BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Epigenetics (Page 1 of 2)

COVID CHANGES THE IMMUNE SYSTEM!?!

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In 2019, a new strain of SARS-coV-2 took the world by storm, sending millions of people into quarantine. While the past few years have seen the virus’s spread ultimately be controlled, the people continue to be infected today—I know this personally as last month I got COVID. Luckily my COVID was very mild, but for many people, the same can’t be said. Unfortunately, in addition to the terrible symptoms that one might have during their Illness, recent research has found that severe COVID-19 could cause long-term immune system changes.

This recent research found that severe COVID-19 causes long-term effects on specific cells responsible for our immune system. They found that a chemical, IL-6, changes how genes are expressed and impacts how cells work as a result. The cells called hematopoietic stem and progenitor cells (HSPC), undergo lasting changes in their characteristics and how their genes are regulated (epigenetic programs). These changes persist for months to a year and result in altered activities of transcription factors (proteins that control gene expression), modifications in how inflammation is regulated, and increased production of certain immune cells (myelopoiesis). The altered HSPC makes so many changes because HSPC, or stem cells, are the only type of cell that can differentiate or repair specialized types of cells.

 

This research is related to AP BIO because the article talks about COVID-19 influences epigenetics (how genes are turned on or off because of environmental factors) and in AP BIO we talked about how proteins are able to be made because of the information on the DNA. In protein synthesis in a cell, the first step is transcription where information on the DNA is transcribed onto mRNA. The mRNA then is sent to the Rough Endoplasmic Reticulum where it is received on the cis face. Then the ribosomes of the rough ER, the protein is synthesized. The type of protein that is synthesized here is determined by the information of the mRNA. Then the protein is sent to the Golgi where, based on the information from the mRNA, molecules are added to the protein to determine its final location.

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This AP BIO information relates to the research because the research is about how a chemical changes how DNA is expressed, this information from AP BIO explains why DNA is important.

Wow! That was so interesting! Reading about epigenetics has made me wonder: what other conditions can influence how DNA is expressed?

 

Changing a baby’s DNA profile by physical contact?

Photograph by Vera Kratochvil, License: CC0 Public Domain

Recent research from the University of British Columbia and BC Children’s Hospital Research Institute proved that the amount of physical contact between infants and their caregivers can affect children at the molecular level. The study demonstrated that children who had been more distressed as infants and received less physical contact had an underdeveloped molecular profile for their age. This is the first study to show that the simple act of physical touching on human children can result in deeply-rooted changes in genetic expression.

The researchers measured a biochemical modification called DNA methylation in which parts of the chromosome are tagged with small molecules made of carbon and hydrogen. These molecules act as “dimmer switches” that help control how active each gene is and affect how cells function. The extent of methylation and where on the DNA it takes place can be impacted by external conditions, especially in childhood.

The team analyzed DNA methylation of 94 healthy children with records of received caregiving from the age of five weeks to four and a half years. The DNA methylation patterns the scientists gathered presented consistent differences between high-contact and low-contact children at five specific DNA sites. Two of the five sites are related to genes: one involves in the immune system, and the other in metabolism. The children who experienced higher distress and received little contact had a lower “epigenetic age” than what’s expected from their age. Such low epigenetic age is conceived as an underdevelopment of the child’s molecular profile. As medical genetics professor Michael Kobor said, “In children, we think slower epigenetic aging might indicate an inability to thrive.”

The researchers intend to further examine whether the “biological immaturity” – epigenetic changes resulted from low physical contact – carries broader implications for children’s health, especially their psychological development. According to the lead author Sarah Moore, “If further research confirms this initial finding, it will underscore the importance of providing physical contact, especially for distressed infants.”

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: https://www.flickr.com/photos/21560098@N06/5642711277

Original Article: https://www.sciencedaily.com/releases/2017/03/170320104008.htm

Epigenetics Fight Against Pancreatic Cancer

Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most deadly forms of of Pancreatic Cancer with a less than 10 percent, 5-year survival rate. Unfortunately, it is the most common form of Pancreatic Cancer.  However, scientist were given hope to increase the survival rate when a protein was identified as a aid to the development of PDAC. The protein is Arginine Methyltransferase 1 (PRMT1) and it is involved in gene transcription, DNA signaling, and DNA repair.

It is said that research done by Giulio Draetta, M.D., PhD “strongly suggest a role for PRMT1 in PDAC development and illuminate a path toward the development of therapies for patients in desperate need of innovative solutions”. Draetta’s  team developed a platform called PILOT, Patient-Based In Vivo Lethality to Optimize Treatment. The PILOT technology allows researchers to systematically identify epigenetic drivers in patient-derived tumors. The research found hat PRMT1 is a epigenetic driver for PDAC. Using CRISPR, the team was able to confirm that when the proteins were removed from DNA, the growth of the cancer cells were significantly impaired. There is hope that this recent development can save many lives and increase the survival rate of Pancreatic Ductal Andeocarcinoma.

https://commons.wikimedia.org/wiki/File:Diagram_showing_stage_T4_cancer_of_the_pancreas_CRUK_267.svg

 

How A Chemical From the Cypress Tree Could Advance Epigenetics Against Cancer

by Czechmate on Wikimedia Commons

Found in the essential oil extracted from the bark of a cypress tree, a chemical named hinokitiol shows potential to impact epigenetic tags on DNA and stop the activity of genes that assist the growth of tumors.

In order to develop an of understanding cancer, researches have had to comprehend the DNA methylation, an epigenetic function which controls gene expression. In regular DNA methylation, genes that work to fight against tumors are turned on, reducing the risk of cancer. However, if DNA methylation is negatively altered, then those cancer-fighting genes will be silenced, helping to progress cancer development. Scientists have tried to combat irregular DNA methylation and over-silencing of genes by creating epigenetic anti-cancer medications that reverse non-beneficial methylation effects. Like in most cases of medication usage, the users face unappealing side effects. Hinokitiol is attractive to scientists because it is a natural compound with many health benefits and way less side effects than modified drugs that can possibly cause mutagenesis and cytotoxicity.

 

Researchers from the Korea University College of Medicine tested the productivity of the hinokitiol chemical in a study by giving doses of it to colon cancer cells. It was found that this chemical helped to inhibit the colon cancer cells efficiency without affecting the colon cells without cancer. The scientists also found through careful inspection that the presence of hinokitiol decreases the expression of proteins DNMT1 and UHRF1; both of which are proteins that encourage carcinogenesis. In summary, the doses of hinokitiol appear to have allowed normal cells to remain healthy, while reducing the ability for the colon cancer cells to thrive and ceasing the production of proteins that promote cancer maturation.

Researchers are continuing their search for natural compounds, as opposed to artificial medications, that can prevent the flourishing of cancer in our bodies through playing a positive role in gene expression and DNA methylation.

http://www.whatisepigenetics.com/cypress-trees-epigenetically-protect-cancer/

 

 

https://commons.wikimedia.org/wiki/File:Raindrops_on_leyland_cypress.jpg

Using CRISPR to Prevent Chronic Pain & Inflammation

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Researchers at the University of Utah have recently figured out a way to use CRISPR gene-editing techniques to reduce chronic pain and inflammation.

Normally, inflammation around damaged tissue signals various cells to produce molecules that destroy the damaged tissue. However, this can quickly devolve into chronic pain when the tissue destruction does not stop.

The researchers have found a way to use CRISPR (Clustered Regularly Interspaced Short Palindromic Repeat) to relieve and prevent chronic pain. Unlike most popular CRISPR techniques, theirs does not involve altering the gene sequences– it instead relies upon epigenetics, and modifying the expression of the genes in the cytokine receptors in inflammatory areas, to prevent cells from producing the molecules that destroy tissue.

The treatment is delivered through a virus, which is injected into the inflammatory site. It is more potentially therapeutic than current treatments for chronic pain, in that it actually prevents tissue destruction and future pain, rather than just relieving present pain. The method is approximately ten years away from being used to treat human patients.

Avenging Lamarck: The Epigenetics of a Fish

The laughingstock of biology classrooms everywhere, the footnote to Charles Darwin and his widely acclaimed theory of natural selection, the scientist who has caused many a biology student to stop and wonder why he or she should even know his name, Jean Baptiste Lamarck has gotten a bad rap among student’s across the country. Predicting that evolution in species resulted from individual species adapting to their environment and morphing their bodies to better survive and reproduce, passing their adapted traits to their offspring, Lamarck has been criticized by students everywhere for simply not being correct. However, he wasn’t entirely wrong. Recent research conducted in the Gulf of St. Lawerence off the Labrador Peninsula has revealed that skate fish  in the area have developed differences in terms of size from other skate fish because individual organisms are able to turn on and off select genes.

https://en.wikipedia.org/wiki/Mottled_skate

The ability to turn on and off certain genes in organisms based on environmental conditions and pass those changes to offspring is called epigenetics. Epigenetics allows individual organisms to change their traits slightly to adapt to their environment. Where evolution by natural selection takes millions of years and results in the evolution of populations on a macro scale rather than individual organisms, epigenetic changes are much quicker.

Researchers were attracted to studying the winter skate fish in this bay because though the fish lies all along the North American coast, in this bay, the fish tends to be significantly smaller than other members of its species. Scientists attribute this to the warm water in this shallow water area which makes smaller organisms more likely to survive and reproduce.

However, DNA tests showed that significant changes in the genome of the fish weren’t what made them smaller, indicating it wasn’t Darwinian natural selection that dominated this process. The researchers discovered that the fish could turn on and off certain pieces of DNA in individual organisms to better adapt to the environment. Thus, the fish are able to adapt more quickly to changes in temperature than other organisms that rely solely on natural selection for changes to their traits.

Thus, Lamarck wasn’t entirely wrong all along (just mostly!).

The researchers hope this new information will help with conservation efforts and will give more insight into how species adapt to climate change.

So, do we owe Lamarck an apology? How can conservationists use this information to draw more interest to their goal?

Sperm Epigenetics and the Next Generation

Jerome Jullien from the Welcome Trust CRUK Gurdon Institute in Cambridge experimented with frogs to see if more than just DNA is passed on to the second generation offspring.  Sperm contain something called epigenetic tags which are “chemical switches attached to the genomes of sperm.”  (It is important to understand that epigenetics does not alter an organism’s DNA.)  In order to test if these sperm epigenetics influence offspring Jullien used two types of sperm; regular frog sperm and spermatids which had different epigenetic tags.  They then injected the sperm and spermatid into genetically engineered eggs which took away some of the epigenetic tags (with specific enzymes) on the sperm.  This lead to abnormal gene expression causing problems for the offspring.

This basically shows that a male does not simply pass down his DNA to his offspring but other factors like epigenetic tags can also effect the life of their kids.  As Jullien says, “The obvious implication is that whatever experiences the father has in life that end up epigentically modifying sperm cells might also be transmitted to the offspring and affect their genetic development and characteristics.”  There is still disagreement over whether epigenetic tags on sperm influence offspring.  For example some feel the experiment tested was not realistic because the frogs were not exposed to different environments as a human would be in his lifetime.  What do you think; would epigenetic tags on male sperm have an effect on a mans offspring?

The Role of Metabolism and Epigenetics in Cancer Development

Cancer most commonly is defined as a “perpetuating mass of dystregulated cells growing in an uncontrolled manner”, however the meaning can be further related to epigenetics, for they appear to be very much interconnected.  Another definition of cancer goes on to note this relationship as the “dynamic genetic and epigenetic alterations that contribute to cancer initiation and progress.” Recent research shows that if epigenetics is disrupted, it might switch to oncogenes or shut down tumor suppressors. Either way, this would lead to the development of tumor cells that would cause cancer. We are already aware of the fact that chemical modification affecting the packaging of our DNA can switch genes on and off. The first time that became aware of an epigenetic code, we learned that that code chemically labels active or inactive genetic information. The focus of epigenetics is on the change caused by the modification of gene expression, not the alteration of the code itself. With recent discoveries through research on epigenetics and its relation to cancer, we learned that there must be a balance of “writers” and “erasers” for the cells. Recent data has shown that methyltransferase EZH2 is an epigenetic writer that is hyperactivated in many cancers, specifically melanomas and lymphomas. This recent research also shows KDM3A (member of the jumonji histone lysine demthylase family) as an epigenetic eraser. KDM3A fulfills an oncogenic role by activating a network of tumor promoting genes. Epigonomic changes also allow tumor cells to evade the immune system so that these cells can thrive and divide without the disruption of the immune system. Ultimately, there are two potential pathways that epigenomic regulators can cause cancer. The first is the result of too much epigenetic activation, which can lead to oncogenes. The second is too much epigenetic protection that conversely blocks tumor suppressor genes. DNA hypermethylation causes the silencing of tumor suppressor genes.

Both of these methods would lead to the development of cancer. Epigenetic regulation involves methods including histone regulation, DNA methylation, and changes in noncoding RNAs such as miRNAs. One of the challenges of studying cancer and researching possible vulnverabilities in pathways is that they are often disrupted by epigenetics. The recent studies also have shown that there are close ties between epigenomic (analysis of global epigenetic changes across many genes) changes and metabolites, or human cellular chemistry. Metabolites initiate, target, or maintain epigenetic factors with the transcriptional complex, and cooperation with them metabolites can target, amplify or mute these coded responses. Since the fields of both epigenetics and metabolism are still developing a great deal, there is hope that these insights with regards to cancer and regulating gene expression to prevent the development of cancer will allow for more precision in targeting cancer, specifically when existing methods of therapy fail to work sufficiently.

Epigenetics – Exercise Runs In The Family

It is common fact that people who exercise frequently are more likely to live a longer healthier life, but now new studies show that if a person exercises it can also result in a better life for his or her children and even grandchildren. Before the study of epigenetics people always thought the genome they are born with it the genome they are stuck with. However new science has shown exercise not only changes the outward appearance of our muscles and overall physical health, but also changes our DNA.

Exercise, astonishingly, can effect gene shape, function, and turn them on and off. Scientists now know that genes can actually be quieted or amplified through exercise because biochemical signals are sent out every time a person exercises. This is where epigenetics comes in. Epigenetics doesn’t simply change the gene all together, but instead works its magic on the outside of each gene through a process called methylation. A cluster of atoms surround the genes either denying or amplifying biochemical signals. Scientists believe that even one day of exercise can change methylation patterns.

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One study done by scientists at the Karolinska Institute in Stockholm put the theory of exercise and epigenetic’s to the test. They studied 23 young and healthy men and women. They asked all the participants to work out half of their lower body for three months. This way each member of the study was his or her own control and experimental group. Obviously, after the three months each members leg that was worked out was stronger than the other, but what was much more intriguing was the results at the molecular level. The scientists found significant methylation changes in the cells of the leg that were worked out, averaging 5,000 sights on the genome where there was a new methylation pattern. Many of these methylation patterns were changed on enhancers, which are important for amplifying gene expression. The genes that were most affected were those that play a role in energy metabolism, insulin response, and inflammation within muscles. Exercise, along with many other healthy lifestyle tasks, has shown to cause changes in a persons epigenome. Changes that make a person healthier, but perhaps even more significantly, can make his or her children and grandchildren healthier.

 

http://well.blogs.nytimes.com/2014/12/17/how-exercise-changes-our-dna/?_r=0

 

Epigenetics and Dopamine Activity

Researchers at the University of California in Irvine have correlated erratic dopamine activity as an underlying cause of complex neuropsychiatric disorders, specifically because of the epigenetic alterations caused by low levels of dopamine. This study, overseen by Emiliana Borelli, a UCI professor of microbiology & molecular genetics, provides clues to the possible causes of complicated disorders like schizophrenia.

Dopamine is a neurotransmitter (and hormone) that fuels our daily life, acting as our prime motivator and pleasure inducer, while also being linked to memory, and cognitive function. Many addictive drugs increase the amounts of dopamine released to exhausting levels, eventually wearing out the neurotransmitters notwithstanding the negative effects of the drugs themselves. High dopamine levels can also be achieved via everyday pleasures like exercise or sex, which can also spur addiction.

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Dopamine, therefore, has an irrefutable role in our everyday lives, and according to Borelli, “Genes previously linked to schizophrenia seem to be dependent on the controlled release of dopamine at specific locations in the brain. Interestingly, this study shows that altered dopamine levels can modify gene activity through epigenetic mechanisms despite the absence of genetic mutations of the DNA.”

In short, it is quite likely that Dopamine is an epigenetic hub of sorts, that can cause powerful changes in gene regulation when functioning in a disrupted or excessive manner. Borelli, knowing the consequences of excess dopamine release, tested the opposite effect on mice, hindering dopamine release by turning off mid brain dopamine receptors in rats, leading to mild dopamine synthesis. The results were profound, as Borelli found there to be decreased expression in approximately 2,000 genes in the prefrontal cortex. This epigenetic surge of decrease in genetic expression was reinforced by the increase in change of DNA proteins called histones, which are associated with reduced gene activity. The now mutated mice suffered from ranging psychotic behavior and episodes, and were then treated with dopamine activators for a duration of time before seeing their behavior normalize.

Borelli’s and others’ work will provide useful clues for understanding these complex neurological disorders, while serving to reinforce the newfound importance of comprehending gene regulation and expression. These studies seem to point to a new era in which it is not just your genetic make up that determines your future, but also the regulation of your genes.

 

 

Genetics and Mental Illness

Brain Lobes

Scientists have tirelessly searched through the genetic makeup of people with metal illnesses trying to find a common variation(s) that could account for conditions such as schizophrenia and bipolar disorder. However this has been inconclusive so researchers have turned to epigenetics, the study of how experience and environment effect the expression of certain genes. Epigenetic marks regulate when and how much protein is made with out actually altering the DNA itself. It is believed that these “marks” can affect behavior, and thus may interfere with metal health. This idea was tested in a study with rats.  Researchers proved that affectionate mothering alters the expression of genes, allowing them to dampen their physiological response to stress, which was then passed on to the next generation. This is thought to be similar in humans and these markers develop as an animal adapts to its environment.  Epigenetic research led scientists to prove that offspring of parents who experienced famine are at a higher risk for developing schizophrenia. Additionally, some people who have autism, epigenetic markers had silenced the gene which helps produce the hormone oxytocin which helps the brain’s social circuit. And therefore a brain that lacks this hormone would most likely struggle in social situations. Thomas Lehner of genomics research at the National Institute of Mental Health says that studies and research have shown that epigenetic modifications impact behavior and he also believes that these effects can be reversed. By studying genes at the “epi” level, researchers are hoping to find patterns that were hidden at the gene level.  Finding and targeting these patterns can lead to more effective treatment of and management of certain mental illnesses. There are many projects and studies at some of the most prestigious institutes, such as Tufts and Johns Hopkins, that are focused on the study of things at the epigenetic level.

Original Article

Further Information:

Epigenetic Markers and Heredity

Epigentetics and Autism 

Genetics and the Brain

 

 

 

 

Epigenetics for Asthmatics


In a recent study, a group of scientists obtained findings that could lead to a new approach to treating allergies. Instead of looking at the genes of their test subjects, they looked at something “above” the genome. Here we reach the field of Epigenetics.
Let us first define “Epigenetics” as the study on the activity and regulation of genes. In the world of Epigenetics, one can think of the epigenome as the on-off switch for the expression of genes. In terms of the study lead by Professors William Cookson and Miriam Moffatt, they focus on genes that trigger Asthma in patients. As Asthma cannot be ‘cured’, is there a way to shut down the genes that cause it?

The research team searched for a correlation between Asthma-causing antibodies and low methylation levels. Methylation is the process by which a methyl group attaches to certain genes in order to regulate their activity. Scientists already know that people with asthma have higher levels of an antibody called “Immunoglobin E” (IgE). This antibody is involved in triggering the symptoms of asthma. It is already known that genes responsible for producing IgE are hyperactive in asthma patients. The question became whether methylation had something to do with it. So to answer this question, the researchers obtained volunteers with asthma, but with varying IgE levels. The group found significant results surrounding lower levels of methylation with the patients that had higher levels of IgE than those with lower levels of IgE in their blood. This suggests that the lower methyl levels on certain genes evokes an overactivity of IgE producing genes.

After reading the article myself, I wonder if asthma patients could find ways to have higher methyl levels in their body to shut down the overactive IgE-producing genes. Perhaps they could consume a methyl rich diet? I guess it’s not that simple. Further research should obviously go into epigenetics, since I feel it is a newly discovered field. Anyways, here are the head scientists reactions to the experiments:

Professor Moffatt: “The genes we identified represent new potential drug targets for allergic diseases as well as biomarkers that may predict which patients will respond to existing expensive therapies.”

Professor Cookson: “Our pioneering approach, using epigenetics, allowed us to obtain insights that we weren’t able to get from traditional genetics. It isn’t just the genetic code that can influence disease and DNA sequencing can only take you so far. Our study shows that modifications on top of the DNA that control how genes are read may be even more important.”

This article (and the entire study of Epigenetics) shows how scientific knowledge and thought is always changing. Before recent research showing a link between one’s living environment and their genetic activity came along, scientists widely believed that one only passes down inherited genes to their offspring. This potentially makes scientists now look twice at Lamarck and Darwin’s theories of evolution. Due to the new research conducted on Epigenetics, Lamarck’s (originally rejected) theory of how an animal’s environment will affect that animal’s offspring can now be regarded in a whole new light.

Original Article: http://www.sciencedaily.com/releases/2015/02/150218073057.htm

Further Reading: http://www.extremetech.com/extreme/180963-lamarcks-revenge-the-epigenetics-revolution-may-redeem-one-of-darwins-oldest-rivals

Editing the Brain Using Epigenetic Tools

Epigenetics is a huge part of our life and influences us in ways we may not be aware of. Did you know that it is impossible to create and save new memories without epigenetic tags? The brain is heavily reliant on Epigenetics to do its functions, and this makes it a huge topic of research to figure out the ways in which the epigenetics of the brain could affect certain diseases or memory. Recently special epigenetic molecular tools have been created that can erase specific epigenetic markers throughout the genome. The possible effects these tools could have on the curing of diseases of the brain or psychological ailments are tremendous.

These “epigenetic editing” procedure use either CRISPR (clustered, regularly interspaced, short, palindromic repeats) or TALE (Transcription activator-like effector) systems of modification. These systems can carry an Epigenome modifying enzyme and deliver it a specific site they are programmed to go to. This allows researchers to target very specific epigenetic changes and either shut them down or turn them on and possibly determine their correlation with certain ailments of the brain. “We’re going from simply being able to observe changes to being able to manipulate and recapitulate those changes in a controlled way,” Day said. This quote from Day, one of the researchers of this project, shows that we advance from only being able to observe epigenetic influences on the brain, to being able to manipulate and control them to potential aid us in combating diseases.

Researchers can catalog all of the epigenetic changes involved in forming and preserving a new memory. If we are able to track these epigenetic changes, then could we implant memories in to a person’s mind, by copying similar epigenetic changes? These researchers where also able to trigger not only the place where epigenetic change happens, but also the exact time using optogenetics. This form of using light to control neurons allows researchers to use the TALE system and a light switch apply epigenetic change to very specific brain regions or cell types.

One of the final goals of this research is to eventually be able to use epigenetic as a form of therapy to benefit PTSD, depression, schizophrenia, and cognitive function using the ability to alter epigenetic marks. This can also be used in a similar way to silence mutated genes that are damaging the cells or the body as whole. This form of using TALE and CRISPR to alter epigenetic tags creates a lot of hope for PTSD, depression, schizophrenia, Alzheimer’s, Parkinson’s, Huntington’s and other similar disease treatment options.

Long Term Effects of Bad Diet Linked to Epigenome

Epigenetics has become an increasingly popular topic of scientific study. It is universally understood that DNA carries genes, however the expression of those genes are at the whim of the epigenome. The long-term control of the epigenome over the expression of certain genes is not yet fully understood. Scientist Erik van Kampen of the Leiden Academic Centre for Drug Research at Leiden University in The Netherlands studies epigenetics. He was interested in the mystery of how the epigenome is influenced by diet. He explored the idea of how the effects of a poor diet continue to persist even after a better diet is adopted.

In his study, he used mice that naturally had a high susceptibility to getting high blood cholesterol and atherosclerosis. He fed these mice either a high fat, high-cholesterol diet or a normal diet. After time had passed, bone marrow was isolated from both the unhealthy and healthy diet mice. This bone marrow was transplanted into mice that had their bone marrow destroyed. The new mice with borrowed bone marrow were given a healthy, normal diet for several months. After this time had passed, the mice were measured for development of atherosclerosis in the heart. In addition to this, the mice were measured for the number and status of immune cells throughout the body and epigenetic markings on the DNA in the bone marrow.

The results of this study were staggering. Mr. Kampen found that DNA methylation (which inactivates the expression of genes) in the bone marrow was different in both types of mice. The transplants received from the unhealthy diet mice were seen as having a decreased immune system and increased atherosclerosis in comparison to the ones who had healthy donors. This study proves at least somewhat of a correlation between diet and long-term effects on the body and the expression of genes.

The original article can be found at this address: http://www.sciencedaily.com/releases/2014/11/141103102359.htm

The Harm Stress Causes

http://upload.wikimedia.org/wikipedia/commons/c/c6/DNA_double_helix_45.PNG

https://www.sciencenews.org/article/chronic-stress-can-wreak-havoc-body

Recently scientists have begun to discover why stress can have a negative effect on the human body. Although stress is needed when dealing with situations which require hormones to trigger a fight or flight, consistent stress can lead to a multitude of health problems. Chronic stress can lead to mental instability, and an increased risk in heart attacks, strokes, infection, etc. The decrease in health is due to inflammation and warped genetic material caused by epigenetics (chemical interactions that activate and deactivate regions of a genome to carry out specific functions). Recently scientists have discovered that  changes in epigenetics can affect activity levels in genes which directly change responsibilities of certain cells including immune cells. The stress causes a genetic response that deactivates certain areas of a genome which stops an immune cell from working properly, which of course leads to an increase in diseases that cannot be properly taken care of. Hopefully, as we continue to understand epigenetics, we will be able to take appropriate steps that will both further our understanding of the human genome, as well as help increase the longevity and immune system of individuals.

Epigenetic breakthrough: A first of its kind tool to study the histone code

 

DNA_methylation

Scientists at the University of North Carolina have recently made a breakthrough in the study of epigenetics, particularly enzyme modification of histones. Histones, the structures to which our DNA binds in the nucleus, play a pivotal role in gene expression. In other words, histone and enzyme interaction control which genes are expressed in which cells during certain times. Epigenetics is the study of how this process works. Tightening or loosening histones can turn a certain gene off or on. The study of this process has been difficult given the size of the genome and number of different histone-enzyme interactions dispersed through the sizable sequence of DNA. The Enzymes place specific chemical markers on the histones that cause the gene regulation to occur, but scientists have been unable to determine which enzymes affect what genes and how. However, the scientists at UNC have recently conducted a study with the fruit fly genome that has given them a large amount of data. The fruit fly genome contains all of its epigenetic markers in the same place. The scientists were able to insert synthesized gene regulating enzymes in place of the originals and determine the function of each individual enzyme by simply observing what was affected by the new enzymes. This research is crucial for the understanding of how the human genome is regulated, possibly leading to the cure for many illnesses.

Article Link: http://www.sciencedaily.com/releases/2015/02/150210142008.htm

A Breath of Fresh Air: Epigenetic Studies Help Asthmatics

Asthma and allergies affect many people worldwide. Up until recently, treatments for both asthma and allergies were administered without an appropriate prediction of responses; However, this is about to change. In a recent study conducted by scientists at Imperial College London, “30 new genes that predispose people to allergies and asthma” were found. The discovery of these genes means that new treatments for allergies are possible and more accurate predictions for current treatment responses will be available.

Photo by Author

Photo by Author

By observing the epigenetic changes, ones that influence gene activity- not genetic code, the scientists were able to identify genes which are linked to triggering allergic responses. Such genes regulate specific antibodies. Genes become inactive through methylation: the attachment of methyl molecules to DNA. The scientists studied white blood cells of families with asthma to see if methylation levels in specific genomic locations were associated with levels of an antibody in the blood. Immunoglobin E (IgE) is the antibody studied in the case. The antibody IgE was known prior to this study, but the genes which activities it regulates were not. After monitoring the IgE levels in the blood, researchers saw a strong correlation between IgE and low methylation at 36 places in 34 genes. These genes are overstimulated in asthmatics, thus the production of IgE is increased, contributing to asthma symptoms. In expanding the investigation, researchers came to believe that IgE-involved genes may activate eosinophils, a type of white blood cell which in asthmatics promotes airway inflammation by gathering and releasing chemicals in airways/lungs. Researchers believed that these genes, and their ability to activate eosinophils, then cause the most damage. In order to test this, researchers isolated eosinophils from the blood of subjects and demonstrated that all 34 genes have high activity levels in asthmatics with high IgE levels. Thanks to the findings of new activation signals, patients can avoid high costs and ineffective “treatment-trials” because we’ll be able to predict responses to treatments with more accuracy. Professors Cookson and Moffatt, the leaders of the investigation, give credit to epigenetics for allowing them to make a breakthrough in discovering new potential drug targets for allergies and asthma and sharpening the accuracy of treatment-response predictions. Professor Cookson explained that, “the genetic code that can influence disease and DNA sequencing can only take you so far. Our study shows that modifications on top of the DNA that control how genes are read may be even more important.”

As someone who suffers from allergic asthma, I find it intriguing how the disease-triggering genes aren’t inactive, thus leading to poor lung function, but rather they are overstimulated. Our genes’ ability to regulate disease-triggering antibody activity is amazing. With new studies like this one, we can see that the solution to proper activity regulation is in epigenetic changes, rather than the broad expectations of “our genes”.  This just goes to show that epigenetics is helping us make strides in the ever-changing world of medicine. It should be interesting to see how epigenetic medical-solutions, the current gold mine of Biological research, evolve in the near future.

 

Does the aging process influence changes on a cellular level or do changes on a cellular level influence the aging process?

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How do humans age? While we are “programmed to die,” there doesn’t seem to be one thing that causes our death by “old age.” For example, one way we carry out our own deaths is found on the cellular level, where we accumulate mutations in the DNA repair process and the cells themselves die, or the enter senescence (non-replicating state) as they age. These processes occur at several different times, overlapping and alternating. Therefore, what appears to be the best time to intervene in order to promote healthy aging? No one knows, but they do know what DNA becomes extremely damaged as time goes on and has an incredible impact on our aging process. The cells have sooner suicide dates where they undergo apoptosis more rapidly than normal, and the loss of too many cells can cause tissue atrophy and dysfunction. In addition to creating a lack of cells, the damaged DNA can even shift epigenetic markers.

Typically, epigenetic marks shift in tumor cells, which can lead to cancerous cells. However, in the early 1990s at Johns Hopkins University, Jean-Pierre Issa was studying changes in DNA methylation in colon cancer cells when he observed shifts in epigenetic markers over time, but not only in tumor cells; he found that (to a lesser degree) these shifts were occurring in healthy cells as well. After mapping DNA methylation in human cells, we know that some areas of the genome become hypermethylated with age while others exhibit reduced methylation. These changes typically occur through DNA replication or DNA damage repair because the histone modifications are not always perfectly reproduced and in order to repair damaged DNA, repair proteins must remove the epigenetic marks to access the damaged genetic material to repair it, and once completed, the epigenetic marks can be omitted or misplaced. These epigenetic alterations have been linked to a reduced regenerative capacity of stem cells with age, and bring up a valuable question:

“Is this an epiphenomenon that happens just because we age, or is it actually causing symptoms or diseases of aging and limiting life span?”

Article source: http://www.the-scientist.com/?articles.view/articleNo/42280/title/How-We-Age/

Biggest Ever Epigenetics Project!!

 

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Identical Twins

 

This article is about a project that has recently been planned out with respect to

epigenetics. It is the largest project to date and will cost around $30,000,000 to complete. Epigenetics is the study of cellular and psychological trait variations that are not caused by DNA sequence, but rather what within the DNA is triggered and shown. It is a relatively new field and has exploded in recent years. The heads of this project are TwinsUK and BGI, both very credited organizations in the realm of epigenetics. Epigenetics is the newest and recently the most popular field of all genetics and the goal of this project is to use the twins and the resources given to understand why and how epigenetics occurs.

The plan is to review the patterns of 20,000,000 sites in the DNA of each identical twin (they must be identical because their DNA must be the same and not vary) and compare the DNA with the other twins. The aim is to not look at similarities, but to look at differences and figure out how twins get different diseases if their DNA is identical. They will focus on obesity, diabetes, allergies, heart diseases, etc. at first. Until recently, science did not understand why twins could receive different diseases since their DNA is identical to their other twin, but by studying epigenetics and how genes can be triggered to do different things based on surroundings and circumstance, this idea is plausible.

Being able to locate what genes turn on to trigger certain diseases along with how to control this is something that will benefit not only our general knowledge but will also advance health care to levels that it has never seen. Experiments such as this have been done before but only with a handful of twins. The goal in this experiment is to increase the amount of twins tremendously in order to increase the accuracy of their data.

The Executive Director of BGI, Professor Jun Wang stated that the goal of this experiment is to “unlock many secrets about human genetics that we don’t currently understand, and to accelerate research and applications in human healthcare.”

 

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