BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Epigenetics (Page 2 of 2)

Fear in Your Genes

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Scientists at the University of Virginia recently conducted a study that suggests a connection between social behaviors and epigenetic markers. The study of these markers could predict the social dispositions of individuals and predict future social issues.

The gene for Oxytocin receptor (OXTR) has the ability to carry various amounts of DNA methylation tags. Those low in methyl tags have a greater ability to utilize oxytocin and therefore have a less amplified fear response. Those with many DNA methyl tags are shown to exhibit a more exaggerated fear response. More finitely, the amount of OXTR methylation affected the amount of brain activity in the amygdala, fusiform, and insula. These regions of the brain are directly correlated with face and emotional processing. To prove this, researchers conducted MRI scans on healthy participants while showing them pictures of angry and fearful faces.

The study not only proved the importance of studying the possible effects of epigenetic markers on susceptibility and resistance to disease, but it also shed a light on the possibility of brain disorders such as autism, anorexia, and depression being linked to DNA methyl tags at the oxytocin receptor.

Broadly, this study changes the way we look at how our environment and upbringing shapes our future susceptibility to illness and disorders. As scientific investigation into this topic continues and expands, we may be able to predict an individual’s reaction to social situations with the prick of a finger.

Article Source: http://www.genengnews.com/gen-news-highlights/fear-response-may-be-epigenetically-amplified-or-muted/81250914/

Identical Twins, Identical Lives, Different Disease

Jack and Jeff Gernsheimer are identical twins. Jack has Parkinson’s disease, and his twin Jeff does not. Up until recently, because they have identical genomes, it would have been a mystery as to why Jack could develop Parkinson’s but not Jeff. However, with the discovery of epigenetics, scientists know that genes alone cannot explain why some people get Parkinson’s and other do not. While there are some genetic mutations linked to Parkinson’s, 90 percent of cases are “sporadic”, meaning that the disease did not run in the family. Even twins often do not develop Parkinson’s in tandem. Naturally, if genes don’t explain the development of Parkinson’s, scientists look to environment. There are several environmental factors that are known to link to the disease. People who were POW’s in WWII, for example, have a higher rate of developing Parkinson’s. But, and here’s the interesting part, Jack and Jeff have lived almost identical lives. For almost all of their lives, they have lived less than half a mile apart. Throughout their lives, they have been exposed to the same air, water, pesticides, etc. When they grew up, they built homes five minutes apart (by walk) on their father’s farm in Pennsylvania. Then, when they entered the professional life, they co-founded a design firm, working with their desks pushed up against each other.

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This anomaly, where a pair of humans exist with the same genetics and the same environment yet only one of them got sick is a research “bonanza” for scientists. All expected variables are being held constant, thus whatever is left must be deeply linked to the origins of Parkinson’s. However, there was a small difference in their lives that could provide insight into this anomaly. in 1968, Jack was drafted into the army and Jeff was not. This led to a series of unfortunate events in Jack’s life: first he served two years stateside in the military, got married, had two children, became involved in a long divorce, and suddenly his teenage son died. After this traumatic event, Jack went on to develop Parkinson’s, glaucoma, and prostate cancer, none of which Jeff has.

Jeff and Jack have been more than willing to undergo several studies in hope of finding something that could alleviate Jack’s Parkinson’s. The first study involved collecting embryonic stem cells from the twins. The benefit of stem cell cultures is that they act similarly to how they would in the body even though they are in a petri dish. The mid-brain dopaminergic neurons grown from Jack’s cells created abnormally low amounts of dopamine. Jeff’s produced normal amounts. Surprisingly, even though Jeff showed no signs of Parkinson’s, both twins had a mutation on a gene called GBA. This gene is known to be associated with Parkinson’s. As a result, both of their brain culture cells produced half the normal amount of beta-glucocerebrosidase, an enzyme linked to that gene. Instead of answering questions, this study only raised more to the fascinating case of Jeff and Jack.

I want to add a bit about how Jack’s son died, because it is unimaginably tragic and can show you just how much Jack had to face. Especially if we are considering Jack’s trauma as a contributor to his development of Parkinson’s, it is important to know the story. When Gabe, Jack’s son, was 14 in 1987, he became fascinated with the Vietnam War. Like any good father, Jack rented his son some movies on the war. One of those being The Deer Hunter, in which there is a scene where two prisoners of the Viet Cong are forced to play Russian Roulette. Gabe told his friend that if it were him, he wouldn’t just sit there. He would rather just get it over with. With that conversation, Gabe got his dad’s pistol, that he knew was hidden in the closet drawer, put one bullet in the chamber, put the gun to his head, and shot.

Jack rarely shows emotion. This “pressure cooker” way of dealing with things could explain his illness. Jeff thinks that the parkinson’s is a physical manifestation of how Jack deals with stress, rather how he doesn’t deal with stress. The connection between stress and disease is a very active research topic. And while their lives were very similar, if compared, Jack’s is by far the life with a more stressful environment. Some research might suggest that this stress differential can have a relation to Parkinson’s disease. In 2002, neuroscientists at UPitt subjected rats to stress, and they found that the stressed rats were more likely to experience damage to their dopamine-producing neurons than the non-stressed rats. This led to the term “neuroendangerment”, which means “rather than stress producing damage directly and immediately, it might increase the vulnerability of dopamine-producing cells to a subsequent insult.”

Another hypothesis as to what caused Jack’s Parkinson’s is that it could be linked to chronic inflammation.  Chronic inflammation is the mechanism by which stress can create neurodegeneration. Evidence that suggests this could be the case in Jack and Jeff is presented in their skin. Jack has psoriasis, a condition linked to chronic inflammation, and Jeff does not.

To this day, the search for what caused Jack’s Parkinson’s continues. Last year, NYSCF scientists conducted a study on the twins’ stem cells. They found a few functional differences between their cells. After finding the GBA mutation, they searched harder for other clues as to what might differentiate their brains. They screened 39,000 SNV’s, single nucleotide variants, which are instances where a single nucleotide in the human genome has been altered (either switched, deleted, or duplicated). They found 11 SNV’s, nine of which are linked to Parkinson’s disease. However, all 9 were found in both twins, meaning that this did not explain why Jack was sick and Jeff wasn’t.

Finally, they were able to uncover a relevant difference. Jack had high levels of MAO-B, which is involved in the breakdown of dopamine, whereas Jeff’s levels were close to normal.This hypothesis supposed that there exists a possible molecular mechanism by which stress could lead to neurodegeneration. What’s nice about this finding is that it could present a possible treatment for Parkinson’s. MAO-B inhibitors exist and are actually drugs currently on the market. They were given to Jack, and while it’s too soon to see the effects and to recommend them as treatment for Parkinson’s disease, it’s definitely a start.

Source: http://nautil.us/issue/21/information/did-grief-give-him-parkinsons

Epigenetics and Brain Development

Pre-natal human brain development helps determine many major qualities a person may have in life. Research at the University of Exeter found that a type of Epigenetics, DNA methylation, helps us understand the differences between male and female brains. They studied that this type of gene regulation in pre-natal brain development may help us grasp more information about “sex differences in behavior, brain function, and disease.”

In the womb, as organs are developing, the brain has extreme plasticity. Professor Jonathan Mill of the University of Exeter explains how it is extremely vulnerable to changes because the brain is creating the structures that “control neurobiological function across life.” The research consisted of measuring genomic patterns of DNA methylation in the womb between 23 and 184 days after conception. DNA methylation is a chemical modification to one of the 4 nitrogen bases that helps create one’s unique genetic code. By studying the DNA methylation, or turning on of selected genes, in the pre-natal period when the brain is being developed, it helps scientists understand the susceptibility of different neurological diseases based on one’s sex. Helen Spiers from King’s College London explains how male and females have unique differences with certain disorders, such as Autism. She says how “autism affects five males to every female.”

The molecular switches that regulate genes were found to be gender specific. They also help differentiate brain cells from other cells in the body. This research gained traction in understanding the unique qualities of the DNA “blueprint” of males and females in their developing stages. The genetic switches that are turned on in pre-natal development for each gender are unique, and a deep topic of study. By doing so, in the future, scientists can research deeper into neurological diseases that are unique to males or females, and how they may be created in the womb.

 

Original Article: http://www.sciencedaily.com/releases/2015/02/150203190223.htm

Link to picture:

http://commons.wikimedia.org/wiki/File:Brain_01.jpg#mediaviewer/File:Brain_01.jpgBrain_01

Regular Exercise Can Change Our DNA

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Most people (hopefully) know that exercise and physical activity are beneficial to almost everyones physical and mental health. Exercising improves one’s mood, boosts energy, controls weight, helps the body fight against diseases, reduces stress, and many more life benefits. A new study  by a group of scientists in Sweden discovered how the influence of physical exercise actually has that beneficial effect on the human body.

The scientists focused their work on 23 young, healthy men and women at the Karolinska Institute in Stockholm. The participants were asked to exercise on stationary bikes for 45 minutes, four times per week, for three months. The scientists understood that it would be difficult to study the full changes on each person because they can’t isolate the other aspects of someone’s life like diet or other behaviors. Because of this issue, each person only exercised one leg so they essentially became their own control group.

After the three months had passed, the scientists clearly saw that the exercised leg was stronger. They also studied the DNA of the muscle cells and compared them between each leg. The genome of muscle cells on the exercised leg had new methylation patterns. DNA Methylation is the process of methyl groups attaching to the outside of a gene and making the gene more or less able to respond to biochemical signals. This entire study is also known as epigenetis. Epigenetics is the study of modifications of DNA influenced by the environment. The scientists found that exercise has a huge effect on human epigenetics based on methylation patterns.

The experiment showed that many of the methylation changes were on the enhancer part of the genome. Enhancers “bind to activator proteins which help connect transcription factors to RNA polymerase and the promotor region to turn on transcription of a gene” (from Mrs. Newitt notes packet). The enhancers amplified the expression of proteins by genes that effect energy, insulin, muscle inflammation and muscle pain.

Exercising is good for you and now we know why. It affects how healthy and fit our muscles become. The results of this study will now help lead other scientists into methylation pattern and gene expression research.

 

Main article:

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

Other articles of interest:

http://www.ncbi.nlm.nih.gov/pubmed/25484259

http://learningenglish.voanews.com/content/study-regular-exercise-can-change-our-dna/2580467.html

http://www.cell.com/cell-metabolism/abstract/S1550-4131(12)00005-8?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1550413112000058%3Fshowall%3Dtrue

http://www.mayoclinic.org/healthy-living/fitness/in-depth/exercise/art-20048389?pg=1

Can Stress Affect Pregnancies in Later Generations?

We all know stress isn’t always a good thing, but it could be important to especially avoid it at certain points in one’s life. Recently researchers from the University of Lethbridge in Canada investigated the effects of stress on pregnancies and how it can influence pre-term births. It is already known that pre-term births them selves lead to health issues later in life, but there were some new discoveries involving epigenetics.

 

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These researchers studied the length pregnancies of rats, due to the generally small amounts of variation between them, and found something intriguing. They carried out the experiment by first splitting the first generation of rats into “stressed” and “not stressed” groups. What they found was that the daughters of stressed rats had a shorter pregnancy than the daughters of not stressed rats.

This trend continued into the granddaughters of the rats. They also displayed high levels of glucose than the control group, and they weighed less. The stress also compounded, or increased, through generations.

This can all translate into human pregnancies. The researchers believe that the epigenetic changes in the rats is due to microRNA (miRNA) – non-coding RNA molecules that play a role in regulating gene expression. They bind to complementary mRNAs and prevent them from being translated. This is different than what is usual belief with epigenetics which is that epigenomes are affected by DNA methylation of the nucleotide base pairs. Metz, a scientist working on this research states that microRNAs “are important biomarkers of human disease, can be generated by experiences and inherited across generations. We have now shown that maternal stress can generate miRNA modifications with effects across several generations.”

It is very similar to the information found with the generational epigenetic effects of famine in the “Ghost in Our Genes” video that we watched in class.

This research can help determine pre-term births and the causalities that can come along with them. While the research is still not the whole picture, it is another step towards understanding our genetics.

 

The New Source of Mental Illness

a three dimensional recreation of DNA methylation

a three dimensional recreation of DNA methylation

For years scientists were convinced that the root cause of diseases such as bipolar disorder and schizophrenia lay somewhere hidden in the human genome. But the particular genetic sequence that would supposedly be linked to these illnesses remained elusive.  So researches turned to the developing theory of Epigenetics.  Studies from King’s College in London and related in this article have shown that Epigenetic (changes in gene activity caused by the environment) changes might be responsible for bipolar disorder and schizophrenia.  Jonathan Mill and colleagues scanned the genome of 22 pairs of identical twins.  For each pair of twins, one of the twins was diagnosed with either bipolar disorder or schizophrenia. With the understanding that chemical methyl groups attached to particular sites on a genome are responsible for the “turning of” and “turning on” of genes, Mill and his team “scanned for differences in the attachment of methyl groups at 27,000 sites in the genome.”  The researches found variations in the amount of methylation of up to 20 percent in the gene ST6GALNAC1 (which has been connected with schizophrenia) and differences in the amount of methylation of up to 25% in the gene GPR24 (which had previously been linked to bipolar disorder).  Interestingly Mill’s team found that “a gene called ZNF659, showed over methylation in people with schizophrenia and under-methylation in those who were bipolar, suggesting that the conditions might result from opposing gene activity.  These findings certainly support the theory of Epigenetic’s being a real factor in behavior and mental illness.  They also serve to confirm that bipolar disorder and schizophrenia are related disorders.  This relates to our unit in the sense that Epigenetics deals with the expression of the DNA and genetic sequence we are learning about.  While we read about how the nucleotides are sequenced, Epigenetics could potentially be responsible for how DNA is expressed.

Related reading:

http://www.nytimes.com/2010/11/09/health/09brain.html?_r=0

http://bipolarnews.org/?tag=epigenetics

http://www.psychiatrictimes.com/bipolar-disorder/psychiatric-epigenetics-key-molecular-basis-and-therapy-psychiatric-disorders

Links Between Human and Mice Obesity

A new study of the genomes and epigenomes of mice and humans is beginning to link the two, especially in regards to obesity.

As Andrew Feinberg, MD states, “It’s well known that most common diseases like diabetes result from a combination of genetic and environmental risk factors. What we haven’t been able to do is figure out how, exactly, the two are connected,”. Therefore, Feinberg began to study epigenetic tags to further understand gene usage.

His project with his team was to study the epigenetics of identical mice that were fed either normal or high-calorie diets. He found that the difference between normal and obese mice was the presence of chemical tags, or methyl groups, that prevent the production of proteins. This is significant because as we have learned, these types of modifications of DNA can be copied and inherited, which is then passed on into the next generation. This revealed that the normal and obese mice did not have the same location sites of their tags, giving them that alteration in their DNA. This is often seen in the alterations of the Agouti gene in mice.

Pictured here is effect of epigenetics on the physical appearances of mice (Agouti gene)

This proves that epigenetic changes are related to the environment and food sources that are around us, creating patterns based on one’s diet (which can create risk if a high-calorie intake is continuous).They also found that epigenetic changes affect genes that are already both linked to diabetes as well as those who aren’t, allowing them to further conclude that genes plays more of a role in diabetes than we previously thought.

This allows hope for future to provide epigenetic tests, which can prevent diabetes in those who are on track to have it later in life.

Article  Source: http://www.sciencedaily.com/releases/2015/01/150106130510.htm

 

Does long-term endurance training impact muscle epigenetics?

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Epigenetics translates to “above” or “on top of” genetics. To be more specific, Epigenetics is the study of how modification of gene expression can cause changes in many organisms.

A new study from Karolinska Institutet in Sweden explores the theory that long-term endurance training alters the epigenetic pattern in the human skeletal muscle. The team that conducted the research also explored strong links between these altered epigenetic patterns and the activity in genes controlling improved metabolism and inflammation.

The study was conducted using 23 young and healthy men and women. The men and woman would perform one-legged cycling – where the untrained leg would be the control of the experiment. Four times a week and over the course of three months, the volunteers would participate in a 45 minute training session. Though skeletal muscle biopsies, supervisors would measure their markers for skeletal muscle metabolism, methylation status of 480,000 sites in the genome, and activity of over 20,000 genes.

At the end of the study, the researchers concluded that there was a strong relationship between epigenetic methylation and the change in activity of 4000 genes in total. Epigenetic methylation is defined as the “addition of a methyl group to a substrate or the substitution of an atom or group by a methyl group. ” Moreover, it was determined that methylation levels increased when involved in skeletal muscle adaptation and the metabolism of carbohydrates. However, methylation levels decreased in regions associated to inflammation.

Furthermore, Carl Johan Sundberg found that “endurance training in a coordinated fashion affects thousands of DNA methylation sites and genes associated to improvement in muscle function and health.” He believes that this determination could be vital to understanding the treatment of diabetes and cardiovascular disease as well as how to properly maintain good muscle function throughout life.

This article relates very much to our work in class as we learn the Molecular Genetics Unit. It connects because we are learning what happens when mutations occur in one’s genome and the impacts those mutations have on someone. For example, cancer is one of the most researched and explored topics in regard to how modification of gene expression alters organisms. Oncogenes and Tumor suppressor genes have vital impacts on cellular division, changes to cellular function, and the growth of tumors.

Diesel Exhaust Causes Changes Within

Diesel Exhaust

Two hours of exposure to diesel exhaust fumes has proven to show fundamental health-related changes in biology by switching some genes on and others off.

A study put volunteers in a polycarbonate-enclosed booth and had them breath diluted and aged exhaust fumes. These fumes were about equal to the air quality along a Beijing highway. The researchers examined how the exposure affected the chemical coating that attaches to many parts of a person’s DNA. The coating they were referring to is carbon-hydrogen coating, also known as methylation. The coating can silence or dampen a gene and prevent it from producing a protein. Methylation is a mechanism for controlling gene expression.

The study found that diesel exhaust caused changes in methylation located at about 2,800 different places along a person’s DNA, which affects about 400 genes. Some places led to more methylation. How these changes affect health is the next topic of research. However, the AstraZeneca Chair in Occupational and Environmental Lung Disease claims that the fact that DNA methylation was affected from only two hours of exposure is a positive implication; when something happens that quickly, it usually means you can reverse it through either therapy, change in environment, or change in diet.

This article is very similar to what we are learning about methylation and epigenetics. It discusses how the environment can affect someone’s genes and their gene expression as opposed to solely being their DNA sequence. I found this interesting because diesel exhaust is something people are exposed to everyday and it is important to know the affects it can have other than just respiratory issues.

Source:

http://www.eurekalert.org/pub_releases/2015-01/uobc-bid010715.php

http://aqicn.org/city/beijing/

http://www.whatisepigenetics.com/dna-methylation/

http://commons.wikimedia.org/wiki/File:Diesel-smoke.jpg

The mutation and spread of Cancer caused by changes in Epigenetics

Epigenetics could be the key to understanding how cancer originates, when it mutates, and how it spreads. Researchers at the Boston University School of Medicine (BUSM) believe that different types of cancer are caused by an “on and off” switch in the epigenome. While many scientists believe  that many cancers originate in cells called progenitor cells, they cannot concoct a model that explains  how cancer spreads from the progenitor cell and mutates into many forms as it continues to grow in a person’s body.

One of the lead researchers, Sibaji Sarkar, posited “there should be a general mechanism that initiates cancer progression from predisposed progenitor cells, which likely involves epigenetic changes.” The researchers believe that the theory of an epigenetic switch is supported by the growth of tumors, which go through many different stages. The team believes that if cells can be altered to become cancerous and remain stuck in their stage of growth while they replicate out of control, then there must also be an off switch to this uncontrolled replication. They also suspect that epigenetic changes can determine the rapidity of growth and the mutability of the characteristics of the cancer and tumors.

Although Sarkar’s team has not yet found specific epigenetic code that causes these mutations and growth, he believes that their hypothesis will cause other scientists to focus their attention on the epigenome and find ways to prevent progenitor cells from spreading and mutating into malignant tumors.

This epigenetic research relates to our study of the relationship between the epigenome and cancer. Specifically the absence of an active p53 protein would prevent a certain part of the DNA from being  read and the cell would therefore lack a protein that inhibits the cell cycle. This would cause uninhibited cell division and the spread of cancer.

 

Methylation of DNA

640px-DNA_methylation

Save the Devils

When most people hear the name Tasmanian Devil, they think of the small and ferocious little animal from the Looney Tunes named Taz. Just like in the show, Tasmanian Devils (carniverous marsupials)  are tough, rugged and very aggressive animals. Unfortunately, over the past two decades, a rare case of contagious facial cancer, with a 100% mortality rate, has decimated the population. Scientists have estimated that this specific cancer has wiped out about 85% of the entire population, almost to the point of extinction. The cancer is typically spread when the Devils bite each other in the face during battle, killing it in a matter of months. Scientists are working tirelessly to find out how this cancer is slipping by the immune system and hope to find a cure.

Until recently, scientists believed that the cancer was able to develop, without

being detected by the immune system, because Tasmanian Devils lack genetic diversity. However, a study led by the University of Cambridge claims it is much more complex. On the surface of most cells are histocompatability complex (MCH) molecules, which determine whether other cells are good or bad. If the cell happens to be a threat, then the cell triggers an immune response. According to the research, these DFTD cancer cells lack theses complexes and can therefor avoid detection.

Researchers also found that the DFTD cells have just lost the expression of MCH molecules and that its genetic code is still in tact (it can be turned on). By introducing specific signaling molecules, scientists believe they can force the DFTD cells to express these molecules, leading to the detection of the cancer. Not only will this research help save the Devils, but it will also give scientists a head start on contagious cancers in other species when the time comes.

Epigenetics, Dads, and Obesity

 

By Ynse. Photo from Flickr http://www.flickr.com/photos/ynse/1531699476/

 

It turns out that kids with obese fathers have unique epigenetic changes that can affect their health… for the worse.

According to a recent study, “children with obese fathers have different epigenetic markings on the gene for insulin-type growth factor 2 (IGF2) than children with fathers of normal weight.”

Children with obese fathers have less methylation on a specific region of the IGF2 gene. Sadly, this occurrence is linked with many types of cancers such as ovarian cancer.

However, it is too soon to tell if these epigenetic changes are directly linked to the children’s’ health.

According to the biologist Gudrun Moore, “it is tempting to over-emphasize the role of a small number of parent-of-origin expressing genes and to speculate about the effects of modest variation in methylation, but we must not be too hasty to blame either parent for their offspring’s health outcomes.”

However, other researchers are sure that that your parent’s environment and habits affect children’s health.

According to Michael Skinner, this research “suggests that environmental epigenetics might be the mechanism for these effects.”

Maybe now both the mother and father have to be careful about what they eat during the pregnancy. Sorry Dads-to-be, you are going to have to eat healthy now!

For more information on epigenetics and health, you can visit these links.

http://www.economist.com/news/science-and-technology/21565573-some-effects-smoking-may-be-passed-grandmother

http://healthletter.mayoclinic.com/editorial/editorial.cfm/i/249/t/Understanding%20epigenetics/

Photo credit: http://www.flickr.com/photos/ynse/1531699476/

Breakthrough in Epigenetics!

 

This file (Arabidopsis thaliana flower) is in public domain, not copyrighted, no rights reserved, free for any use

 

For several dozen years scientists have searched for a way to understand the role of a single RNA strand in gene expression.  Scientists have been without a method to pinpoint 1 type of RNA strand and isolate its effect thus discovering its influence and its corresponding proteins role in influencing the way our bodies work.

However a breakthrough was made this march regarding such obstacles.  A team of scientists from Michigan Technological University discovered a way to turn off small RNA strands in order to figure out what they are up to.  They did this by inserting their own custom DNA strand that codes for something called a small tandem target mimic or “STTM” into a plant known as “Arabidopsis“.  Inside the plant, these DNA strands gave rise to STTM’s that blocked the ability of a target RNA to express itself.  The particular target for the STTM was a type of RNA strand suspected to be involved with facilitating vertical growth of the plant.  The STTM’s stopped the RNA from being able to cut itself into smaller bits, and prompted the target RNA’s to destroy all of its own smaller RNA’s that would normally slice the target RNA.  This effectively lead to the disappearance of the target RNA’s protein products thus resulting in no expression of the gene the target RNA from transcribed from.

The result was outstanding.  “The control Arabidopsis plants grew upward on a central stem with regularly shaped leaves and stems. The mutant plants were smaller, tangled, and amorphous.”

The above process is said to be “a highly effective and versatile tool” for studying the functions of small RNA.  One researcher on the team who discovered this method stated that she intends to use this discovery to study type 2 diabetes.

 

Reference

http://www.sciencedaily.com/releases/2012/03/120301143756.htm

Identical but Not the Same

 

Some Rights Reserved. More Information: http://www.flickr.com/photos/timoni/3390886772/sizes/s/in/photostream/

After studying genetically inherited traits and diseases it could be easy to assume that genes determine everything about us. While it is true that colorblindness is a sex-linked trait – there is certainly more to the story.

Monozygotic “identical” twins are genetically identical, so they should be the same in all ways shouldn’t they?

Why, then, does one twin get early onset Alzheimer’s disease and the other “identical” twin doesn’t? The same is true for height, autism, and cancer. Although, when one twin has a disorder the other is more likely to get the disease also, that is not always the case.

In the January edition of National Geographic, author Peter Miller discusses the newest theories about how genes, environoment and epigenetics affect our life (and the end of it).

Twins offer scientists a unique opportunity to study how genetically identical people differ. Basically, that means scientists can study how things other than genes affect human development and lifespan. Already, scientists have found that a persons height is only 80% determined by genetics because the heights of “identical” twins differ by about .o8 on average. Using IQ tests, scientists have nearly disproved John Locke’s Tabula Rasa or blank slate theory (the idea that children are born with a blank mind that is either stimulated – (and made intelligent) – or not –  (kept unintelligent)). Specifically, scientists studied twins who had been separated at birth and adopted into different families. In this way, scientists have found that intelligence  is about 75% controlled by genetics.

So that leads to the question, what is it besides genes that affects us humans so drastically?

Environment has something to do with our differences. However, that cannot be the whole story. “The Jim Twins” as they are called in the twin science community, were studied in the 1870’s. They were adopted into different families where both boys were named Jim. Then went on to have the same jobs, marry wives of the same name (two Lynda’s first then two Betty’s), enjoy the same hobbies, enjoy the same brand of cigarette and beer, name their sons James Allan and James Alan… the list goes on. These two lived very similar lives, yet they grew up in very different environments. If environment isn’t the only factor in creating difference then what is?

Scientists have recently come to believe that epigenetics plays a significant role in our lives. Epigenetics (site 2) can be seen as the meshing of environment and DNA. In the words of author Peter Miller “If you think of our DNA as an immense piano keyboard and our genes as keys – each key seach key symbolizing a segment of DNA respinsible  for a particulare note or trait, and all the keys combining to make us who we are – then epigenetic prcesses determine when an how each key can be struck changing the tune.”  Environmental changes do have some impact.  When a pregnant mouse is put under stress during the pregnancy it can create changes in the fetus that lead to abnormal behavior as the rodent grows into adulthood.

However, scarily enough, many epigenetic changes appear to occur randomly (thus creating a probelm for the organized nature/nurture theory). Currently work is being done studying DNA methylation, which is known to make the expression of genes weaker or stronger. Specifically, Andrew Feinburg, director of the Center for Epigenetics at Johns Hopkins School of Medicine, is working to find how DNA methylation relates to autism. Currently, he is using scanners and computers to search samples of DNA from autistic twins who have the disease in varying degrees. He is looking to compare how and why

the genes are expressed differently.

In the end, all we know is that there is more to our future than our genes can tell us. Yes, our genes play a huge role in who we are as people – in terms of appearance, character, intelligence and more – but there are some variables that our environment and epigenetics control.

Main Article: Miller, Peter. “A Thing or Two About Twins.” National Geographic. Jan 2012: 38-65. Print.

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