Self Regional Hall(Photo: Craig Mahaffey/Clemson University)

A new facility that will house the Clemson University Center for Human Genetics has opened at the Greenwood Genetic Center.

The 17,000-square-foot structure, named Self Regional Hall, will allowClemsons growing genetics program to collaborate closely withresearchers at the center and to focus on early diagnostic tools for autism, cognitive developmental disorders, cancer and rare metabolic disorders.

Opening Self Regional Hall means that we will be able to do even more to help children with genetic disordersand their families, and to educate graduate students who will go out into the world and make their own impact, said Clemson University President James P. Clements, who has a child with special needs.

As you all know," he added, "an early diagnosis can make a huge difference for a child and their family because the earlier you can figure out what a child needs the earlier you can intervene and begin treatment.

The building will house eight laboratories and several classrooms, conference rooms and offices for graduate students and faculty, officials said.

GCC director Dr. Steve Skinner said the facilityis the nextstep in a collaboration of more than 20 years.

"We look forward to our joint efforts with both Clemson and Self Regional Healthcare to advance the research and discoveries that will increase our understanding and treatment of human genetic disorders, he said.

For more information about GGC, go towww.ggc.org.

Read or Share this story: http://grnol.co/2lcrenp

Read the original here:
New research facility opens at Greenwood Genetics Center - Greenville News

February 16, 2017 by Andy Fell Honey bees provide 'pollination services' worth billions of dollars to US agriculture. Understanding honey bee populations requires understanding their origins in the Middle East and Africa. New work from UC Davis and UC Berkeley clears up some of the confusion around honey bee origins. Image: Honey bees collecting pollen Credit: Kathy Keatley Garvey

Where do honey bees come from? A new study from researchers at the University of California, Davis and UC Berkeley clears some of the fog around honey bee origins. The work could be useful in breeding bees resistant to disease or pesticides.

UC Davis postdoctoral researcher Julie Cridland is working with Santiago Ramirez, assistant professor of evolution and ecology at UC Davis, and Neil Tsutsui, professor of environmental science, policy and management at UC Berkeley, to understand the population structure of honey bees (Apis mellifera) in California. Pollination by honey bees is essential to major California crops, such as almonds. Across the U.S., the value of "pollination services" from bees has been estimated as high as $14 billion.

"We're trying to understand how California honey bee populations have changed over time, which of course has implications for agriculture," Ramirez said.

To understand California bees, the researchers realized that they first needed to better understand honey bee populations in their native range in the Old World.

"We kind of fell into this project a little bit by accident," Cridland said. "Initially we were looking at the data as a preliminary to other analyses, and we noticed some patterns that weren't previously in the literature."

The new study combines two large existing databases to provide the most comprehensive sampling yet of honey bees in Africa, the Middle East and Europe.

Unrelated Bee Lineages in Close Proximity

Previously, researchers had assumed an origin for honey bees in north-east Africa or the Middle East. But the situation turns out to be more complicated than that, Cridland said.

"You might think that bees that are geographically close are also genetically related, but we found a number of divergent lineages across north-east Africa and the Middle East," she said.

There are two major lineages of honey bees in Europe - C, "Central European," including Italy and Austria and M, including Western European populations from Spain to Norway - which give rise to most of the honey bees used in apiculture worldwide. But although C and M lineage bees exist side by side in Europe and can easily hybridize, they are genetically distinct and arrived in different parts of the world at different times.

M lineage bees were the first to be brought to north America, in 1622. The more docile C lineage bees came later, and today many California bees are from the C lineage, but there is still a huge amount of genetic diversity, Ramirez said.

"You can't understand the relationships among bee populations in California without understanding the populations they come from," Cridland said.

In the Middle East, the O lineage hails from Turkey and Jordan, and Y from Saudia Arabia and Yemen. The main African lineage is designated A.

At this point, the researchers cannot identify a single point of origin for honey bees, but the new work does clear up some confusion from earlier studies, they said. In some cases, diverged lineages that happen to be close to each other have mixed again. Previous, more limited studies have sampled those secondarily mixed populations, giving confusing results.

"We're not making any strong claim about knowing the precise origin," Cridland said. "What we're trying to do is talk about a scientific problem, disentangling these relationships between lineages, the genetic relationships from the geography."

The study is published online in the journal Genome Biology and Evolution.

Explore further: Bee rescue mounted after hospital breaks out in hives

More information: Julie M. Cridland et al, The complex demographic history and evolutionary origin of the western honey bee, Apis mellifera, Genome Biology and Evolution (2017). DOI: 10.1093/gbe/evx009

It was a sticky situation.

Agricultural demand for pollination is growing more quickly than the supply of honey bees, the dominant species managed for crop pollination. Increasing the efficiency of pollination represents a way of increasing crop yield ...

In a new study published in the Journal of Apicultural Research, scientists have compared the ability of two strains of honey bees to defend themselves against the parasitic mite varroa by grooming the mites from their bodies.

Scientists from The University of Western Australia's Centre for Integrative Bee Research (CIBER) tagged 200 honey bee workers to find out how a highly-contagious fungal parasite (Nosema apis) impacts their ability to pollinate ...

A study conducted by biologists at UC San Diego has found that the Africanized honey beean aggressive hybrid of the European honey beeis continuing to expand its range northward since its introduction into Southern ...

For the last 30 years, Drummond, professor of insect ecology at the University of Maine, has studied the biology, ecology, disease susceptibility and pesticide exposure of Maine's 275 native species of bees, as well as the ...

Facial recognition is a biometricsystem that identifies or verifies a person from a digital image. It's used to find criminals, identify passport and driver's license fraud, and catch shoplifters. But can it be used to ...

A smart trap for mosquitoes? A new high-tech version is promising to catch the bloodsuckers while letting friendlier insects escapeand even record the exact weather conditions when different species emerge to bite.

Where do honey bees come from? A new study from researchers at the University of California, Davis and UC Berkeley clears some of the fog around honey bee origins. The work could be useful in breeding bees resistant to disease ...

Timothy Blake, a postdoctoral fellow in the Waymouth lab, was hard at work on a fantastical interdisciplinary experiment. He and his fellow researchers were refining compounds that would carry instructions for assembling ...

A new WCS study in India shows that three carnivorestigers, leopards, and dholes (Asian wild dog)seemingly in direct competition with one other, are living side by side with surprisingly little conflict. Usually, big ...

A University of Michigan biologist combined the techniques of "resurrection ecology" with the study of dated lake sediments to examine evolutionary responses to heavy-metal contamination over the past 75 years.

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

See the original post here:
Honey bee genetics sheds light on bee origins - Phys.Org

Thursday February 16, 2017

As Canada's national opioid crisis continues, scientists at the University of British Columbia are trying to figure out why some people may be more susceptible to addiction at a genetic level.

"There have been a number of researchers who have taken patients or people who have drug abuse issues and compared their genes to people who do not have drug abuse issues," says Shernaz Bamji, a professor in the department of cellular and physiological sciences.

"And they have identified a number of mutations in many genes that actually help the brain communicate or cells within the brain communicate with one another. "

Her new research, published this week in thejournal Nature Neuroscience,suggests a stronger connection between genetics, biology andaddictionand may provide more clues on how to treat addiction in the future.

"The study adds to a growing body of work that suggests that addiction ... is not just a matter of being weak-willed,but really isa matter of genetics, biology and circumstances," says Bamji.

The UBC research involved injecting cocaine into genetically-modified mice to see if differences in their brains made them more susceptible to addictive behaviour than ordinary mice. The results surprised the whole team. (Darryl Dyck/Canadian Press)

Bamjitells The Current's guest host Laura Lynchhow this study could help with treating and even preventing addiction.

"[This study] explains to us differences in how we learn and different parts of the brain. And this has got impact down the line ... for humans because that might point to avenues of therapy," Bamji says

"Once we really, fully establish exactly how learning and synaptic plasticity in the area of the brain that's involved in addiction is different from learning in other areas of the brain."

As part of the research Bamji injected cocaine into genetically-modified mice to see if differences in their brains made them more susceptible to addictive behaviour than ordinary mice.

Bamji says the results were the exact opposite of what the team expected.

"Well it was, you know, completely counter-intuitive to what we thought was going to happen," says Bamji explaining that unlike the normal mice, the genetically-modified mice displayed less addictive behaviour even after multiple doses of cocaine over days.

According to Bamji, this reaction suggests that addiction may be more connected to genetics and biology than previously thought.

Bamji is excited about the potential practical uses of this research, but says clinical trials involving this research is years away.

"You have to be very cautious when you're only interpreting genetic data. You have to go back and do the experiments that we are doing to validate that these particular genes are indeed involved in whatever disease that you're talking about."

Listen to the full conversation at the top of this web post.

This segment was produced by The Current's Liz Hoath.

See more here:
New UBC research suggests stronger connection between addiction and genetics - CBC.ca

Mendels laws, like any laws in science, are wonderful because they make predictions possible. A woman and man both carry a recessive mutation in the same gene, and each of their children has a 25% chance of inheriting both mutations and the associated health condition. Bio 101.

In contrast to our bizarre new world of alternate facts, multiple interpretations, and both are true scenarios, science is both logical and rational. If an observation seems to counter dogma, then we investigate and get to the truth. Thats what happened for Millie and Hannah, whose stories illustrate two ways that genetic disease can seem to veer from the predictions of Mendels first law: that genes segregate, one copy from each parent into sperm and ova, and reunite at fertilization. (Ill get to embryo engineering at the end.)

Millies situation is increasingly common exome or genome sequencing of a child-parent trio reveals a new (de novo), dominant mutation in the child, causing a disease that is genetic but not inherited.

Hannahs situation is much rarer: inheriting a double dose of a mutation from one parent and no copies of the gene from the other.

MILLIE AND BAINBRIDGE-ROPERS SYNDROME

Millie McWilliams was born on September 2, 2005. At first she seemed healthy, lifting her head and rolling over when most babies do. But around 6 months, her head became shaky, like an infants. Then she stopped saying dada, recalled her mother Angela.

By Millies first birthday, her head shaking had become a strange, constant swaying. She couldnt crawl nor sit, had bouts of irritability and vomiting, and bit her hands and fingers.

In genetic diseases, odd habits and certain facial features can be clues, but none of the many tests, scans, and biopsies that Millie underwent lead to a diagnosis. Nor were her parents carriers of any known conditions that might explain her symptoms. Still, it was possible that Millie had an atypical presentation of a recessive condition so rare that it isnt included in test panels.

By age 6 Millie couldnt speak, was intellectually disabled, and was confined to a wheelchair, able to crawl only a few feet. Today she requires intensive home-based therapies. But Millie can communicate. She likes to look at what she wants, with an intense stare, said Angela. She loves country music and Beyonc, and every once in awhile something funny will happen and shell break into a big smile.

Millies pediatrician, Dr. Sarah Soden, suggested that trio genome sequencing, just beginning to be done at Childrens Mercy Kansas City(where the child already received care) as part of a long-term project, might help to assemble the clinical puzzle pieces to explain the worsening symptoms. So the little girl and her parents, Angela and Earl, had their genomes sequenced in December 2011. Analyzing the data took months, but Dr. Sodens team finally found a candidate mutation in the child but not her parents. However the gene, ASXL3, hadnt been linked to a childhood disease. Yet.

Its typically a matter of time for gene annotation to catch up to sequencing efforts and clinical clues. In February of 2013, a report in Genome Medicinedescribed four children with mutations in ASXL3 who had symptoms like Millies. Even her facial structures arched eyebrows, flared nostrils, and a high forehead matched those of the other children, as well as the hand-biting. They all haveBainbridge-Ropers syndrome.

One copy of Millies ASXL3 gene is missing two DNA bases, creating an inappropriate stop codon and shortening the encoded proteins. From this new glitch somehow arose the strange symptoms. Because neither Earl nor Angela has the mutation, it must have originated in either a sperm or an egg that went on to become Millie.

Since the paper about Bainbridge-Ropers syndrome was published three years ago, a few dozen individuals have been diagnosed and families have formed a support group and a Facebookpage. Thats huge. Even if a disease has no treatment, as is the case for Bainbridge-Ropers, families find comfort in reaching the end of the diagnostic odyssey and locating others. Said Angela, It was a relief to finally put a name on it and figure out what was actually going on with her, and then to understand that other families have this too. Ive been able to read about her diagnosis and what other kids are going through.

HANNAH AND GAN

Hannah Sames will be celebrating her 13th birthday next month, and is showing what may be early signs of strength in her muscles after receiving gene therapyinto her spinal cord last summer to treat giant axonal neuropathy (GAN).

When I first met Hannahs mom Lori in 2010, she told me that Hannah had inherited the exact same deletion mutation in the gigaxonin gene from her and her husband Matt. At that time, only a few dozen children were known to have the condition, and that number hasnt risen much. Because of the diseases rarity, I politely asked ifLori and Matt could be cousins but not know it. Shared ancestry seemed a more likely explanation for two identicalextremely rare gene variants occurring in the same child than the parents having the same length deletion just by chance. But no, Matt and Lori arent related.

The answer came just a few months ago: Hannah inherited both of her gigaxonin deletion mutations from Lori, and none from Matt. This is a very rare phenomenon called uniparental disomy (UPD), meaning two bodies from one parent. Like Millie, UPD seemingly defies Mendels law of segregation, with a pair of chromosomes (or their parts) coming solely from one parent, rather than one from each parent.

UPD happens during meiosis, the form of cell division that sculpts egg and sperm. And it requires two exceedingly rare events.

First, something goes wrong during the separation of one chromosome in which the DNA has replicated to form two chromatids, like two squiggly lines of DNA linked at the middle. Instead of those chromatids separating into different eggs, a pair went into the same egg, providing two copies of the chromosome 16 that bears the mutation, instead of the normal one. For a child with GAN to have resulted from Loris meiotic glitch, her double-dose egg must have met with a sperm cell that just happened to be missing chromosome 16 thats the second rare event. Or, more likely, the one-celled Hannah indeed had a chromosome 16 from her dad yet had two from her mom, an anomaly in chromosome assortment called nondisjunction. In fact an extra chromosome 16 is the most common trisomy(3 instead of 2 chromosomes) associated with miscarriage. But then Matts chromosome was lost, leaving two from Lori.

Neither Millies Bainbridge-Ropers syndrome nor Hannahs GAN actually counters Mendels law. Although Millie didnt inherit her mutation, if she were able to have children, she would pass it on with a probability of 1 in 2 to each child, just like the law predicts for dominant inheritance. Likewise, a child of Hannah would inherit one copy of the mutation that causes GAN when present in a double dose, just like the law predicts for recessive inheritance.

FORGET EDITING THE GERMLINE GENOME AND HELP SICK KIDS

As I was writing this post, the National Academy of Sciencesreleased its long-awaited tome on whats being called, among other things, embryonic engineering. Rather than banning editing of the human germline forever, the report foresees certain situations in which gene or genome editing, using CRISPR-Cas9 or some other variation on the theme, might be deployed to prevent disease.

WhileI think its great that the rare scenarios in which genome editing might be useful are finally being spelled out, instead of flaming fears of genetic enhancement spawning designer babies, my thinking aboutMillie and Hannah made me wonder why we would ever need to edit a genome to prevent disease in the first place. To quote the eminent mathematician from Jurassic Park, Ian Malcolm, Yeah, yeah, but your scientists were so preoccupied with whether or not they could that they didnt stop to think if they should.

Preventing illness in a future child of course isnt the same as designing theme park dinosaurs, but like Jurassic Parks technology, I cant imagine why genome editing at very early developmental stages is necessary.Even for an exceedingly rare family situation in which passing on an inherited disease is unavoidable, according to Mendels laws, there are alternatives, although they do not yield a biological child: replace, select, or adopt:

Instead of replacing errant genes early in prenatal development, or even before, I think we should focus instead on helping the Millies and Hannahs who are no longer fertilized ova or early embryos, but are kids. Thats already starting for Hannah, thanks to the gene therapy technology that has been gestating since 1990. Millies turn hasnt come yet.

So yes, lets set rules for editing the human germline but lets also consider whether this type of intervention will ever even be necessary in our overcrowded world.

See original here:
Defying Mendelian Genetics and Embryo Engineering - PLoS Blogs (blog)

An Asian American born in Connecticut in 2009 could expect to live89.1 years. An African American, on the other hand, couldexpect to live 77.8 years. Its seldom surprising tosee large discrepancieswhen comparing life expectancies indeveloped and developing nations, considering the vast differences in availablehealth care. But how do we explain such a wide variance between two populations or ethnic groups living in the same region?

The complicated relationship between population, ethnicity and raceand how it impacts our health involves a complex equation offactors,includingmedicine,economics, psychology, anthropology, sociology andgeography. But it also seems clear that there are so-called race-related genetic factors in play .

Cultures and health behaviors

At this point in the history of medicine, there are a handful of behaviors withwell-established health impacts onour health. Among this is tobacco smoking,which has been linked unequivocallyto lung cancer and chronic obstructive pulmonary disease (COPD). Its also associated withcardiovascular and cerebrovascular conditions (leading to high blood pressure, atherosclerosis, heart disease, and strokes), and a host of non-pulmonary cancers. Yet different ethnic groups react differently to prolonged exposure.

Consider that therate of smoking among Native Americans is higher than for any other group in North America, at 26.1 percent, according toAmerican Lung Association. At the other end of the smoking spectrum areAsian Americans, at 9.6 percent, andHispanics at12.1 percent. In the middle areAfrican Americans, 18.3 percent, andCaucasians,19.4 percent.

Source: American Lung Association

Based on smoking rates alone, youd expect Asians and Latinos to have lower lung cancer rates, and they do. However, youd also expect Native Americans to have higher lung cancer rates. Yet their lung cancer rates are only slightly worse thanthose of Latinos. Strikingly, the ethnic group with the highest lung cancer rate is African Americans, according to the Center for Disease Control (CDC).

A similar phenomenon is seen inalcohol use. According to the National Institute of Alcohol Abuse and Alcoholism (NIAAA), the most common drinkers are white males, 74.27 percent, while Asian-American women were the least common, at 36.11 percent. In terms of daily heavy drinking, the highest rates were recorded among Hispanic males, at 40.48 percent, while Asian American men had the lowest rate, at 18.84 percent. Alcohol abuse relates to liver disease, nutritional disorders, and various cancers, but as with smoking the disease rates among ethnic groups do not correlate precisely with consumption.

Black men (25.81 percent)and women (19.02 percent), for example, reported lower rates of daily heavy drinking, when compared to white men and women. Yet, African Americans have a higher risk of developing alcohol-related liver disease, according to the National Institutes of Health.

Health genetics

With majorkillers like heart disease and stroke,there are a multitude of genetic factors, making forcomplex relationships between genetics and disease.For example, despite having a relatively high risk of developing cardiovascular disease, Latinos have alower risk of actually dying from the disease. Thus, studies are constantly underway to examine genetic risk factors and markers. African Americans have a notoriously high rate of high blood pressure compared with other ethnic groups, and for decades there has been a debate regarding whether genetic factors or environmental factors are more important.

What about discrimination?

A potentially troubling possibility has emerged from a University of Florida study that was published in December 2016in thejournal PLOS ONE. By interviewing 157 African American subjects in creative ways, researchers were able to show a relationship between the feeling of discrimination and high blood pressure. The study pointed toeight genetic variants of five genespreviously known to be associated with cardiovascular disease. The cause ofhigh blood pressure iscomplex, given that its related both to physical phenomena such as factors controlling how tightly blood vessels squeeze, as well as psychological factors, since blood pressure rises in nearly everyone when they become anxious or stressed.

Putting all of these factors into a coherent picture of how diseases are generated appears to be a daunting task. Year by year, month by month, the science community is inundated with new data, especiallyfrom genomic studies. Various new instruments are in use too, and yet, when the goal is to assess anything related toethnicity or race, the task grows progressively more difficult.

David Warmflash is an astrobiologist, physician and science writer. Follow @CosmicEvolution to read what he is saying on Twitter.

View original post here:
Race, genetics and health: Our ancestry both limits and exacerbates ... - Genetic Literacy Project