day African bichir fish having similar structures for taking in air at the water’s surface,” commented Dr. Choo. In light of these findings, the team began to consider how the supplementary breathing apparatuses contribute to our evolutionary heritage. “The ability to supplement gill respiration with aerial oxygen likely afforded an adaptive advantage,” added Professor Long. Harajicadectes is a member of those intrepid water dwellers who brought life to land. Elpistostegalians gave way to limbed tetrapods in the evolutionary family tree.

The evolutionary edge that supplementary breathing gave Harajicadectes is not to be underestimated. It is widely understood that oxygen sustains life, but its immense significance can only be realized when looking at the molecular level of respiration. Mitochondria are one of the most ancient organelles and, according to the endosymbiont theory, preceded eukaryotic cells as aerobic bacteria. In the final and most powerful stage of Cellular respiration – oxidative phosphorylation – oxygen plays an essential role in ensuring that ATP is churning. Oxidative phosphorylation takes place in the mitochondrial inner membrane, where proton pumps transport hydrogen protons from the mitochondrial matrix to the intermembrane space where a gradient builds. Then, through simple diffusion, protons cross through the ATP synthase complex back into the matrix where they bind with O2 molecules, forming H2O as a byproduct. If Harajicadectes didn’t have access to oxygen on land, it would have only been able to leave the water for brief periods of time. This would have greatly reduced its competitive advantage on the shores and reduced the likelihood of limbed tetrapod evolution. 

I think the field of paleontology is an underappreciated field of biology and science. Just as the field of history provides context for the problems of today, paleontology better helps modern biologists understand how, when, and why species evolve as they do. This naming of the animal has been fifty years in the making, but thanks to the team of Australian scientists, we understand our evolutionary beginnings slightly better. I find the mapping of ancient biomes fascinating, and as more advanced chemistry develops, maybe one day scientists will be able to bring these prehistoric animals back to life. 

Sticky Viruses – How Strengths of Adhesion Influence the Transmission of COVID-19

SARS-CoV-2 without background

Keeping track of each new SARS-CoV-2 strain and variant may feel like learning a new language. The myriad of Greek letters used to designate each one quickly turns science into classics, so it’s understandable how one may get lost in the confusing terms. But keep calm, these identifiers are crucial for understanding how COVID-19 evolves. They help scientists organize the virus’ different traits and open a window into understanding its behavior at the molecular level. A recent experimental study has just discovered how one of the determining factors that contribute to virulence could be the strength with which the virus binds to the host cell. In a joint effort between the University of Auburn, University of Munich, and Utrecht University, scientists analyzed the virus’ atomic structure.

The team observed how the different variants’ spike proteins interacted with the human ACE-2 protein and found that Alpha’s docking sequence is much stronger than those of Beta and Gamma. However, these latter variants appeared equally virulent as Alpha, leading researchers to conclude that it was their ability to evade immune responses that compensated for their relatively weak adhesion. The lead experimental scientist, Dr. Bauer, took an innovative approach by using force stability – essentially the net force with which the virus binds to the protein receptor of the host cell – as a means of determining the strength of adhesion.

Being a respiratory virus, the cells to which COVID-19 primarily binds are those along the path air takes from the nostrils to the lungs. After making contact with one of these cells, the virus begins a docking sequence that will allow it to assume control of the cell’s replicative mechanisms. In one of the universe’s most fascinating existential tricks, the virus is neither living nor dead: it is simply an envelope filled with genetic material. If it wants to replicate itself, it can’t do it alone. The virus binds to an ACE-2, a common receptor protein on the outside of the phospholipid bilayer. Once firmly connected, the host cell sends lysosomes to digest the envelope, revealing the virus’ genetic information, which enters the cell through a pinocytotic vacuole. Once inside, the virus then hijacks the existing cell structures to replicate itself. After assembling an army of fellow viruses, the host cell ruptures, releasing legions of viruses to neighboring cells in an attempt to repeat and amplify the process. This rupturing is often the source of the soar throats from which infected patients suffer.

As someone who has in the past gone toe-to-toe with COVID-19, I can say that it is a formidable opponent. It is clever, elusive, and stubborn. For a while I felt only the most bitter animosity towards this microscopic speck, but after developing an understanding of its behavior and anatomy, I can now respect its sophisticated biological processes that aid in its reproduction. I still view it as the most heinous and lowest “life” forms in the universe, but at least I understand its point of view. Let me know what you think about this groundbreaking research! Will it prove pivotal for engineering future vaccines for specific variants? How fascinating and haunting that the severity of the illness can be determined by how firmly the virus snatches at your cells!

Marathon Mice – How an Exercise Mimicking Drug is Helping Mice Lose Weight

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Our little furry friends are well known for their appetite for cheese and delectable crumbs, so it’s entirely understandable if they put on a couple of extra pounds. But modern medicine may have just found a safe and reliable remedy to their gluttony. In a study conducted by a University of Florida professor of pharmacy, a new wonder drug has allowed mice to get into marathon shape without them even “lifting a paw.” SLU-PP-332 belongs to a class of drugs known as “exercise mimetics” – pharmaceuticals that allow the body to reap the benefits of working out while simultaneously circumventing any physical exertion.

The study found that mice that received the drug experienced a sharp drop in body fat percentage without a change in appetite. By boosting and catalyzing the body’s existing metabolism of fat, the drug is able to burn fat that would usually require endurance exercise or prolonged aerobic threshold exertion. Thomas Burris, the lead researcher, summarized its metabolic effects, saying, “This compound is basically telling skeletal muscle to make the same changes you see during endurance training.”

So why is body fat so stubborn to metabolize in the first place? The answer lies in its chemical structure. Lipids, unlike their carbohydrate cousins, are particularly difficult to break down. Take the mouse’s coveted Swiss cheese as an example: it’s a saturated fat that, although delicious, is unhealthy. It has fatty acid chains with single bonds between its carbon atoms; consequently, the chains pack closely together and layer upon each other. Carbohydrates, on the other hand, are the body’s quick and accessible source of energy. It’s going to choose the easier task and consume carbs in the bloodstream over stored fat. Hydrolysis, which occurs extensively in the digestive system, facilitates the breaking apart of carbohydrate polymers. It’s a primary and preferred means of sourcing energy via glucose, ribose, or fructose that doesn’t require the extra thirty minutes of jogging to tap into fat reserves.

I think exercise mimetics could be useful for athletes who are sidelined by medical treatment for an extended period of time, but I find its commercial application for dietary convenience troubling. I think it could become a cheap way to circumvent the discipline and timely cost of serious physical exercise. What do you think: will these mimetics compromise the integrity of exercise? Maybe one day humans will be able to maintain an elite physique while sustaining a diet of cheese and crackers, but for now, bike, run, swim, dance, lift, push, and use the human body to the fullest of its wondrous capabilities!

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