BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Genes (Page 1 of 2)

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.”

Build A Baby?!

Have you ever wanted a baby to be a super fast swimmer like Michael Phelps? How about a child who has more talent than Mozart? Well, that can’t happen.

According to the  New York Times Article, Scientists in Oregon have successfully modified the DNA of human embryos. This led to the new hope that designer babies are in our near future. But, designer babies are more likely to be seen in movies than in reality.

The main reason why designer babies are unlikely is because great vocals and amazing coordination does not come from a single gene mutation, or even from an easily identifiable number of genes.

Hank Greely, director of the Center for Law and the Biosciences at Stanford, said,“Right now, we know nothing about genetic enhancement,”. “We’re never going to be able to say, honestly, ‘This embryo looks like a 1550 on the two-part SAT.’”File:Baby Face.JPG

Physical traits, like height or arm length, will also be difficult to genetically manipulate. Some scientists estimate height is influenced by as many as 93,000 genetic variations. A recent study identified 697 of them.

Talents and traits aren’t the only thing that are genetically complex. So are most physical diseases and psychiatric disorders. The genetic message is not a picture book ,but it actually resembles a shelf full of books with chapters, subsections and footnotes.So talents, traits and most medical conditions are out of the equation.

But about 10,000 medical conditions are linked to specific mutations, including Huntington’s disease, cancers caused by BRCA genes, Tay-Sachs disease, cystic fibrosis, sickle cell anemia, and some cases of early-onset Alzheimer’s. Repairing the responsible mutations in theory could eradicate these diseases from the so-called germline, the genetic material passed from one generation to the next. No future family members would inherit them.

Although this is challenging, it is proven to be more possible for scientists to alter the genes that lead to genetic diseases.

Last but not least, it is illegal.
There are debates regarding ethics and “playing God”. “I’m totally against,” said Dr. Belmonte. “The possibility of moving forward not to create or prevent disease but rather to perform gene enhancement in humans.”

Other people are scared of a super children takeover.

“Allowing any form of human germline modification leaves the way open for all kinds — especially when fertility clinics start offering ‘genetic upgrades’ to those able to afford them,” Marcy Darnovsky, executive director of the Center for Genetics and Society, said in a statement. “ We could all too easily find ourselves in a world where some people’s children are considered biologically superior to the rest of us.”

In summary, genetic modification for babies will only be used in dire cases. Therefore, the only way I can have a red head child who can play the piano and the flute simultaneously with their feet is through Sims 4.

Not to worry… you’re someones (blood) type!

 

BLOOD

Blood types were first discovered in 1901 by Austrian immunologist, Karl Landsteiner. The classification of human blood is based on the inherited properties of red blood cells as determined by the presence or absence of the antigens A and B, which are carried on the surface of the red cells. So what is the difference between types A,B,AB and O blood?

This picture demonstrates the possibilities of different blood types and their characteristics.

 

Blood Type is Hereditary 

Hereditary is defined as genetic factors that are able to be passed on from parents to their offspring or descendants. If someone has blood type A, they must have at least one copy of the A allele, but they could have two copies. Someone who is type B must have at least one copy of the B allele.  Alleles are one or two or more alternative forms of a gene that arise by mutation and are found at the same place on a chromosome.

Blood types are either positive or negative.  It is important to note that blood cells do not have a charge, the + or – is used to determind specific traits of the cell. For example, the + or – is determined on wether or not the blood cell has the antigen “Rh factor”. If there is a + attached to your blood type, the antigen is present; if there is a – next to your blood type, the antigen is not present.

So What?

Dealing with blood types is very interesting because, according to “Scientific American”, blood type may affect brain function as we age, concluded from a new large, long-term study. However those with AB show a 10% increase of having cognitive problems. From that same study, it was determined that…

In addition to blood types affecting health, blood types also contribute to a persons personality.  According to James and Peter D’Adamo’s work, type A tends to be cooperative, sensitive, clever, passionate and smart where type B people tend to be balanced, thoughtful and ambitious.

Blood type’s current impact on society is very crucial because it gives insight to future diseases, the ability to donate blood to those who need it, and for new born babies be a backbone for their personality.

Comment your blood type below!

 

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

The Miracle of CRISPR/Cas9 in Gene Editing

Some scientists say, “you can do anything with CRISPR” and others are absolutely astonished and amazed.

CRISPR can rapidly change any gene in any animal or plant with ease. It can fix genetic diseases, fight viruses, sterilize mosquitos and prepare organs for transplant. The possibilities are endless – and the prospect of designer babies isn’t far off.

https://en.wikipedia.org/wiki/CRISPR#/media/File:Crispr.png

Dead Cas9 can fix a single base pair typo in DNA’s genetic instructions. It can convert a C-G into a T-A pair. Also, we can attach fluorescent tags to dead Cas9 so researchers can locate and observe DNA or RNA in a living cell. Dead Cas9 can also block RNA Polymerase from turning on a gene, in CRISPRi. In CRISPRa, a protein that turns on genes is fused to dead Cas9.

CRISPR can be used for anything involving cutting DNA. It guides molecular scissors (Cas9 enzyme) to a target section of DNA & works to disable or repair a gene, or insert something new.

Many scientists have been thinking of improvements for this miracle gene editor. RNA Biologist Gene Yeo compares the original Cas9 to a Swiss army knife with only one application – a knife. He says that by bolting other proteins and chemicals to the blade, they transformed the knife into a multifunctional tools.

CRISPR/Cas9 is special because of its precision. It is much easier to manipulate and use compared to other enzymes that cut DNA. By using “guide RNA” it can home in on any place selected by the researcher by chemically pairing with DNA bases.

While Cas9 does have some problems, scientists definitely see the potential for greatness with a few tweaks. They wanted to ensure permanent single base pair changes, and they increased that from 15 to 75 percent. Liu used a hitchhiking enzyme called cytidine deaminase.

Scientists researched chemical tags on DNA called epigenetic marks. When scientists placed the epigenetic marks on some genes, activity shot up. This provided evidence that the mark boosts gene activity.

Case can also revolutionize RNA biology. The homing ability of CRISPR/Cas9 is what makes this seem possible. It was found that Cas9 could latch on to mRNA.

CRISPR/Cas9 was first found in bacteria as a basic immune system for fighting viruses. It zeroes in on and shreds the viral DNA. Half of bacteria have CRISPR immune systems, using enzymes beyond Cas9.

Overall scientists predict that in the next few years, results will be amazing. The many ways of using CRISPR will continue to multiply and we will see where science takes us.

Source: https://www.sciencenews.org/article/crispr-inspires-new-tricks-edit-genes

Other Sources: https://www.neb.com/tools-and-resources/feature-articles/crispr-cas9-and-targeted-genome-editing-a-new-era-in-molecular-biology

8 Genes That May Be Affecting Your Sleep Patterns

Have you ever wondered why you struggle to fall asleep at night, while your sibling has no issues sleeping soundly for eight hours? What causes your sleep patterns? While your sleep may occasionally be affected by a particularly stressful event, leading to irregular sleep patterns, for

While your sleep may occasionally be affected by a particularly stressful event, leading to irregular sleep patterns, for many, it is simply caused by the way their brains and bodies work. New research has identified for the first time eight specific genes that are linked to insomnia or excessive daytime sleepiness. The data also revealed that some of the genes associated with disturbed sleep identified in this study seemed to be linked to certain metabolic and neuropsychiatric diseases too, like restless leg syndrome, schizophrenia, and obesity.

Richa Saxena, one of the co-authors and assistant professor of  anaesthesia at the Massachusetts General Hospital and Harvard medical school, explained why this research was so important: while “it was previously known that sleep disturbances may co-occur with many diseases in humans, but it was not known that there are shared genetic components that contribute both to sleep problems and these conditions.” Furthermore, while studies have previously identified genes linked to some sleep disorders, this is the first study that has specifically linked genes to insomnia.

Link to Original Image

The study looked at the prevalence of insomnia, sleep problems and excessive daytime sleepiness in 112,586 European adults who had participated in a UK Biobank study. All participants had their genes mapped, as well as additional information like weight and diseases/chronic conditions. The results revealed fascinating linkages between certain genes. For example, the genes linked to insomnia were most strongly related to those associated with restless legs syndrome, insulin resistance, and depression, while the genes associated with excessive daytime sleepiness were also linked to obesity. Saxena remarked again that “it was not known until this study that there are shared genetic components- shared underlying biological pathways- that contribute to both sleep problems and these shared conditions.”

Of course, this study is not 100% conclusive- people who have trouble sleeping are not necessarily at higher risk for restless legs syndrome, schizophrenia, and obesity. In reality, it is likely that many different genes contribute to both sleep problems and these medical problems, Saxena said. But this new study does suggest that these problems share genes and underlying pathways.

So what does this research do for the average person? Well, not much. Right now, it’s just fascinating news that there may be a genetic reason people with these disorders are more likely to have troubled sleep. However, there is hope that in the future researchers will be able to design and test various drugs to target these genes. This would bring immense benefits to people who struggle to keep normal sleep patterns, as well as helping individuals proactively avoid diseases they may be more at risk for (for example, obesity).

 

Transgender- Science Behind Sexual Identity

Stop Homophobia - NUS Sports Gay Protests, London

Darren Johnson Image Link

Transgender concepts have been a prevalent issue. It has been seen on a celebrity level with Caitlyn Jenner but on smaller levels as well. Schools are struggling to make decisions of whether to make bathrooms same-sex or unisex. While administrative figures are struggling to make accommodations for the increasing number and popularity of LBGT rights, society is also struggling to determine whether trans-gender identity is a social or biological doing.

One recent finding has shown that anatomical sex- gender identity and orientation- is determined in the womb. However, once the anatomy is settled, there is about a six month lag before the brain masculinizes or feminizes. Research has concluded that through some combination of genetics, hormones and the uterine environment, sometime between six months and delivery the sexual orientation is set in the brain. The only question that rises is what happens when the brain does not match the genitals.

Genetics has been proved to play a role in transgender identity. Researches studied a group of twins where either one or both were transgender.  In identical twins, 39% were both transgender. Of the fraternal twins, there were zero pairs where both were transgender. In fact a study in the Journal Biological Psychiatry, researchers found a gene variant that was associated with being a trans woman.

For the 61% of identical twins where only one is transgender, the prenatal environment, or womb, had a key role. While identical twins share genetic codes, the genes that get expressed or remain unexpressed differ. Identical twins have separate umbilical cords , separate amniotic sacs, and develop in separate locations of the womb. All these things can have an affect in the mixing of chemicals and the sexual identity process.

Lastly, the structure of the brain also plays a role. A 2014 study from the Journal of Neuroscience found that “differences in the brain’s white matter tracts [fall] along a perfect spectrum of gender identity with cisgender men and women at the ends and trans men and women in the middle.”

 

CRISPR/Cas9 Provides Promising Treatment for Duchenne Muscular Dystrophy

There are nine kinds of muscular dystrophy and of these, Duchenne MD is the most common severe form of childhood MD. It affects about 1 in 5000 newborn males, only in very rare cases has it affected females. DMD is a genetic disorder that causes progressive muscle degeneration and weakness. Patients usually die by age 30 to 40.

DMD is caused by the absence of a protein, dystrophin, that helps keep muscle cells intact. In 1986 it was discovered that there was a gene on the X chromosome that, when mutated, lead to DMD. Later, researchers discovered that the protein associated with this gene was dystrophin. From this information, we can tell that this disorder is sex-linked, which explains why women are mainly carriers.

No one has found an absolute cure for this genetic disorder until now. Even in recent years, people have discovered treatments that will make patients’ lives more bearable, but never reverse the disorder. As a result of these advances, mostly in cardiac and respiratory care, patients are able to live past teen year and as long as in to their fifties, though this is rare. Although there are still drugs being tested like Vamorolone (a “dissociative steroid,” is an anti-inflammatory compound), more treatments on the molecular level are now being considered. However, thanks to recent discoveries and research with the new genetic technology, CRISPR/ Cas9, scientists may have found a treatment for DMD.

This new approach to gene correction by genome editing has shown promise in studies recently. This particular correction can be achieved in a couple ways: one is by skipping exon 51 of the DMD gene using eterplirsen (a morpholino-based oligonucleotide). Studies over four years show prolonged movement abilities, and a change in the rate of decline compared to controls. The newest approach to gene correction using CRISPR/Cas9, which the article I’m writing about focuses on, was performed in this study as next described: the CRISPR/Cas9 system targets the point mutation in exon 23 of the mdx mouse that creates a premature stop codon and serves as a representative model of DMD. Multiple studies in three separate laboratories have provided a path and laid the groundwork for clinical translation addressing many of the critical questions that have been raised regarding this system. The labs also discovered by further demonstrations, that this is a feasible treatment for humans. Functional recovery was demonstrated in the mice, including grip strength, and improved force generation- all of which are very important and hopeful discoveries. It is estimated from these studies that this new method will pass clinical trials and go on to benefit as many as 80% of DMD sufferers. Even greater success rates are expected if this is performed in young and newborn DMD patients.

The Relationship Between Girls and Their “Skinny Jeans”

New findings suggest that the dynamic between a girl’s gene and her early socio-economic environment can dictate if they have a larger fat intake or healthier consumption in relation to others within the same class background. The gene variant is called the DRD4 repeat 7 (7 repeats). According to the McGill Centre for the Convergence of Health and Economics, girls from poorer families with DRD4 repeat 7 have an increased fat intake than other girls from the same socio-economic environment. However, girls with the gene variant from wealthier families and backgrounds have a lower fat intake. These studies portray how it isn’t solely the gene that determines an individual but how the gene influences an individuals sensitivity to environmental factors that contribute to a child’s preference to fat.

This research was done by collecting diaries by parents of 200 Canadian children (about 4 years old). Their fat, protein, and carbohydrate percentages were all measured along with their BMI and also saliva tests to see who are carries of the DRD4 repeat 7 gene. To categorize the children in their socio-economic environment, the family income was used while acknowledging the food environment (what type of foods are available in that neighborhood).

Plasticity genes,” where carriers of gene variants might be more “open” to their environment rather than those who are not carries of gene variants, is a term used to describe the DRD4 repeat 7 gene. Researchers realized that the fat intake has a direct correlation with any modification of the girls social environment and how they are raised. Therefore, the gene itself is not to blame for a high fat intake.

The data had only shown to be consistent with girls, not boys. From an evolutionary perspective, in order to sustain hard conditions and be able to reproduce, girls had to have more weight on them. Another reason may be because the age four is not old enough to measure the gene’s activity in boys because boys can gain weight at different stages than girls.

Furthermore, this research contributes to the idea that preventing childhood obesity cannot have a general and “one size fits all” type of approach. Instead, specific approaches for certain populations is what’s needed. Especially populations that are vulnerable in adverse conditions because they are more likely to respond better if their conditions improve.

 

Original article can be found here.

Serious Monkey Business Going on with these Tanzanian Monkeys

https://commons.wikimedia.org/wiki/File:Udzungwa_Red_Colobus_Stevage.JPG

https://commons.wikimedia.org/wiki/File:Udzungwa_Red_Colobus_Stevage.JPG

A team from the University of Oregon comprised of Maria Jose Ruiz-Lopez, a postdoctoral researcher, and Nelson Ting, a corresponding author and professor of anthropology, have discovered why a specific species of endangered monkeys in Tanzania are living in various different geographical areas that are increasingly becoming isolated from one another. It has been concluded that this situation is due to the monkey’s closeness to villages and the intentional forest fires by humans in an effort to create space for crops. Lopez collected 170 fecal samples of the Udzungwa red colobus monkey, a specific monkey used as indicator species in ecological change, for DNA analysis over five distinct forests in the Eastern Afromontane Hotspot. To approach this experiment, the team used landscape-genetics, a method that merges landscape ecology and population genetics. Though odd to use in tropical settings, this technique allowed them to investigate the dissimilarities between 121 monkeys and how human activity influences ecological changes. The largest difference between monkeys were of those who were separated by villages and/or zones that had a history of the highest density fires. The researches studied multiple variables at once and the monkey’s proximity to villages and man-made fires was still the most significant. Because these fires are stopping the monkeys from migrating, smaller groups of them are becoming more isolated, resulting in a decrease of genetic diversity and yielding to extinction variables.

This experiment regarding behavioral ecology, a way in which organisms react to abiotic factors in their environment, made me contemplate the human’s role in the environment and how we are strongly affecting the possible extinction or conservation of animals. This particular ecosystem is rich in diversity and it would be a tragedy for it to fall to extinction! There is no direct solution to this problem; after all, to have the power to alter a human’s ecological footprint and their decision whether to burn a forest or not is quite hard to seize control of. Do you believe with enough awareness and education, local communities would be able to create a local solution to save the diverse genes of these monkeys?

Original article can be found here.

Bullying and its Epigenetic Effect

Unfortunately, bullying is commonplace in most schools in America.  Most people are aware of the mental and psychological harm that bullying can cause, but not until very recently have they been aware of the lasting physical changes it can cause.  With the discovery of epigenetics, or the study of genetic traits or expressions that are not caused by DNA, but rather by the methylation or concealing of genes, a new door into the effects of bullying was opened. A group of researches from the UK and Canada performed a study on identical twins.  At age 5, the twins had not been exposed to bullies and expressed almost all of the same traits, physically and emotionally.  The researchers then waited until the twins were 12, imageand revisited only the twins that had different experiences with bullying (one twin was bullied when the other was not).  The researches found big disparities in the twins epigenome, or the way they express their genes.

 

The bullied twin’s protein that codes for a protein that helps move the neurotransmitter serotonin into neurons called SERT had significantly more DNA methylation in its promoter region.  This change is thought to dial down the amount of proteins that can be made from the SERT gene — meaning the more it’s methylated, the more it’s “turned off.”  Therefore, the bullied twin is unable to produce as much serotonin.  This effect is thought to persist through a person’s life.  The effects of bullying will persist an entire lifetime.

 

The researchers also tested how the twins responded to stressful situations differently.  The bullied twin had a much lower cortisol response than the twin that had not experienced bullying.  Cortisol is a hormone that helps people through stressful situations, like being bullied.  However, having too much cortisol is harmful to the body.  The bullied twin’s body turned off the gene that aids in cortisol production because they were being put in stressful situations so often by bullies that their body couldn’t tolerate the amount of cortisol they were producing.

 

This study is not only interesting from a scientific standpoint, but it is also very important in the movement against bullying.  These scientists proved that bullying not only does immense psychological harm, but it also effects people’s well being in a very real and lasting way.

 

 

 

Link to article: http://www.huffingtonpost.com/sharon-moalem/bullyings-terrible-legacy_b_5142857.html

 

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

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?

800px-Nucleosome_1KX5_2

 

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.

Fat lies: Did you inherit your body?

While obesity is typically attributed to over eating and a lack of exercise, researchers at Kings College London have identified a type of gut bacteria, called Christensenellacae, which influences a person’s genetic makeup and body weight. The study focused on fecal samples from 416 pairs of twins. Of these participants, identical twins had a larger abundance of the gene microbe than fraternal twins suggesting that the bacteria is highly heritable. Furthermore, researchers found that Christensenallacae is most common in the intestines of lean people and in experiments with mice they determined that this microbe alone promoted thinner mice. Thus far, research results suggest that a person’s genes influence his body weight by determining the types of bacteria that live in his intestines and that altering the Christensenallacae population could have a direct impact on his susceptibility to obesity. This research gives a very important window into the study of obesity prevention and gut microbes. Although the information is groundbreaking, further studies need to be conducted to determine if altering levels of this gut microbe is actually effective.

As researchers continue to expand their study, how do you think this discovery will be used in the future to combat obesity?

weight loss by pixabay

weight loss by pixabay

The Ability to Control Genes with Your Thoughts

A research group led by Martin Fussenegger, a professor of Biotechnology and Bioengineering at the Swiss Federal Institute of Technology, has developed a method by which brainwaves control the creation of proteins from genes. The technology wirelessly transfers brainwaves to a network of genes that allows the human’s thoughts to control the protein synthesis of the genes. The system uses a uses an electroencephalogram (EEG) headset, which records and transmits a human’s brainwaves and sets it to the implant in the gene culture.

A successful experiment of the system included humans controlling gene implants in mice. When activated by brainwaves, the gene implant culture would light up by an installed LED light. The researches used the human protein SEAP as the protein that would be generated in the culture and diffused into the blood stream of the mice. The humans were categorized by their states of mind: “bio-feedback, meditation and concentration”. The concentrating group caused an average release of SEAP. The meditation group released high concentrations of the protein. Finally, the bio-feedback group produced varying degrees of SEAP, as they were able to visually control the production of the protein as they could view the LED light turning on and off during the production process. The LED light emits infrared light, which is neither harmful to human nor mice cells. The system proved successful in its ability to translate brainwaves into gene control and protein production and its potential for harmless integration into the living tissue of humans.

The research group hopes that in the future a thought-controlled implant could help prevent neurological diseases by recognizing certain brainwaves at an early stage of the disease and translating the brainwaves into the production of proteins and other molecules that would work to counteract the disease.

Lights of ideas

To Know or Not to Know: Cancer Risk Gene Testing

Breast Cancer Cells

Genetic mutation testing has been a hotly debated and controversial topic since its initial prevalence in 1990.  Originally genetic testing was used to test females who have cancer in their family history for the BRCA 1 and 2 gene mutations.  Early detection of these mutations allowed for precautionary measure sure to be exercised prior to cancer even being diagnosed. The hereditary breast cancer risk testing was done mainly by Myraid Genetics but just last year the Supreme Court invalidated Myraid’s patents on the testing of the BRCA genes.  This ruling opened up many windows for the competition of Myraid in the field of genetic testing.  Many other companies and Myraid itself began not only offering BRCA testing but also more elaborate multi gene testing for the same price (apron $4000) as it would have been to test just the two BRCA genes.  This “bargain” influenced many patients to have more genes (up to 25) tested for mutations despite the fact that they may not have a family history to tendency towards certain cancers.  This multiplex testing has raised many eyebrows in the medical field because patients and doctors are getting information that sometimes they are unsure as to what they should do.  Doctor Kenneth Offit of Memorial Sloan Kettering Cancer Center stated when referring to multiple gene mutation testing, “because they could be tested,not necessarily because they should be…individuals are getting results we’re not fully educated to council them on. ” However Memorial Sloan Kettering Cancer Center is working on setting up a database for more knowledge on genetic testing.  This online forum, the Prospective Registry of Multiplex Testing (PROMPT) will allow for more research to be done and for patients to learn more.   Often genetic mutations are found and doctors are unsure how to react to the information due to lack of knowledge in that specific field of mutation leading to a specific type of cancer with out any family history.   Professor Mary-Claire King of the University of Washington voiced her opinion that, “We need to report back only what is devastating and clearly devastating.”  Meaning she felt that patients and physicians should only receive specific information as opposed to a full list of all the genetic mutations that tested position or inconclusive.  When do we know when to much information become frivolous? When it come to human health, the more we know the better the outcomes.  How will doctors be able to sift through extraneous data to find what truly are indications for higher risk of cancer?  Is this “extra” testing and information skewing the data and prognosis of many patients?

 

Main Article Used:

http://www.nytimes.com/2014/09/23/health/finding-risks-not-answers-in-gene-tests.html?ref=health&_r=0

 

Where Does Language Come From?

Somewhere in Britain, there is a family where each member has varied speech difficulties. Some members can’t say words like “hippopotamus”, others have trouble reciting words that begin with the same letter. This family, known as the KE family, was subject to research by Oxford University in the early 2000’s to find that they had a rare gene mutation. The subtle mutation took place in the FOXP2 gene, where only one nucleotide was misplaced. However, this research has opened up the world to the search for the so called “language gene” in our bodies.

 

There are approximately 6,900 languages in existence today.

For a while, scientists thought that the FOXP2 gene was the “language gene” in our bodies. But further tests show that the gene has much broader capabilities in humans and other animals, such as mice. This evidence suggests that there is no one language gene but instead it relies on a much broader neural support system. With the existence of a language gene being much less concrete, understanding where language originates from becomes much more difficult. A 2010 study by neuroscientist Aldo Faisal showed that what led humans from making stone flakes to axes was a shift in cognitive capacity, not an improvement in physical coordination. Researchers believe that as toolmaking became more common in the world, humans may have acquired the mental capacity for language. Liverpool archaeologist Natalie Uomini says: “A lot of people would say that toolmaking came [before language], I would just say that they co-evolved.” 

Liverpool archeologist Simon Kirby takes a different perspective on the origin of language, arguing that the human brain alone is not enough to explain language and that we must look at the evolution of human culture as well. Through several experiments with fictional languages, Kirby has found that as a language passes from one person to the next, it develops a unique structure and evolves in such a way that participants could guess words that they weren’t even trained to know. This shows that there is a lot more than just brain function in the evolution language. There is a huge social component, and this makes the discovery of language’s origin even messier than originally thought.

The fact that such an integral part of our society is still relatively unknown biologically is fascinating, and many breakthroughs in this topic have been made within the last 5 years. What’s fascinating about the search for language is that it shows that as modern science progresses, we may not find the answer to the question that we asked, but instead find a whole new set of questions that we would never have thought to ask. What do you think about the origin language? Did it come to fruition before or after toolmaking? Leave your thoughts in the comments section below, thanks for reading!

 

Source: http://nautil.us/issue/17/big-bangs/the-family-that-couldnt-say-hippopotamus

 

Queen Bee and her special gene

A recent article, “Single gene separates queen from workers“, discusses a study published in Biology Letters carried out by scientists from Michigan State University and Wayne State University. They found a gene, which affects not only leg and wing development in bees but also the evolution of a bee’s ability to carry pollen. This gene, known as Ultrabithorax (UBX), gives worker bees the physical feature of their hind legs, which they need to carry pollen. 

Photo taken by: Christopher Down http://en.wikipedia.org/wiki/File:Bee_gathering_pollen,_Montreux.jpg

Thanks to Ubx, workers develop a smooth spot on their hind legs that is home to their pollen baskets. Elsewhere on their legs, the gene causes the formation of 11 bristles, known as the “pollen comb” and it synthesizes a pollen press, a “protrusion” that packs and transports pollen back to the hive. Queens don’t have these features that the Ubx gene is responsible for. The scientists isolated Ubx and silenced it. The results were the disappearance of the pollen baskets, the growth of pollen combs, and reduction in the size of pollen presses. The scientists also concluded that pollen baskets play a smaller role in bees that are “less socially complex”, and the main scientist, Huang states that:  “We conclude that the evolution of pollen baskets is a major innovation among social insects and is tied directly to more-complex social behaviors.” 

So why is this information important? Well, given the recent downhill trend of bee populations, this research can contribute towards future attempts to make bees better pollinators. Do you think scientists should pursue this?

 

Microglia! Here to the Brain Rescue?


MicrogliaRecently, Massachusetts General Hospital (MGH) investigators have used a new sequencing method to identify a group of genes used by the brain’s immune cells, called microglia, to sense pathogenic organisms (bacteria that cause bacterial infection), toxins or damaged cells. Identifying these genes could lead to better understanding of the role of microglia both in normal brains and in neurodegenerative (nervous system) disorders. This discovery could also lead to ways to protect against brain dysfunctions caused by conditions like Alzheimer’s and Parkinson’s diseases.

The set of genes microglial have also been able to react with their environment. “We’ve been able to define, for the first time, a set of genes microglia use to sense their environment, which we are calling the microglial sensome,” says Joseph El Khoury, MD, of the “MGH Center for Immunology and Inflammatory Diseases and Division of Infectious Diseases, senior author of the study”. A type of macrophage microglia are known to consistently test their environment in order to sense any indication of infection, inflammation, and injured or dying cells. Depending on the situation they are involved in, the microglia reacts in a neurotoxic response, replying in a defensive protective manner. The microglia can “engulf pathogenic organisms, toxins or damaged cells or release toxic substances that directly destroy microbes or infected brain cells”. In this way microglia is extremely beneficial to the brain because it is able to identify infections before they have any direct contact with the brain. However, this neurotoxic response can also damage healthy cells and can “contribute to the damage caused by several neurodegenerative disorders”, so keeping the response under control is crucial.

El Khoury’s team’s “next step is to see what happens under pathologic conditions” and to define the sensome of microglia and other brain cells in humans, identifying how the sensome changes in central nervous system disorders, and eventually finding ways to safely manipulate the sensome. Discovering the microglia gene is a large and successful step to eventually finding a cure for infectious brain diseases, such as Alzheimer’s and Parkinson ’s disease.

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