henribosome – BioQuakes

Author: henribosome

In the book of Genesis, Satan tells Eve that “God knows that when you eat from [the tree of knowledge] your eyes will be opened, and you will be like God.” As molecular biology and genetic science discover and elevate human knowledge, scientists find themselves considering compelling ethical questions. CRISPR, or clustered regularly interspaced short palindromic repeats, is one of these methods that demands ethical scrutiny. Throughout the course of human history, innovation and technological advancements provoke these philosophical investigations. And for inventions of great destructive and creative potential, a fundamental question arises which confront both CRISPR and the atom bomb. Is it just for humanity to wield divine power?

On June 28, 2012, CRISPR pioneer Jennifer Doudna and her colleagues published a groundbreaking paper titled “A Programmable Dual RNA-Guided DNA Endonuclease in Adaptive Bacterial Immunity.” Just as Oppenheimer’s atomic bomb started the nuclear arms race, Dr. Doudna recalls how she “remember[s] thinking very clearly… [publishing this paper is] like firing the starting gun at a race.” Despite the extraordinarily dense title, the paper actually revealed revolutionary systems for editing DNA. CRISPR technology’s access to modifying DNA has led to advancements in crop resilience, medical breakthroughs, and anthropological knowledge. Using an enzyme called Cas9 that temporarily separates the 5’ and 3’ strands of DNA similar to the effects of helicase during transcription, scientists can access the nucleobases and match a guide RNA up to the relevant strand. If the guide RNA is complementary, then Cas9 will cut the DNA strand. At this point, the repair mechanisms inherent to cell regulation pounce on the DNA strand in an attempt to repair it. In the repair process, the cell must use an identical DNA strand as a template strand to repair the broken one. But scientists are clever, so at this point, a specially engineered and previously inserted DNA strand becomes the template strand. In Summary the CRISPR process takes advantage of the cell’s repair system by cutting DNA and presenting the cell with the blueprint for how to reconstruct it.

But how does this insertion end up changing our DNA? After all, how can such a tiny difference in DNA affect any biological processes when a single strand of human DNA is six feet long when uncoiled? The answer lies in DNA transcription and translation. After transcription in which a messenger RNA complementary to the template DNA strand is synthesized and processed, the mRNA leaves the nucleus and travels to the cytoplasm where translation occurs. The mRNA is effectively the blueprint for a corresponding amino acid. The mRNA enters a ribosome, where anticodons on tRNA read for the codons on the mRNA. As tRNA carries amino acids into the ribosome’s A site, the right codon-anticodon match will trigger a transfer of the amino acid from the tRNA in the P site to the one in the A site, which shifts over into the P site as its predecessor exits through the E site. The process chugs along until the polypeptide chain is complete, at which point a growth factor terminates the synthesis. Triplets of codons correspond to specific amino acids. As a result, having the right nucleobases and codons in place is crucial for attaining the desired amino acid. Thanks to CRISPR, scientists can now identify weaknesses in present DNA structures and engineer potential solutions by inserting the right DNA instructions.

I think that CRISPR will bear the greatest fruit in the agricultural sector (no pun intended). I think that there aren’t many ethical dilemmas when it comes to engineering more resilient and abundant crops, as few would oppose solving world hunger. However, regarding livestock and poultry, CRISPR could reveal some ethical problems, specifically when the well-being of the animal is sacrificed for more short-term agricultural gain. What do you think? Will CRISPR lead the world into a new era of food security, or will it open a Pandora’s box of moral issues just as the atomic bomb did.

After 50 Years, Ancient Fish Finally Named

By henribosome

On February 27, 2024

In Student Post

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

By henribosome

On December 7, 2023

In Student Post

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

By henribosome

On October 21, 2023

In Student Post

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!

BioQuakes

AP Biology class blog for discussing current research in Biology

Author: henribosome

CRISPR: Ethical Dimensions and The Race for the New Agricultural Revolution

After 50 Years, Ancient Fish Finally Named

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

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

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