AP Biology class blog for discussing current research in Biology

Tag: genetics (Page 1 of 2)

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:

A brief summary of Dr. Vijg’s findings (a bit shorter than the NY Times article):

An interesting article about an entrepreneur’s quest to make people live even longer:


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.


(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


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!


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!


“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.


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:

Is it Really Your Choice to Make Better Choices?


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

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!!



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:


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?


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?

Link to Photo:
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.


Epigenetics, Dads, and Obesity


By Ynse. Photo from Flickr


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

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

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

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

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

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

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

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

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

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Incredible New Gene-Searching Software

MIKI Yoshihito

Joseph T. Glessner, of the Center for Applied Genomics at the Children’s Hospital in Philadelphia recently invented a new software tool that will revolutionize accuracy in genetic disease studies. The software called ParseCNV is an algorithm that “detects copy number variation associations with higher levels of  accuracy than that available in existing software,” says Mr. Glessner. This incredible software automatically corrects for variations in the length of deleted or duplicated DNA sequences from one individual to another and produces high quality, replicable results for researchers studying genetic diseases.

CNV stands for copy number variations which are sequences of DNA, ranging from 1000 to millions of nucleotide bases, which may be deleted or duplicated. These CNV’s are very difficult to find because they are so rare but so important in the discovery of genetic diseases. Previous methods to find the link between CNV’s and disease involved individual case-control studies, in which diseased DNA is compared to healthy DNA. This method does not work accurately because different people have different CNV’s which can effect the outcome of the diagnosis.

ParseCNV is incredible in that it can account for and adjust to so many differences in genes and has so much versatility in that it is applicable to family studies and quantitative analyses of continuous traits. I am really looking forward to seeing the future of this amazing algorithm and its contributions to genetic research.

The True Origins of HIV

There’s no doubt you’ve heard of HIV, or Human Immunodeficiency Virus. The HIV virus, if left untreated can lead to AIDS, or Acquired Immunodeficiency Syndrome, which leads to progressive immune system failure ( HIV didn’t become a problem in the United States until the 1980s, but was around long before then. Alfred Roca, an assistant Professor at the University of Illinois believes HIV was around for much longer than we believe.


The Origins 

HIV was thought to be originated from SIV, or Simian Immunodeficiency Virus, that infected Chimpanzees in Central Africa. About ninety percent of humans infected with HIV are infected with a strain called HIV-1 Type M, which was believed to have crossed the species barrier anywhere between 1884 and 1924. However, believes that HIV crossed the species barrier many times before 1884, but was most prevalent in rural areas, so it remained undetected.


Why it was a mystery

If HIV was around long before we initially thought, why did it remain undetected. According to Roca, “the persistence of HIV in humans requires population densities typically of larger cities that appeared in West Central Africa during the colonial period.” HIV didn’t spread amongst humans pre-1884 because the population was not dense enough. In addition, diseases spread much faster. Many people would have died early from diseases such as smallpox, and those with compromised immune systems would have been hit first, thus the disease couldn’t spread.

Map of the prevalence of HIV in the world, according to the 2008 UNAIDS Preport

Roca also believes that different strains of HIV could affect people with different genes. Using data from The Human Genome Project, Roca was able to analyze the DNA of the Biaka people, who live in the forests where the chimpanzees responsible for our current HIV pandemic reside and 4 other African populations which live outside the chimpanzees’ range. Research done in the 1980s concluded there are 26 genomic locations that help resist HIV.

The results of the research were astounding. Roca and his team identified four genes that code for proteins that affect the ability of the HIV to affect the host or the progression of the disease. Several of these genes were common among the Biaka people. Though the results aren’t definitive, they show that natural selection does play a part in the transfer of HIV to human populations, which is why the disease didn’t thrive earlier.



New Deadly Virus Discoved in Africa

Recently an article was released summarizing the discovery of a new disease in Africa. In 2009 a fifteen year old boy in a small village in the Democratic Republic of the Congo fell ill. The initial symptoms were malaise and a bloody nose, but quickly the boy developed an acute hemorrhagic fever. Within two days of the showing symptoms the boy died. Approximately eleven days later a thirteen year old girl who went to the same school as Patient One developed similar symptoms, and died three days later. At the local health center which both Patients One and Two visited, a thirty-two year old male nurse began to experience identical symptoms. He was moved to the hospital in Boma, Democratic Republic of the Congo, where the doctors drew blood and began to test for known viruses; they found nothing. However, very recently a research team used deep sequencing to determine the pathogen,which they dubbed “Bas-Congo Virus”, and posted their results in the Public Library of Science Journal. It was discovered that the virus belonged to the Rhabdoviridae family, best known for the Rabies virus. Interestingly enough, though, the Bas-Congo virus only shares 34% of the amino acids found in other Rhabdoviruses, meaning that it is very different. The discovery of this virus may end up being of great importance due to the possibility that the virus may return. In any case, we will have one less pathogen on this planet to identity lest there be another, more deadly, outbreak.

Identical but Not the Same


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

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

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

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

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

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

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

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

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

the genes are expressed differently.

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

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

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