AP Biology class blog for discussing current research in Biology

Author: cellwalz

DYING to Know Your Predicted Lifespan? Look No Further!

Have you ever wondered how long you’ll be around for? Well, scientists at the German Cancer Research Center, Saarland Cancer Registry, and the Helmholtz Research Center for Environmental Health have made great strides in predicting human mortality. How so? Through a controlled study in which they analyzed patterns in DNA methylation.

DNA methylation, an epigenetic phenomenon, occurs in the body in order to inhibit the transcription of DNA. Methyl groups attach to specific combinations of DNA building blocks called CpGs. In this experiment, the scientists analyzed the DNA from blood cells taken from 1,900 participants fourteen years prior. As they were all older adults, many of the participants had died within that fourteen years. The scientists analyzed methylation at 500,000 of the CpGs, trying to figure out if there was a correlation to chances of survival. Spoiler alert: at 58 of these CpGs there proved to be a strong correlation between methylation level and mortality.

One interesting discovery was that 22 out of the 58 influential CpGs were identical (in terms of amount of methylation) to the CpGs of smokers that the scientists had analyzed in a previous study. What does this mean? Smoking definitely leaves its mark on your genome. However, the good news is that DNA methylation can be reversed, so if a smoker quits his or her risk of dying could drop significantly.

The second major finding of this study was that only 10 out of the 58 CpGs can actually determine mortality risk. The scientists took the 10 CpGs with the strongest correlation with mortality and created an epigenetic risk profile. This profile can predict “all-cause mortality”. Participants who were overly-methylated at five or more of these spots were seven times more likely to die in the fourteen year span than their properly-methylated counterparts.

This study is a major breakthrough in understanding human mortality, because analyzing DNA methylation is so much more accurate than looking at SNPs. The researchers plan on using their new knowledge to find out how to improve methylation profiles at these CpGs.

Does it surprise you that only 10 spots on the genome can have such a profound effect on duration of life? Do you think there could be an even more accurate predictor of mortality than DNA methylation levels? Let me know in the comments!

Don't Smoke!

Credit: Nina Matthews Photography, URL:

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Long Island Sound May Be Getting a Timely Makeover

In its glory days, the Long Island Sound has supported many fisheries for lobsters, oysters, crabs, etc. It still boasts of 170 species of fish and more than 1,200 species of invertebrates. In recent years, however, the Sound has been plagued with excess nitrogen. The build-up causes eutrophication, in which the extra nitrogen feeds seaweed and algae blooms, causing them to use up more oxygen. As a result, the fish don’t have adequate oxygen and perish, and the ecology of the Sound makes it uninhabitable for shellfish.

Where does all of this nitrogen come from? The main sources of nitrogen are septic tanks and sewers, fertilizers from lawns and parks, certain agricultural practices, and atmospheric deposition from dust, rain, and snow. Because the severity of the problem is based largely on human practices, it is much worse in some areas than in others.

Bridgeport  Seaside Park looking over Long Island Sound 2011

View of Long Island Sound from Bridgeport Seaside Park (credit: 826 Paranormal)

Jamie Vaudrey and her team at the University of Connecticut wanted to make this issue a priority for people, so they made a model displaying the level of nitrogen runoff in the Sound. They painstakingly collected data for four years from each of the 116 estuaries, harbors, rivers, and bays of the Sound. This allowed people to see how this problem affected not only the Sound but their local beach or the coast they sail on.

The model is an Excel spreadsheet that can be easily downloaded. In addition, the “scenario” section of the model allows people to alter a communities’ settings (such as lessening fertilizer usage) to see how it can lessen the nitrogen runoff. Another feature of the model shows the places that are impacted the most by the issue.

The model is already in use by the Connecticut Department of Energy and Environmental Protection and the Nature Conservancy. Vaudrey is creating a second model to shed more light on how every bay is affected differently by the introduction of excess nitrogen.

Do you think that this model will prompt local governments to enact legislation to solve this problem? Will this model be extended to other bodies of water suffering from this same fate? Let me know in the comments!

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Gut Microbes and Parkinson’s Disease: A Fascinating New Study

Parkinson’s, a disease of the central nervous system, affects approximately one million people in the United States. While the disease known for impairing motor skills, it can also have digestive symptoms such as constipation years before diagnosis. Because of this phenomenon, scientists have begun to investigate the role of gut microbiome composition in this awful disease. One such study conducted by a team at Caltech used transgenic mice to get to the answer. All of the mice overexpressed the protein human a-synuclein, which can form the insoluble fibrils that lead to Parkinson’s. However, the researchers raised some of the mice germ-free, or gave them antibiotics, so no intestinal microbes formed. In these mice, Parkinson’s-like symptoms and brain pathology decreased. In addition, the researchers found that the mice that did have gut microbiota had brain inflammation that the germ-free mice didn’t. Only when the researchers fed the germ-free mice short-chain fatty acids (to stimulate gut microbiota) did they show signs of inflammation and other Parkinson’s symptoms. This suggests that gut microbiota that produce short-chain fatty acids could be what triggers this disease.

The researchers then tried to investigate more about which gut bacteria could cause Parkinson’s. Since different communities of gut bacteria live in people with Parkinson’s disease than in healthy people, they wanted to find out if these different communities are merely a byproduct or a cause of the disease. To do so, they transplanted human gut-derived microbes from Parkinson’s patients into some mice, and microbes from healthy people into others. The transgenic mice with microbiota from the Parkinson’s patients ended up with typical Parkinson’s symptoms like motor dysfunction. However, wild-type mice (mice that didn’t overexpress human a-synuclein) weren’t affected. This finding shows that people who are genetically predisposed to Parkinson’s can be afflicted with symptoms if introduced to microbes that are associated with the disease.

This is such groundbreaking work because it establishes a causality between the gut microbiome and Parkinson’s. It also raises questions about the negative affects of short-chain fatty acids on the mice in this study, since they’ve been known to be beneficial in humans. The researchers wish to continue their work by investigating the types of microbes in people with Parkinson’s to get to the fundamental cause of the disease and possible cures.

Do you think that short-chain fatty acids are actually harming humans in unseen ways? Is investigating human gut microbiomes is the right path to find the cure to Parkinson’s? Let me know in the comments!

Three-dimensional Human Intestinal Cells

Human Intestinal Cells Cultured with Gut Bacteria

Credit: Scitechnol Publisher, URL:


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Just Keep Swimming…and Fixing Paralysis!


Zebrafish (Danio rerio)

Zebrafish (Danio rerio)- from Flickr

The zebrafish may just look like a cute aquatic animal, but they actually have a unique power that humans don’t: they can heal a severed spinal cord. While this uncanny ability sounds almost magical, it can be explained by the work of a certain protein, CTGF (connective tissue growth factor), that humans have as well. Because of this commonality, recent research conducted by Duke University suggests that by learning from the mechanism that allows the Zebrafish to do this, humans may eventually be able to regenerate their lost spinal tissue!

Essentially, the zebrafish is able to regenerate their spinal cord by forming a cellular bridge across the damaged or missing area. They can be fully healed in as little as 8 weeks! But how is this “bridge” possible on a molecular level? When the fish get injured, dozens of genes get activated. Seven of these genes code for proteins that are secreted from cells. The researchers at Duke found that CTGF, one of these proteins, is crucial to the bridge-making process. They found this by looking at the glia, which are the supporting cells that help initially form the bridge before the arrival of nerve cells. After forming the bridge, CTGF levels rose marginally in these glia. When the researchers genetically deleted CTGF from the glia, the whole regeneration process failed. This research proved exciting because humans also have a very similar form of CTGF, and when they added this human-version of the gene to the glia, regeneration was even faster, only taking 2 weeks! The researchers even discovered which of the four parts of CTGF was the important one in this regeneration phenomenon, which in the future would make it easier to create therapies modeled after this part for humans.

However, using this knowledge to help human tissue regeneration is not as straightforward as it may seem. Mammals such as ourselves form scar tissue around damaged areas, complicating the matter further. The group plans on experimenting with other mammals, namely mice to compare and contrast their CTGF levels with those of zebrafish. Do you think that CTGF research is the best way to achieve human tissue regeneration? Is there any way to prevent scar tissue from forming around our wounds? Let me know in the comments!


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Photo Credit to Tohru Murakami:

XRN1: The Virus Hitman

When I think of the words killer and assassin, my mind drifts to shady men in all black equipped with sniper rifles. However, recent research conducted by the University of Idaho and the University of Colorado Boulder has indicated that I should expand that mental list to include XRN1, a gene in saccharomyces cerevisiae which, according to a recent study, kills viruses within the yeast. Upon stumbling onto this subject, I was intrigued because it was a fairly simple procedure that led to a huge discovery. To grasp the significance of such a discovery, one must understand it on a molecular level. XRN1’s duty in yeasts is to create a protein which breaks down old RNA. The image below shows the generic process of the creation of a new protein through gene regulation.

Wikipedia- Regulation of Gene Expression

Wikipedia- Regulation of Gene Expression

Yeasts also contain viral RNA since practically all yeasts are infected by viruses. When scientists removed XRN1 from the yeasts, the viruses within yeasts replicated much faster, and when they expressed high amounts of XRN1, the virus was completely eradicated. This is because the XRN1 gene was inadvertently breaking down the viral RNA, mistakenly taking it for the yeast’s RNA. Scientists continued the research by using XRN1 from other saccharomyces yeast species. The virus continued replicating rapidly but the XRN1 did continue its job of breaking down the yeast’s RNA. This shows that the XRN1 from each yeast species evolves to attack the specific viruses that occur in its host while still maintaining their basic role as the RNA eaters. Scientists are hopeful about this study’s human health implications. Viruses such as Polio and Hepatitis C work by degrading XRN1 and not allowing it to break down RNA, respectively. Dengue Fever also occurs when XRN1 is unable to perform its function of RNA breakdown. These studies on Dengue Fever and Hepatitis C elaborate on the implications of XRN1 not breaking down RNA. Scientists hope that this discovery could lead to the triumph of XRN1 over these viruses. Could this really be the discovery that leads to the first ever Hepatitis C vaccine? Do you think that XRN1’s success against virus in yeasts guarantees eventual success against viruses in humans?


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