BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: genetics (Page 1 of 2)

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.

Tree Lobsters Are Back!

Image result for Stick insects Tree lobsters Lord Howe

Lord Howe Tree Lobster

Tree Lobsters are actually not lobsters at all. Nor are they crustaceans.  They are actually just insects with a similarly shaped exoskeleton. But that’s not what makes them interesting. What does, is that Tree Lobsters have seemingly come back from extinction.

The Species, originally from the Lord Howe Island in the Tasman Sea between Australia and New Zealand, went extinct during the 1920’s due to becoming the main food source for an invasive rat species that came onto the island. The Tree Lobsters were only formally declared extinct in 1960 though. Since then scientist had pretty much forgotten about them.

Image result for Stick insects Tree lobsters Lord Howe

Ball’s Pyramid Stick Insect

Thus, when scientists found a small group of stick insects similar to Lord Howe Tree Lobster’s on Ball’s Pyramid, a volcanic stack 12 miles away from Lord Howe Island, in 2001, they were quite surprised. The Ball’s Pyramid stick insects were skinnier and darker but scientists were still hopeful the newly discovered insects were, in fact, the same species as the extinct Lord Howe Tree Lobsters. Scientists tested the genes of the stick bugs from Ball’s Pyramid with genes extracted from preserved Lord Howe Tree Lobsters and found out that despite some morphological variance, they are still the same species. They speculate that diet, age, and environment had caused the Ball’s Pyramid Stick Insects to look a little different. How the species got to the volcanic stack is still a mystery as the insects cannot swim but they infer that they had been carried over by birds.

The newly discovered Tree Lobsters are now being bred at the Melbourne Zoo and elsewhere in an attempt to reintroduce the species to Lord Howe Island. However, the invasive rat species on Lord Howe Island still remains a problem as it threatens the lives of over 70 different native species. In order to successfully reintroduce the Tree Lobsters back to Lord Howe, the rat problem needs to be taken care of first.

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

Preferential Gene Expression: Not As Random As We Thought

Our conventional knowledge of genetics dictates that the activation of genes in our DNA is random. It is equally likely that our body will express our mother’s alleles as it is that our body will express our father’s. In the case that one parent donates a defective copy, it will be silenced; the other parent’s healthy set of DNA takes precedence and becomes activated.

However, a new study indicates that gene expression and activation is not as random as we thought. In certain regions of the body, our genes demonstrate preferential expression.

A team of scientists at the University of Utah found that almost 85 percent of genes in juvenile mice brains displayed preferential treatment. The mice brains activated one parent’s set of DNA over the other’s. This phenomenon was observed in other areas of the body, as well as in primates.

Although the preferential expression came to a close within ten days, it could provide explanations for vulnerability to brain diseases such as schizophrenia, ADD, and Huntington’s. The temporary preferential treatment to one parent’s copy of DNA could trigger a host of problems specific to that cell site that lead to such disorders, if the parent had given a defective copy of genes.

The study has the potential to alter our basic understandings of genetics, and how we are more prone to certain specialized diseases.

Image: (Public Domain, https://pixabay.com/en/dna-biology-medicine-gene-163466/)

The Grey Area of Human Gene Editing

The process of Human Gene Editing developed with the goal to prevent future generations from suffering from genetic diseases present in past generations, like our own. Human gene editing, provided it is done only to the correct disease, alters the DNA in embryos, eggs, and sperm to the when reproduction occurs, the gene for the disease or disability is not inherited. However, two weeks ago the National Academies of Sciences and Medicine issued a report stating that human gene editing is being used to enhance people’s health or abilities. This is considered unethical according to organizers of a Global Summit on human gene editing.

Human gene editing has been given a “yellow light” because the process is not yet approved to be done on people. There are high hopes that diseases caused by only 1 genetic mutation such cystic fibrosis and Huntington’s disease will be eliminated due to this process. Unfortunately diseases that are caused by more than one genetic mutation, such as autism or schizophrenia, are not curable by this process.

National Cancer Institute

Gene Editing on humans is such a controversial topic right now: is it ethical to change genes? should the practice be used to change physical appearances? Ultimately, if Human Gene Editing is approves, who decides when it becomes too much, or unethical. This grey area is presented to be somewhere between when it is appropriate to help aid the life of a human, ridding them of a disease, and when enhancements are made.

 

Is There a Limit to How Old Humans Will Get?

In the 1900s, the life expectancy for humans in the United States was approximately 50 years. Since then, the age to which humans can live has only grown. In 1997, a woman by the name of Jeanne Calment died at the age of 122- an astounding increase from the life expectancy less than a hundred years ago. A new study written about in the New York Times explains that Dr. Vijg, an expert on aging at the Albert Einstein College of Medicine, feels that we have now reached our “ceiling. From now on, this is it: Humans will never get older than 115.” Dr. Vijg and his graduate students published their pessimistic study in the journal Nature, presenting the evidence for their claim.

For their study, Dr. Vijg and his colleagues looked at how many people of varying ages were alive in a given year. Then they compared the figures from year to year, in order to calculate how fast the population grew at each age. For a while, it looked as though the fastest-growing group was constantly becoming older; “By the 1990s, the fastest growing group of Frenchwomen was the 102-year-olds. If that trend had continued, the fastest-growing group today might well be the 110-year-olds.” (NY Times Article). Instead, the increases slowed and eventually stopped, leading Dr. Vijg and his colleagues to conclude that humans have finally hit an upper limit to their longevity. Further research into the International Database of Longevity seemed to validate their findings; No one, except in rare cases like Ms. Calment, had lived beyond the age of 115. It appears as though human beings have hit the ceiling of longevity.

There was a varied mix of responses to the study. Some, like Leonard P. Guarente, a biology professor at MIT, praised it, saying “it confirms an intuition he has developed over decades of research on aging.” Others, like James W. Vaupel, the director of the Max-Planck Odense Center on the Biodemography of Aging, called the new study a travesty and said, “It is disheartening how many times the same mistake can be made in science and published in respectable journals.”

This study is by no means conclusive. It is simply one more piece of research in the ongoing debate over whether human beings will continue to live longer, and will continue to be debated by many experts in the field.

However, one must wonder whether living longer should be the goal. After all, as Dr. Vijg pointed out, “aging is the accumulation of damage to DNA and other molecules. Our bodies can slow the process by repairing some of this damage. But in the end, it’s too much to fix. At some point, everything goes wrong, and you collapse.” While morbid, he makes a valid observation: Humans can only go so long until necessary bodily functions begin to break down. Rather than worrying about whether we will live to an extraordinary age such as Ms. Calment, I concur with Dr. Vijg; the focus should be on living the most amount of healthy years and taking care of our bodies. While it may seem like a great idea to live to the age of 125, what good would that do if you aren’t able to continue with the activities you enjoy because your body is breaking down?

 

Other Relevant Articles:

In Depth Explanation of Longevity: https://en.wikipedia.org/wiki/Longevity

A brief summary of Dr. Vijg’s findings (a bit shorter than the NY Times article): http://www.newser.com/story/232121/human-lifespan-has-likely-maxed-out.html

An interesting article about an entrepreneur’s quest to make people live even longer: https://www.theguardian.com/science/2015/jan/11/-sp-live-forever-extend-life-calico-google-longevity

 

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.

Crispr-Cas9: Coming to a Theater Near You

This sequel to GATTACA is to be released shortly, and this time, they’re transcending the movie screen and bringing the experience to reality!

Crispr-Cas9 is a fairly recent DNA-editing technique that has been developed, and allows for extremely easy and precise gene editing, a development said to be at least on par with PCR for bio engineering. In many ways, this is great. Now biologists won’t have to spend the time nor undergo the difficulty of creating variant DNA through old methods, meaning that all these cool genetic breakthroughs should be happening at an unprecedented pace! The problem is, it may be going too fast for humans to wrap their head around.

Similar to the ethical questions raised by the film GATTACA, countries and scientists are debating what regulations should be put on this new and powerful tool. With Crispr-Cas9, the possibility to genetically modify humans becomes a very real option to consider. Scientists could remove DNA sequences which lead to defects and diseases such as albinism and Huntington’s Disease. Or anything else, really.

(The miracle protein)

The main point of Crispr-Cas9 is not necessarily the ability it gives to scientists to easily modify DNA, but the increased rate at which we can understand what specific sequences of DNA do by altering them. Not only are we more able to modify DNA, we are now able to figure it out at breakneck speed.

 

Where it gets complex is, as always, how humans deal with it. Some people, such as Mark Leach, whose daughter has down-syndrome, believes that children with disabilities not only are still able to live rich lives, but also teach others to be more compassionate. Although debating if I would choose to let my child have down-syndrome or not for that reason seems like an absurd consideration, and most likely a coping mechanism, the point still stands that some people are uneasy with fixing genetic-related problems because “they wouldn’t be the same person.” (That’s the point!)

People are really afraid of change, aren’t they?

 

However, for those on the more lethal/completely disabling part of the genetic spectrum, the answer is more than clear.  Charles Sabine, the brother of the renown British lawyer John Sabine, who both have Huntington’s Disease at varying stages, says “If there was a room somewhere where someone said, ‘Look, you can go in there and have your DNA changed,’ I would be there breaking the door down.” Similarly, Matt Wilsey, a parent of a child with a terminal genetic illness, is awestruck at the ridiculousness of the situation: “As a parent with an incredibly sick child, what are we supposed to do — sit by on the sidelines while my child dies?” The oddity of the situation is, we have the capability to start figuring out how to solve these genetic issues with a very effective and efficient technique, it’s just that humans are riding the brakes, trying to slow down the almost inexorable progress of the freight train that is Crispr-Cas9. The irony is that many are afraid with tampering with the “sanctity” of human embryos. I would agree, except that humans defile it all the time. Birth defects, genetic diseases, miscarriages, etc. Of course, this is not intentional, but the parents have the largest hand in these outcomes, as they provide all the material,genetic and otherwise, to create the embryo, fetus, and eventually child. We are already making horrible mistakes with human embryo’s that cripple or kill the resulting child through the natural birth process. Personally, I would go off of this to say we should at least learn from this, so we could eventually progress far enough to prevent these things from ever happening, but I only ask all of the readers to keep this in mind: Nature (very badly) screws up too.

File:Crispr.png

(The process Cas9 facilitates)

I’m not saying that we should be careless with this new and potentially dangerous or aberrant-spawning technology, but I think it’s time that humans come to terms with the fact that their world, and their lives, are entering a new era of existence. For millennia, structured humans have lived in a world where the outside world is the only thing we can manipulate, but now the very structure and formation of ourselves as well. I understand that such a change from a thousands-year-running viewpoint can be hard to make. We’ve never had to think about these things before as a species, because it wasn’t understood and out of our reach. It is daunting. It is terrifying. Only because it is unknown. But how are we to learn, to benefit, from this great potential, if we are too afraid to explore it? I understand that like any form of potential, it can go either way, but this is a great new time of possibilities that simply won’t go away, but reemerge constantly.

I think it’s time we gathered the courage to face it.

Should We Use It: Crispr-Cas 9 Edition

hqdefault

https://www.youtube.com/watch?v=7C20s4eAGtU

Arguably the greatest thing to happen to genetics since the Human Genome Project, Crispr-Cas 9 has been getting a lot of attention.  The Los Angeles Times wrote an article approximately 4 months ago discussing the ins and outs of the new gene editing breakthrough.  The concept of editing genes is nothing new for scientists.  They’ve been doing it since the 1970s.  So many people are asking “What makes Crispr so special?”  The answer is convenience.  Crispr-Cas 9, although still filled with flaws, is the easiest gene editing tool to use out there right now.  Scientists from UC Irvine and UC San Diego have used it on mosquitoes to fight malaria and scientists have begun to use it on human embryos as well.  Crispr is an acronym for Clustered Regularly Interspaced Short Palindromic Repeats which is a relatively complicated way of saying “gene editing tool.”  What Crispr does is it can target certain parts of a strand of DNA and “delete” them from the strand.  In reality they aren’t being “deleted” but “turned off” so RNA doesn’t code it and begin to manufacture proteins for it.  But the real question is why certain people are against gene editing.  Everyone’s seen the movie GATTACA where gene editing is not only commonplace, but discriminatory.  However in today’s world, the fear is much more strongly rooted than a fear of “geneticism” (genetic rascism).  Using Crispr on viable human embryos to edit genes may have undesired effects.  The turning off/on of one gene could result in the unintentional turning on/off of another.  Also, many scientists believe that a parent making decisions for an unborn child can be unethical and unfair if the child did not want those changes to be made.  And who knows, maybe in the future with the continuous use of Crispr and the development of more complex gene editing tools, “geneticism” could be a reality.

Other articles pertaining to Crispr are linked here and here for more information on the subject.

Forget DNA, Let’s Talk RNA!

8737208097_f9441a4000_b

Photo of RNA (licensing information here)

The genetic code within DNA is responsible for determining who we are and what we are capable of. Because of this, scientists have been interested in cracking the genetic code and finding ways to alter it. There are many diseases linked to DNA, as well as RNA. However, scientists have not been as successful in targeting RNA in living cells as they have been in targeting DNA. Recently, using CRISPR-Cas9, researchers at University of California, San Diego School of Medicine have figured out how to do what has been troubling scientists.

Senior author Dr. Gene Yeo described how the researchers at UCSD have been tracking the movement of RNA throughout cells and plan to measure other RNA features and help to correct disease-causing RNA behaviors using CRISPR-Cas9. The location of RNA in a cell determines whether proteins are produced at the right time and in the right place. When defective RNA transport occurs, diseases ranging from autism to cancer can occur. In order to successfully treat these conditions, researchers must find a way to track and measure the movement of RNA. This process was first seen with DNA: scientists found they could use CRISPR-Cas9 to track and edit genes in mammalian systems. Now, however, Yeo and his colleagues at UC Berkeley have started to target RNA in live cells (RNA-targeted Cas9 or RCas9), as well as DNA in live cells.

When CRISPR-Cas9 is used for normal DNA-involved purposes, researchers design “guide” RNA to match the DNA sequence of the gene Cas9 is targeting. The “guide” RNA then directs the Cas9 enzyme to the target spot in the genome. The Cas9 enzyme then cuts the DNA, which causes the DNA to break in a manner that inactivates the gene. Researchers can also replace the section of the genome next to the cut DNA with a corrected version of the gene. In order to allow Cas9 to work for RNA as well as DNA, work originated by co-author Dr. Jennifer Doudna at UC Berkeley laid a base foundation for researchers to design the PAMmer: a short nucleic acid. The PAMmer works with the “guide” RNA to direct Cas9 to an RNA molecule, instead of DNA.

All in all, CRISPR-Cas9 is responsible for a revolution in genomics with it’s ability to target and modify human DNA. Although this breakthrough is crucial, scientists are now trying to use their lead to target and modify RNA. With an extension on already existing research, there is no doubt that scientists will soon be able to do more than just track RNA. So, let’s forget about DNA and shine a light on RNA for a little while!

Source

“Selfish” DNA Defies Mendel’s Laws

R2D2 may be a heroic Star Wars character but in living animals it is a piece of DNA which violates laws of both genetic inheritance and Darwinian evolution. It has swept through mouse populations by mimicking helpful mutations when in fact it damages fertility. These new findings, described in this article by ScienceNews,  propose that even genes that are dangerous to an organism’s evolutionary chances can trick their way to the top. This is a warning for scientists looking for signs that natural selections has picked certain genes because they offer an evolutionary benefit. What looks like survival of the fittest may actually be a “cheater” prospering.

4671355277_a84f2f20a4_o

Image Link

Geneticist John Didion and colleagues examined DNA samples from wild mice from Europe and North America to determine how widespread R2d2 has become. The proportion of mice with the selfish gene more than tripled in one laboratory population from 18 percent to 62 percent within 13 generations. In another breeding population, R2d2 shot from being in 50 percent of the lab mice to 85 percent in 10 generations. By 15 generations, the selfish element reached “fixation” — all the mice in the population carried it. The rate of spread was much faster than researchers predicted—it was projected it would take 184 generations for the selfish DNA to spread to all of the mice.

R2d2 is a “selfish element,” a piece of DNA that causes itself to be inherited preferentially. It is a stretch of DNA on mouse chromosome 2 that contains multiple copies of the Cwc22 gene. When seven or more copies of that gene build up on the chromosome, R2d2 gets “selfish.” In female mice, it pushes aside the chromosome that doesn’t contain the selfish version of the gene and is preferentially placed into eggs. This violates Gregor Mendel’s laws of inheritance in which each gene or chromosome is supposed to have a fifty-fifty chance of being passed on to the next generation. But there is a cost to R2d2’s selfishness: Female mice that carry one copy of the selfish element have small litter sizes compared with mice that don’t carry the greedy DNA. The loss of fertility should cause natural selection to sift out out R2d2. But the selfish element’s greed is greater than the power of natural selection to combat it, as the lab experiments show.

But based on further lab experiments, researchers may have found that even this successful cheat can get caught. These other results revealed a relatively low proportion of wild mice carrying R2d2. Evolutionary geneticist, Matthew Dean says this could mean that some mice have developed ways to suppress the gene’s selfishness. There is still much more research to conduct on this topic.

Original Source

Additional Reading:

https://www.sciencedaily.com/releases/2016/02/160224133715.htm

 http://www.futurity.org/r2d2-gene-natural-selection-1110832/

Is it Really Your Choice to Make Better Choices?

diet-398613_960_720

Picture of scale (licensing information here)

Obesity has become an increasingly prevalent epidemic around the globe and especially in the United States. Obesity has numerous roots. Recently, researchers from the McGill Centre for the Convergence of Health and Economics found that in some circumstances, it is possible to blame obesity not solely on genetic make-up, but rather on genetic make-up and socio-economic background combined. The McGill researchers discovered that the fat intake of a female who is a carrier of DRD4 VNTR with 7 repeats, a specific gene variant, is determined by the interaction of the female’s socio-economic environment with the gene. This gene variant affects about 20% of the population and is commonly related to obesity, especially in females. Males are typically not as affected by the gene because when comparing males and females at the same age, males do not typically show the same pattern of food preferences.

In order to research this topic, McGill researchers randomly selected about 200 Canadian children with an average age of 4 from the MAVAN birth cohort in Montreal, Quebec and Hamilton, Ontario to take place in the experiment. The McGill researchers used food diaries kept by the parents of every child in order to determine what was being eaten and how often the child was fed. The researchers were able to calculate the percentages of fat, protein, and carbohydrates the children were consuming, as well as the BMI of every child. Since the children were selected at random, the researchers tested every child for the gene variant using a saliva test. The researchers also analyzed the socio-economic background of every child and availability of particular foods based off of the family’s income.

Laurette Dubé, Scientific Director at this particular Centre at McGill and lead researcher on the study, analyzed the results. Dubé found that when comparing two females from the same socio-economic background, one with the gene variant and one without, the female with the gene variant had a higher fat intake, even though the two females came from the same socio-economic background. She also discovered that when comparing two females with the gene variant, one coming from a wealthy family and one coming from a poor family, the female coming from the poorer family had a higher fat intake, despite the fact the two females were both carriers of the gene variant. This newly found research led the McGill research team to believe that the gene alone does not determine an individual’s fat intake, but instead the gene causes an individual to be more sensitive to his or typically her environmental conditions that determine what are “good” eating patterns and what are “bad” eating patterns. Dr. Robert Levitan, co-invesitgator on the project, leader of the childhood obesity program of the MAVAN cohort, and Senior Scientist at the Centre for Addiction and Mental Health (CAMH), is an expert on the DRD4 gene in adult female “overeaters”. Levitan said, “We previously assumed that the 7-repeat variant caused weight gain in these patients by increasing the rewarding aspects of certain foods. These new results suggest a different way that the gene might affect food choices” (Biology News).

In certain cases, obesity isn’t all about genetic make-up, but the likeliness of obesity is determined by the socio-economic background of an individual as well! So, if you are a carrier of the DRD4 VNTR with 7 repeats gene variant, which, because of your environment, impacts your decisions, is it really your choice to make better choices?

Source: Biology News 

 

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.

Biggest Ever Epigenetics Project!!

 

Marian_and_Vivian_Brown

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.”

 

Could There be Good Gene Mutations?

Is there an epic battle occurring within our bodies right now? The classic battle royale between good and bad? I suppose in the body’s case the fight between good and bad genes.  There is a new field in medical research in which researchers are on the quest to find good gene mutations that fight against the disease causing mutations.  One individual, Doug Whitney, sparked the interest of a few doctors because he has fought his genetic odds to be health at 65 years old.  Whitney has a gene mutation, presenilin, that causes early onset Alzheimer’s disease in those who has inherited it. Whitney’s mother and 9 out of his 13 siblings were killed by this mutation and so Whitney’s fate seemed to be sealed.  However when Whitney reached his 40s and 50s having no symptoms he assumed he did not have the gene.  At 62 years old, Whitney, decided he would get a gene test.  He did have the gene.  This was an anomaly, He was doomed to have early onset Alzheimer’s Disease but had absolutely no symptoms. Although Whitney still have changes of getting Alzhiemers but the effects of his bad gene have been greatly delayed by another gene in Whitney’s DNA.  Whitney joined a study at Washington University in St. Louis led by Doctor Randall Bateman which recruited people with the early onset Alzheimer’s disease gene. This attracted the attention of Doctor Eric E. Schadt and Doctor Stephen H. Friend.  Doctor Schadt said that searching for good genes that protect against bad gene mutations is completely turning genetic research on its head.  Researchers have found gene mutations that partially protect diseases like osteoporosis, Type 2 diabetes, heart disease, and Alzheimer’s.  These good gene mutation’s partial protect have help to develop drugs to help fight certain diseases. Finding good gene mutations are substantially more difficult to find than bad genes, but the search has gotten a little easier with fast and inexpensive methods of sequencing DNA. Doctor Schadt and Doctor Friend decided to start the Resilience Project and search for good gene mutations that counteract bad gene mutations to help develop new break though treatments and drugs. They have contacted the researchers at Washington University, the research that Whitney is currently participating in.

For more information:

Article from NYT

Prokaryotic positive genetic influences

Genetics used for intrusion protection

About genetic testing

 

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

 

Echinacea’s Habitat Decline

The plant that is commonly used to treat flu and cold symptoms, Echinacea, is beginning to suffer from a disappearing habitat. A flowering plant part of the daisy familyEchinacea grows in central and North America in mostly dry, wooded areas. As one of the “top five” herbal remedies sold in retail stores, the coneflower is regarded as an American staple to relieve suffers’ of the cold and flu. However, their habitat is in decline from human activities, bees, and deadly aphids

EchinaceaPurpureaMaxima1a.UME          Certain human activities have caused wildlands to shrink and splintered the landscape. As one of the most endangered habitats in the world, tailgrass prairie is throughly studied by scientists in order to track how Echinacea reacting to its changing environment and they are also working to save these prairie patches.

Bees have been known by scientists to pollinate the coneflower plant, Dr. Wagenius says “A bee might have been able to fly across a hundred mile expanse of coneflowers. Could it still do that today? No way.” Pollination for these plants is not at all where it should be, as bees can only pollinate these plants up to short distances.

Coneflower plants are now becoming genetically related in the prairies. If a bee brings pollen to these different plant siblings, the plant may reject the pollen. Therefore, there are no new seeds and populations decrease. A new danger to the coneflower is aphids; they devour prairies of Echinacea. As well, scientists urge prairie farmers to set fire to habitats (since they are necessary to these ecosystems). By inducing the plant to flower, new genetic diversity may be reached.

Junk DNA Shaping Your Face?

DNA_Double_Helix

So called “junk DNA” found in mice have been identified as major factors in the shaping of their faces. These findings are important because the same sequences are found in humans, and might be shaping ours. Junk DNA is named as such because it doesn’t code proteins, so it was originally thought to be “junk”. Scientists believe that these findings can help with research for congenital conditions such as cleft palates.

Geneticists have only, as of yet, been able to define a small number of the genes that influence human face shape, however there is a large variety of human faces. Axel Visel of the Lawrence Berkeley National Laboratory believes that this variation is caused by “distant acting enhancers“: non coding regions of DNA that can influence facial shape.

Visel discovered these findings by using a technique called optical projection tomography where he developed three dimensional models of mouse embryos and saw how gene expression varied the faces.

Discovering enhancers that affect face shape could be an important step in preventing or fixing conditions such as cleft palate syndrome. What do you think about this research or its implications?

GATTACA review

Who ever knew a movie staring Jude Law, Uma Therman and Ethan Hawke does not just explore romance and drama but also takes a look into the revolutionizing and weary scientific future our world has yet to see!  The movie, GATTACA(standing for the 4 DNA bases-Guanine, Adenine, Thymine, Thymine, Adenine, Cytosine, Adenine), starts with the birth of Vincent Freeman, an ordinary child just like you and me.  But unfortunately for him, Vincent falls way below average in his society that revolves around eugenics.

I belonged to a new underclass, no longer determined by social status or the color of your skin. No, we now have discrimination down to a science. –Vincent Freeman in GATTACA

This discrimination that Vincent is referring to is based on ones genetic profile.  In the GATTACA world, the creation of a child occurs in a lab, where there parents can choose what genes they want and don’t want their child to inherit, making for one, almost genetically perfect kid.  In the movie, they have facilities that resemble bank tellers but are in fact genetic “profilers”.  One can bring a strand of hair they found to the facility and receive a print out of that persons genetic profile, along with it stating if that person is Valid(genetically engineered) or invalid(ordinarily created).  Because Vincent was not created this way he is forever categorized as In-valid, causing him to have limited options in life, like not getting hired.

I don’t want to give away more of the story, but it goes into deep investigation of what this world, that potentially can one day happen, would be like.  It questions the morality and ethics behind genetic modification, profiling and discrimination.  It also shows a very depressed world devoid of joy.

In today’s world, we already have genome services similar to the ones in GATTACA. The company 23andMe can create your genetic profile with a swab of your DNA.  You can find out what your genetic ancestry is life, what disease you are at risk for, why you like the foods you like and so on.  Some people are very hesitant to viewing their genetic profile. after reading this article, of a women who had her genetic profile made through 23andMe, do you think you would want yours made?  Why or why not?

License: http://creativecommons.org/licenses/by/2.0/deed.en
Link to Photo: http://www.flickr.com/photos/wonderferret/2854706889/
Photographer: wonderferret

Genetically Modified Food? Now You Can Know For Sure.

Whole Foods Market has officially become the first grocery store to require the labeling of all genetically modified foods. In an article published by The New York Times, on Friday, March 8th, Whole Foods Market announced that they will be labeling all genetically enhanced food products.

According to Whole Foods president A. C. Gallo, the new labeling requirement was implemente due to consumer demand. Mr. Gallo stated that that their “manufacturers say they’ve seen a 15 percent increase in sales of products they have labeled.”

Today, genetically modified foods are of great abundance in the global food supply. For example, most of the corn and soybeans grown here in the United States are genetically altered. The alterations make the soybeans resistant to a herbicide used in weed control, and causes the corn to produce its own insecticide. Scientists are currently working on producing a genetically modified apple that will spoil less quickly, and genetically modified salmon that will grow faster.

What do you guys think of the position Whole Foods is taking with labeling their products? What are your thoughts on genetically modified food in general? Do you believe that genetically modified foods are safe for humans to consume? Please leave your thoughts and comments below.

 

Page 1 of 2

Powered by WordPress & Theme by Anders Norén

Skip to toolbar