Self Regional Hall, a new 17,000-square-foot, state-of-the art facility that will house the Clemson University Center for Human Genetics, has opened on the campus of the Greenwood Genetic Center.

The facility will enable Clemsons growing genetics program to collaborate closely with the long tradition of clinical and research excellence at theGreenwood Genetic Center, combining basic science and clinical care. The center will initially focus on discovering and developing early diagnostic tools and therapies for autism, cognitive developmental disorders, oncology and lysosomal disorders. The building will house eight laboratories and several classrooms, conference rooms and offices for graduate students and faculty.

According to theCenters for Disease Control and Prevention, one in six children between the ages of 3 and 17, roughly 15 percent, suffers from some type of developmental disorder.

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

As the parent of a child with special needs, the kind of research that you are doing here is especially meaningful and important to me and my family, Clements said during the event. As you all know, 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.

Self Regional Hall is a state-of-the-art facility that provides the resources our scientists need to understand the genetic underpinnings of disorders, said Mark Leising, interim dean of theCollege of Scienceat Clemson. This facility, and its proximity to the Greenwood Genetic Center, elevates our ability to attract the brightest scientific talent to South Carolina and enhances our efforts to tackle genetic disorders.

The facilitys name recognizes the ongoing support fromSelf Regional Healthcare, a health care system in Upstate South Carolina that has grown from the philanthropy of the late James P. Self, a textile magnate who founded Self Memorial Hospital in 1951.

Self Regional Healthcares vision is to provide superior care, experience and value. This vision includes affording our patients with access to cutting-edge technology and the latest in health care innovation and genomic medicine, without a doubt, is the future of health care, said Jim Pfeiffer, president and CEO of Self Regional Healthcare. The research and discoveries that will originate from this center will provide new options for those individuals facing intellectual and developmental disabilities, and will provide our organization with innovative capabilities and treatment options for our patients.

We are pleased to welcome Clemson University to Greenwood as the first academic partner on our Partnership Campus, added Dr. Steve Skinner, director of the Greenwood Genetic Center. This is the next great step in a collaboration that has been developing over the past 20-plus 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.

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Clemson Center for Human Genetics opens in Greenwood - Clemson World magazine

George Marks Getty Images

Michael W. Young has been studying sleep disorders for more than 45 years. When he started his research, as a graduate student at the University of Texas in the early 1970s, the field was largely unformed.

We still dont know exactly why we sleep, but in the intervening decades weve learned a lot about the underlying mechanisms. For one, we now know about circadian rhythm, or the bodys internal clock, which dictates sleep-wake cycles. More specifically, were starting to pinpoint why this cycle often gets disrupted. By isolating the mutations responsible for changes in the circadian rhythm in flies and mice, researchers are beginning to identify corresponding genes in humans. Its a slow and imperfect processwere (reassuringly) far more complex than either speciesbut were gaining a better understanding of how our genes influence our sleep. For example, Young and a team of researchers recently published a paper in Cell that links delayed sleep phase disorder to a mutation in the CRY1 gene.

Whereas in the past, being a night owl or a morning lark was attributed to vague mix of genetics and personal preferences, the study gets specific. Those with either one or two copies of the variant CRY1 gene, it found, displayed a more than two-hour shift in night sleep times. Their circadian cycle was delayed, meaning they had a difficult time falling asleep before 2 a.m. or 3 a.m., and, if able, would sleep until 10 a.m. or later.

While its unclear the percentage of people with the mutationits likely far less than the percentage of people who identify as night owls, which suggests environmental factors are also at playthe study is a good reminder that sleep is complicated. Our understanding is evolving; theres still a lot we dont know.

What is clear: a lack of sleep predisposes us to a host of health issues, including diabetes, obesity and depression. Thats a problem, because many of us arent getting enough of it. Between 50 million and 70 million adults in the U.S. have a sleep disorder, according to The Centers for Disease Control and Prevention.

Below, Young outlines some factors believed to play a large role in determining when, and how well, we sleep, along with strategies for adopting a more normal sleep-wake cycleeven when our genetics seem to be hardwired against it.

We evolved on a planet governed by cyclical fluctuations in light and temperature. Over the course of millions of years, our circadian rhythms developed to anticipate these changes, says Young. Our internal clocks work on a cellular level; appetite, metabolism, and sleep, along with other bodily functions, are designed to align with daily and yearly shifts in brightness and heat.

A standard circadian rhythm, then, essentially tracks the sun. Enzymes are released in the morning to stimulate metabolism, in anticipation of breakfast. Meanwhile, in the evening, your body temperature falls, and melatonin levels rise in anticipation of sleep. The energy moving through your body is quite rhythmic, says Young. Messing with this cellular schedulestaring at a bright light right before bed, for examplecan throw these synchronized clocks out of whack.

As mentioned above, a disrupted cycle is often due to environmental factors, and can be cured with better sleep hygiene. But thanks to researchers like Young, we know thats not always the casenot every individuals circadian rhythm neatly aligns with external temperature and light cues. In the Cell study, one of the participants habitual bedtime was at 3 a.m. or 4 a.m., with a desired wakeup time between 10 a.m. and noon. She tested positive for the CRY1 gene mutation, an indication that her internal clock was delayed in comparison with the normal population.

You can imagine what that does to someone with a normal work schedule, says Young. Theyre exhausted all the time.

So what if youre a night owl living in a world designed for early mornings? Youngs first suggestion is to figure out whether genetics are actually to blame (a CRY1 mutation can be determined by a spit test, as can other gene mutations linked to sleep disorders). Likely, part of the problem is tied to external, controllable factors, such as going to bed too late, or lying in the dark, staring at the glow from your smartphone. Or perhaps delayed sleep is a contained phase (college students have a tendency sleep in later than the adults they will grow up to become.)

But for individuals who have a lifelong problem...something that persists and is seemingly hardwired into their biology making adjustments is more difficultbut not impossible, says Young. One of the participants in the study, a lifelong night owl, tested positive for the CRY1 mutation; she also had a job that required her to wake up around 5 a.m. By sticking to a strict schedulesetting an alarm and waking up at 5 a.m., even on weekendsshe was able to partially rewire her sleep-wake cycle. But as with individuals who are genetically predisposed to weight gain, maintaining a meaningful shift required constant vigilance. If she lets her guard down, and sleeps in at a weekend, it produces all kind of problems, says Young.

As with a diet, where meals and calories are tightly controlled, Young recommends late-sleepers adopt a schedule in which a variety of factors, including meals, bedtime, wake up time, and exposure to light, are regulated.

The analogy to dieting is useful as circadian rhythm is deeply involved in metabolic control, says Young. While recreating a similar result in humans isnt feasible, Young believes, as with sleep, our eating patterns evolved to align with cyclical fluctuations in the environment. Our ancestors meals were constricted by external factors, including daylight. Today, of course, thats no longer the case. We can switch on the light at any time and make a sandwich, says Young, A great amount of people eat around the clock, says Young, which he believes could be a factor in Americas growing obesity crisis.

We know that obesity has become a problem in the last century, he says. Over that same period, our genes havent changed. Yes, the amount of caloriesparticularly via saturated-fats, refined grains, and sugarhas trended steadily upwards. But Young isnt convinced that this, alone, is enough to explain the spike in our average BMI. Instead, changes in behavior, particularly the American tendency to snack consistently, including right before bed and, frequently, during the night, are also contributors.

Too often, in both sleep and appetite, our schedules are erratic. Modern life has enabled our internal clocks to fall out of whack with the earths cycle. Above everything else, Young recommends sticking to a schedule. We were built to be rhythmic.

See the rest here:
Night Owl or Early Bird? The Reason Might Be Genetic - Fortune

A high ranking employee for the Pennsylvania Department of Corrections went viral on social media Thursday after he posted a tweet suggesting "there is a genetic component to crime."

Bret Bucklen, the director for the DOC's Office of Research and Statistics, was engaged on May 1 in a political debate on Twitter that appears to have been based on the new Republican health care bill.

"There are those who are unfortunate. There are many more who made bad choices," Bucklen said. "Why can't liberals come to terms with that."

The debate took a turn, though, when Bucklen suggested crime was genetic.

One Twitter user responded, writing that "this could go toward a racist fallacy really quick and I hope it doesnt." To which Bucklen replied, "You doubt that there is a genetic component to crime?"

Race and crime have been scientifically linked with racists promoting the idea that Blacks and other ethnic minorities are genetically disposed to criminality, are less intelligent and lack work ethic to justify white superiority.

The ideas also go along with eugenics, a strain of thought from the early 20th century and adopted by the Nazi regime of Adolf Hltler that believed controlled breeding could improve the human race.

In recent years though, linking criminality and genetics has become more acceptable in science and a New York Times article from 2011 about it said researchers estimate about 100 studies showed a link between genes and crime.

But with nearly 2,000 retweets by Thursday afternoon, including one from new era civil rights activist Deray McKesson, Bucklen's comments were looked at through a racial lens by many social media users.

Secretary of Corrections John Wetzel noted the limits of social media in an email that was sent through a spokesperson to The Tribune.

"Complex subjects rarely are adequately defined in 140 characters," Wetzel said. "Department of Corrections employees have the right to freedom of expression on their personal social media accounts on their own time.

"With that being said, we recognize the sensitivity to a subject like this given the historic connotation of race in criminal justice policy," he added. "I have spoken to Dr. Bucklen, our Director of Planning, Research and Statistics, and that was not the intent of his remark and he should have used better judgment in his word choice and lack of context for his comments.

"That said," Wetzel said, "Dr. Bucklen has been a leader on my team in reducing biased and unjust policies in Pennsylvanias criminal justice system, including criminal justice reforms through the Justice Reinvestment Initiative and leading the fight against new mandatory minimums."

Continue reading here:
Official's tweet causes flap in linking crime, genetics - The Philadelphia Tribune

Scientists from University College London and Imperial College London in the United Kingdom have identified new genetic locations that might make some people more prone to developing type 2 diabetes.

Type 2 diabetes affects hundreds of millions of people worldwide, and the numbers have skyrocketed in recent years. According to the World Health Organization (WHO), the number of people with diabetes has almost quadrupled in the past few decades, from 108 million in 1980 to 422 million in 2014.

In the United States, 29 million people currently have diabetes, and 86 million are thought to have prediabetes.

Until now, researchers were aware of 76 chromosomal locations, or "loci," that underlie this metabolic disease. However, new research analyzed the human genome further and found an additional 111.

The new study - published in the American Journal of Human Genetics - was co-led by Dr. Nikolas Maniatis of University College London's (UCL) Genetics, Evolution, and Environment department, together with Dr. Toby Andrew of Imperial College London's Department of Genomics of Common Disease.

Using a UCL-developed method of genetic mapping, Maniatis and team examined large samples of European and African American people, summarizing 5,800 cases of type 2 diabetes and almost 9,700 healthy controls.

They found that the new loci - together with the ones previously identified - control the expression of more than 266 genes surrounding the genetic location of the disease.

Most of the newly discovered loci were found outside of the coding regions of these genes, but within so-called hotspots that change the expression of these genes in body fat.

Of the newly identified 111 loci, 93 (or 84 percent) were found in both European and African American population samples.

After identifying genetic loci, the next step was to use deep sequence analysis to try to determine the genetic mutations responsible for the disease.

Maniatis and colleagues used deep sequencing to further examine three of the cross-population loci with the aim of identifying the genetic mutations. They then investigated a different sample of 94 Europeans with type 2 diabetes, as well as 94 healthy controls.

The researches found that the three loci coincided with chromosomal regions that regulate gene expression, contain epigenetic markers, and present genetic mutations that have been suggested to cause type 2 diabetes.

Dr. Winston Lau, of UCL's Genetics, Evolution, and Environment department, explains the significance of these findings:

"Our results mean that we can now target the remaining loci on the genetic maps with deep sequencing to try and find the causal mutations within them. We are also very excited that most of the identified disease loci appear to confer risk of disease in diverse populations such as African Americans, implying our findings are likely to be universally applicable and not just confined to Europeans."

Dr. Maniatis also highlights the contribution their study brings to the research community:

"No disease with a genetic predisposition has been more intensely investigated than type 2 diabetes. We have proven the benefits of gene mapping to identify hundreds of locations where causal mutations might be across many populations, including African Americans. This provides a larger number of characterized loci for scientists to study and will allow us to build a more detailed picture of the genetic architecture of type 2 diabetes," says the lead author.

Dr. Andrew also adds, "Before we can conduct the functional studies required in order to better understand the molecular basis of this disease, we first need to identify as many plausible candidate loci as possible. Genetic maps are key to this task, by integrating the cross-platform genomic data in a biologically meaningful way."

Learn how gene discovery could yield new treatments for type 2 diabetes.

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Scientists find new genetic locations for type 2 diabetes - Medical ... - Medical News Today

The lost function of two genes prevents infant laboratory mice from developing motor skills as they mature into adults, a new study from Cincinnati Childrens Hospital Medical Center and the City University of New York School of Medicine reports. Researchers also suggest in the study that people with certain motor development disabilities be tested to see if they have altered forms of the same genes.

The study demonstrates that neural circuits between the brains motor cortex region and the spinal cord did not properly reorganize in maturing mice. The circuits are part of the cortical spinal network, which coordinates the activation of muscles in limbs.

Researchers bred the mice to lack molecular signaling from the Bax/Bak genetic pathway. Investigators demonstrated in a variety of experiments how Bax/Baks downstream molecular targets are vital to developing appropriately sophisticated connections between the motor cortex, spinal circuits and opposing extensor/flexor muscle groups in the animals.

Lead author Yutaka Yoshida, PhD, of the Division of Developmental Biology at Cincinnati Childrens, said:

If mutations in the Bax/Bak pathway are found in human patients with developmental motor disabilities, these findings could be very translational to possible medical application. Our goal is for future studies to determine whether disruptions in Bax/Bak pathway are implicated in some people with skilled motor disabilities and whether it also regulates reorganization of other circuits in the mammalian central nervous system.

The researchers stress that because the study was conducted with mice, additional research is required before it can be confirmed whether the data apply directly to human health.

Young postnatal mammals, including human babies, can perform only basic unskilled motor tasks. Citing a number of previous studies on this point, the authors of the paper write one reason for this is that infantile neural circuitry is wired to activate antagonistic (or opposing) muscles at the same time.

As humans and mammals age beyond infancy, and try repeatedly to perform skilled movements, neural circuit connections between the motor cortex of the brain and spinal cord reorganize. Connections to the spine and to opposing muscle groups become more sophisticated.

This enables antagonistic muscle pairs to be activated reciprocally when certain tasks call for it.

An estimated six percent of children worldwide suffer from developmental motor disabilities that affect skilled motor control, according to Yoshida. A significant number of these individuals maintain an immature pattern of co-activating opposite muscle pairs into adulthood, which impedes skilled movements and manual dexterity.

One lifelong disorder is dyspraxia, also called developmental coordination disorder (DCD). According to the National Institute of Neurological Disorders and Stroke, developmental dyspraxia is characterized by an impaired ability to plan and carry out sensory and motor tasks.

People with the disorder may appear out of sync with their environment and symptoms can vary, including: poor balance and coordination, clumsiness, vision problems, perception difficulties, emotional and behavioral problems, difficulty with reading, writing, and speaking, poor social skills, poor posture, and poor short-term memory.

Although people with the disorder can be of average or above average intelligence, they may move their limbs immaturely.

To explore connections between corticospinal neurons in the mouse brains motor cortex and muscles and to identify genetic pathways involved in their development scientists in the study used trans-synaptic viral and electrophysiological assays. This allowed them to observe and trace how these connections develop in maturing mice.

Yoshida and colleagues point to earlier studies showing that the initial formation of prenatal motor circuits are determined genetically by the effects of transcription factors (which turn genes on and off in a cells control center, the nucleus). This control in turn triggers molecular processes that influence the development of never fibers, which transmit impulses.

Knowledge is limited about how initial motor circuits are reorganized after birth to become more sophisticated in adulthood. Even less is known about why this organization fails to occur as mammals mature, according to the researchers.

But trans-synaptic tracing in the current study highlighted how the presence of Bax/Bak signaling resulted in sophisticated circuity as mice matured. It also triggered the development of circuits that allowed opposing muscle groups to activate reciprocally.

The absence of Bax/Bak signaling resulted in continued formation of inappropriate circuitry that did not allow reciprocal activation of these muscles.

In skilled motor tests involving adult Bax/Bak mutant mice, the animals exhibited abnormal co-activation of opposing extensor and flexor muscle pairs. Although they demonstrated normal reaching and retrieval behaviors when given mouse chow, the mice had deficits in skilled grasping.

Mice lacking the Bax/Bak pathway signaling also had difficulty with walking tests on a balance bar and metal grid as measured by the number of foot slips.

Image: Cincinnati Childrens

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Genetics May Underlie Impaired Skilled Movements - ReliaWire

Its Star Wars Day, and thats got everyone celebrating the awesome lore and amazing detail of the Star Wars universe. So, lets talk about one question thats never really been explained: How exactly does the ability to use the Force get passed on in the Star Wars universe?

Helix, a personal genomics company, hastaken a closer look at that question. And theyve used science to come up with some possibleanswers

We have theorized that based on the lineage of the Skywalker-Solo clan, theres abundant evidence that Force-sensitivity is genetic. This is due to the similarity in traits between Skywalker family members raised in isolation from one another, and in totally separate environments (with the exception of Ben Solo who was raised with his mother and trained by his uncle). Luke and Leia grew up on entirely different planets. Neither knew their father (until later in life), and Leia was raised as galactic rebel royalty, whereas Luke was a simple moisture farmer bullseyeing womp rats in his T-16.

The experts at Helix have come up with a number of other fun science-y theories about how the Force is inherited in the Star Wars universe:

Its okay if you dont understand the genetics terminology. What this actually means is that the Force is a trait which parents pass on to their kids who pass them onto their kids. You see the trait in every single generation, just like the Skywalkerfamily.

Now, without getting too technical, this is a special type of genetic mutation which can have repeating effects. In some cases, repeat mutations can increase with each generation, and when the number of repeats exceeds a certain number, resulting traits can appear. So, for example, Shmi Skywalker may have had a repeat number just below the threshold, but it expanded in Anakin to the point where it appeared as if he had suddenly inherited the Force.

Of course, Star Wars is a fantasy and science doesnt necessarily apply, especially to things as mystical as the Force. But its fun to think about.

Want to know more?Read the full story on Helix.

Would you like to be part of the Fandom team? Join our Fan Contributor Program and share your voice on Fandom.com!

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How Do the Genetics of the Force Work in Star Wars? - Fandom (blog)

What happened

Shares of genetic-testing pioneer Myriad Genetics (NASDAQ: MYGN) received a much-needed boost today, rising as much as 16%, after the company announced fiscal third-quarter 2017 financial results. The stock has witnessed a 42% decline in the last year, although it is now up roughly 28% year to date, as investors see signs of life for the company's most important revenue machine and are holding out hope for a pipeline of promising growth products.

The strong performance in the most recent quarter prompted management to raise its full-year fiscal 2017 financial guidance for revenue and narrow the range for earnings per share. As of 12:45 p.m. EDT, the stock had settled to a 15.5% gain.

Image source: Getty Images.

There were reasons for optimism and pessimism in the financial update. Consider how the most important products fared compared to last year's fiscal third quarter:

Metric

Fiscal Q3 2017

Fiscal Q3 2016

% Change

Hereditary-diagnostic-testing revenue

$140.8 million

$156.3 million

(10%)

GeneSight testing revenue

$23.9 million

N/A

N/A

Vectra DA testing revenue

$11.2 million

$12.3 million

(9%)

Prolaris testing revenue

$3.4 million

$5.2 million

(35%)

EndoPredict testing revenue

$2.3 million

$1.1 million

109%

Other revenue

$3.6 million

$2.5 million

44%

Data source: Myriad Genetics.

A 10% year-over-year drop in revenue from hereditary diagnostic testing may not seem like much reason to celebrate, but it marks the second consecutive sequential gain for Myriad Genetics after many quarters of decline. It's a silver lining investors aren't willing to overlook.

Of course, the array of promising growth products is turning in more mixed results. Products excluding GeneSight combined for a year-over-year drop in revenue of $1.7 million. In fact, if not for GeneSight, Myriad Genetics' total revenue would have declined. It's a major reason for the updated revenue guidance -- and investors should be happy to have GeneSight growing into a significant contributor to the overall business and performing well against offerings from competitors.

Metric

Fiscal Q3 2017

Fiscal Q3 2016

% Change

Total revenue

$196.9 million

$190.5 million

3%

Operating expenses

$139.7 million

$107.7 million

30%

Net income

$4.2 million

$34.5 million

(88%)

Data source: Myriad Genetics.

Efforts to rapidly scale new products and services have resulted in a large increase in operating expenses in recent quarters, eating away at net income. Last quarter was no different, but the increase in operating expenses is a necessary evil for investors looking for the company to turn the page long-term.

The company now expects full-year fiscal 2017 revenue to fall between $763 million and $765 million, compared to $754 million in fiscal 2016. Meanwhile, diluted earnings per share are expected to fall between $0.23 and $0.25, compared to $1.71 in fiscal 2016.

Investors are aware that Myriad Genetics is a company in transition, turning away from proprietary testing products (driven by price) and toward cheaper, larger-scale, and more flexible services such as GeneSight (driven by volume) that are in high demand from patients and clinicians. Viewed through that lens, there were no major surprises in the most recent quarter. The company continues to work toward its long-term goals.

10 stocks we like better than Myriad Genetics

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Here's Why Myriad Genetics Rose as Much as 16% This Morning - Madison.com

What happened

Shares of genetic-testing pioneer Myriad Genetics (NASDAQ:MYGN) received a much-needed boost today, rising as much as 16%, after the company announced fiscal third-quarter 2017 financial results. The stock has witnessed a 42% decline in the last year, although it is now up roughly 28% year to date, as investors see signs of life for the company's most important revenue machine and are holding out hope for a pipeline of promising growth products.

The strong performance in the most recent quarter prompted management to raise its full-year fiscal 2017 financial guidance for revenue and narrow the range for earnings per share. As of 12:45 p.m. EDT, the stock had settled to a 15.5% gain.

Image source: Getty Images.

There were reasons for optimism and pessimism in the financial update. Consider how the most important products fared compared to last year's fiscal third quarter:

Metric

Fiscal Q3 2017

Fiscal Q3 2016

% Change

Hereditary-diagnostic-testing revenue

$140.8 million

$156.3 million

(10%)

GeneSight testing revenue

$23.9 million

N/A

N/A

Vectra DA testing revenue

$11.2 million

$12.3 million

(9%)

Prolaris testing revenue

$3.4 million

$5.2 million

(35%)

EndoPredict testing revenue

$2.3 million

$1.1 million

109%

Other revenue

$3.6 million

$2.5 million

44%

Data source: Myriad Genetics.

A 10% year-over-year drop in revenue from hereditary diagnostic testing may not seem like much reason to celebrate, but it marks the second consecutive sequential gain for Myriad Genetics after many quarters of decline. It's a silver lining investors aren't willing to overlook.

Of course, the array of promising growth products is turning in more mixed results. Products excluding GeneSight combined for a year-over-year drop in revenue of $1.7 million. In fact, if not for GeneSight, Myriad Genetics' total revenue would have declined. It's a major reason for the updated revenue guidance -- and investors should be happy to have GeneSight growing into a significant contributor to the overall business and performing well against offerings from competitors.

Metric

Fiscal Q3 2017

Fiscal Q3 2016

% Change

Total revenue

$196.9 million

$190.5 million

3%

Operating expenses

$139.7 million

$107.7 million

30%

Net income

$4.2 million

$34.5 million

(88%)

Data source: Myriad Genetics.

Efforts to rapidly scale new products and services have resulted in a large increase in operating expenses in recent quarters, eating away at net income. Last quarter was no different, but the increase in operating expenses is a necessary evil for investors looking for the company to turn the page long-term.

The company now expects full-year fiscal 2017 revenue to fall between $763 million and $765 million, compared to $754 million in fiscal 2016. Meanwhile, diluted earnings per share are expected to fall between $0.23 and $0.25, compared to $1.71 in fiscal 2016.

Investors are aware that Myriad Genetics is a company in transition, turning away from proprietary testing products (driven by price) and toward cheaper, larger-scale, and more flexible services such as GeneSight (driven by volume) that are in high demand from patients and clinicians. Viewed through that lens, there were no major surprises in the most recent quarter. The company continues to work toward its long-term goals.

Maxx Chatsko has no position in any stocks mentioned. The Motley Fool has no position in any of the stocks mentioned. The Motley Fool has a disclosure policy.

See the original post:
Here's Why Myriad Genetics Rose as Much as 16% This Morning - Motley Fool

May 3, 2017 Western spotted skunk. Credit: Robby Heischman.

Climate plays a key role in determining what animals can live where. And while human-induced climate change has been causing major problems for wildlife as of late, changes in the Earth's climate have impacted evolution for millions of yearsoffering tantalizing clues into how to protect animals facing climate change today. In a new paper in Ecology and Evolution, scientists have delved into the effects of Ice Age climate change upon the evolution of tiny, hand-standing skunks.

"By analyzing western spotted skunk DNA, we learned that Ice Age climate change played a crucial role in their evolution," says lead author Adam Ferguson, Collections Manager of Mammals at The Field Museum in Chicago and affiliate of Texas Tech University. "Over the past million years, changing climates isolated groups of spotted skunks in regions with suitable abiotic conditions, giving rise to genetic sub-divisions that we still see today."

Western spotted skunks are really stinkin' cute at two pounds, they're smaller than the striped Pepe Le Pew variety, their coats are an almost maze-like pattern of black and white swirls, and when they spray, they often do a hand-stand, hind legs and fluffy tail in the air as they unleash smelly chemicals to ward off predators. They're found throughout the Western US and Mexico, in a wide variety of climates they thrive everywhere from Oregon's temperate rainforests to the Sonoran, the hottest desert in Mexico.

There are three genetic sub-groups, called clades, of western spotted skunks. Often, clades develop when a species is split up by geography. If a species is separated by, say, a mountain range, the groups on either side of the mountain may wind up splitting off from each other genetically. However, the division of the skunks into three clades doesn't seem to have been driven solely by geographical barriers populations separated by mountains are more or less genetically identical. Instead, the skunks vary genetically from one historic climate region to another, due to Ice Age climate change.

"Western spotted skunks have been around for a million years, since the Pleistocene Ice Age," explains Ferguson. "During the Ice Age, western North America was mostly covered by glaciers, and there were patches of suitable climates for the skunks separated by patches of unsuitable climates. These regions are called climate refugia. When we analyzed the DNA of spotted skunks living today, we found three groups that correspond to three different climate refugia."

"That means that for spotted skunk evolution, climate change appears to have been a more important factor than geographical barriers," says Ferguson.

In the study, scientists used DNA samples from 97 skunks from a variety of regions and climates in the American Southwest. Upon sequencing the DNA, the scientists were surprised to see that the skunks split into three clades based on pockets of suitable climate present during the Pleistocene.

"Small carnivores like skunks haven't been well-studied when it comes to historical climate change," says Ferguson. "We know how small mammals like rodents respond to changing climates, and we know how bigger carnivores like wolves respond, but this study helps bridge the gap between them."

Ferguson also notes that skunks don't deserve the bad rap they get. "Skunks are a really interesting family of North American carnivores they're well-known, but not well-studied. And studying them comes with a cost they stink, even their tissues stink, and you run the risk of getting sprayed. But they're important to their ecosystems for example, they eat insects and rodents that damage our crops," he says.

Moreover, Ferguson says, the study can illuminate the bigger picture of biodiversity in the face of climate change an issue that grows increasingly relevant as human-driven climate change affects more and more of the world's animals.

"What we know about the past can inform what we expect to see in the future," says Ferguson. "Understanding these genetic subdivisions that happened as a result of changing climatic conditions can help us conserve skunks and other animals in the future."

Before working at The Field Museum, Adam Ferguson was affiliated with Texas Tech University and completed this research there. Ferguson's co-authors are affiliated with Angelo State University, the National Museum of Natural History, the National Zoological Park, the US Fish and Wildlife Service, and the University of New Mexico.

Explore further: Study finds climate, landscape changes may lead to more rabid skunks

Journal reference: Ecology and Evolution

Provided by: Field Museum

While striped skunks already have a nose-worthy reputation for being avoided, new research at the Kansas State University College of Veterinary Medicine finds they carry a serious health threat for humans and animals: rabies.

A fascinating new study in the January/February 2007 issue of Physiological and Biochemical Zoology looks at the benefits of huddling vs. solitude, comparing strategies used by striped skunks to get through long, cold winters ...

Predators with experience of skunks avoid them both because of their black-and-white coloration and their distinctive body shape, according to UC Davis wildlife researcher Jennifer Hunter. The study was published online Oct. ...

A government wildlife researcher has found that rabbits and skunks can become infected with the bird flu virus and shed it enough to infect ducksoffering scientists one more clue about how bird flu may move in the environment ...

New research by University of Montana forest landscape ecology Professor Solomon Dobrowski shows that organisms will face more hardships as they relocate when climate change makes their current homes uninhabitable.

Skunks are very common throughout much of the United States. Their scent glands, located near the tail, serve as the primary defense for these nocturnal animals. Although online sources associate "skunking" with a variety ...

For Indian jumping ants (Harpegnathos saltator), becoming royalty is all about timing.

Researchers from the University of Bristol have discovered that some fish within a shoal take on the responsibilities of leader when they are under threat from predators.

Within a group of meerkats, call patterns vary with factors including sex, rank and reproductive seasonbut not with stress hormones, according to a study published May 3, 2017 in the open-access journal PLOS ONE by Jelena ...

Female Drosophila buzzatii cluster fruit flies may be drawn to the specific courtship songs of males of their own species, according to a study published May 3, 2017 in the open-access journal PLOS ONE by Patricia Iglesias ...

Climate plays a key role in determining what animals can live where. And while human-induced climate change has been causing major problems for wildlife as of late, changes in the Earth's climate have impacted evolution for ...

Research by wildlife biologists from Clemson University and the Tom Yawkey Wildlife Center near Georgetown is shattering conventional scientific understanding about American alligator growth and reproduction.

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Ice Age climate change played a bigger role in skunk genetics than ... - Phys.Org

Newswise The Harvard Medical School-based Personal Genetics Education Project (pgEd.org) and the Sanford Program for the Midwest Initiative in Science Exploration (PROMISE) at Sanford Research have teamed to bring the latest developments in genetics into classrooms and communities in Massachusetts and South Dakota.

The Building Awareness, Respect and Confidence through Genetics project, or ARC, is part of pgEds broader initiative to engage high school students and the general public in conversations about the benefits and implications of advances in personal genetics. The Sanford PROMISE will contribute experience and expertise in biomedical science education programming in the northern Plains and extend the project into rural America.

The ARC project, which is supported by a five-year Science Education Partnership Award from the National Institutes of Health, includes creating curriculum and rolling out new and existing curriculum to teachers.

Given where genetic technologies are heading, its now more important than ever to be discussing the possibilities for improving our health and wrestling with the implications of knowing more about our genetic make-up, said Marnie Gelbart, ARC principal investigator and director of programs at pgEd. ARC is a project that sees opportunities for talking about genetics in many settings and relies on the expertise of and collaboration with teachers to bring these conversations into classrooms, schools, and communities.

The curriculum is transdisciplinary and focuses on genetics, identity and diversity through topics such as gender, race, behavior and genome editing. The first module on genome editing was released in February. Additional modules will be released as the grant progresses.

These topics are making their way into workshops for educators, particularly those teaching in middle schools, high schools, colleges and universities.

ARC hopes to empower teachers across all disciplines to stimulate dialogue about personal genetics, said David Pearce, executive vice president of Sanford Research. It has become increasingly important that we all, regardless of status or education background, better understand the benefits and implications the human genome has and will have in their everyday lives.

In the first year of the program, pgEd held a three-day workshop titled Genetics and Social Justice at Harvard Medical School that attracted nearly 50 educators from across the nation. This group included teachers from Brockton High School in Brockton, Mass., (Jonathan Shapiro, science chair, and David Mangus, science) and Harrisburg High School in Harrisburg, S.D. (Lisa Cardillo, science, and Colby Peterson, social studies).

Working with these four lead teachers, pgEd and The Sanford PROMISE are paving the way for future workshops and community events. In April, the pgEd team visited Harrisburg High School for a community experience, and the team will host professional development workshops in Brockton, Mass., in June 2017 and Sioux Falls, S.D., in summer 2018. This summer, two rural high school educators from South Dakota will travel to Brockton with The Sanford PROMISE and work together with the Harrisburg teachers to help bring awareness of genetics to other South Dakota educators.

About Sanford Health Sanford Health is an integrated health system headquartered in the Dakotas. It is one of the largest health systems in the nation with 45 hospitals and nearly 300 clinics in nine states and four countries. Sanford Healths 28,000 employees, including more than 1,300 physicians, make it the largest employer in the Dakotas. Nearly $1 billion in gifts from philanthropist Denny Sanford have allowed for several initiatives, including global children's clinics, genomic medicine and specialized centers researching cures for type 1 diabetes, breast cancer and other diseases. For more information, visit sanfordhealth.org.

About pgEd

The mission of the Personal Genetics Education Project (pgEd.org) is to raise awareness and spark conversation about the benefits as well as the ethical, legal, and social implications of genetic information. We aim to be inclusive of all voices in these discussions,regardless of socioeconomic or educational background, cultural or religious affiliation, and ethnic or personal identity. Founded in 2006, pgEds efforts include providing online curricula, organizing workshops for professionals, holding congressional briefings in Washington, D.C, engaging producers and writers of film and television, convening conferences, supporting an online learning tool (Map-Ed.org), collaborating with museums and libraries, and partnering with communities of faith.

This projectissupported by the National Institutes of Health under grant number R25OD021895. The content is solely the responsibility of the authors anddoes not necessarily represent the official views of the National Institutes of Health.

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Harvard Medical School, Sanford Research to Engage Classrooms and Communities Through Genetics - Newswise (press release)