Throughout human existence it has been our nature to push the envelope. More speed. More power. More performance. Ingenuity combined with trial and error spawn new peaks in technology.

As we strive to stay ahead of the technological advancement curve, we sometimes forget about the interconnected systems that might need time and adjustment to catch up. Too much torque and the transmissions or drivelines wear out easily. Increases in output translate into greater input requirements and higher priced fuels. At some point, the law of diminishing returns kicks in, making that next increase to performance or production too costly and economically inefficient. Much of the same can be said of beef genetics.

It is amazing how much progress our industry has made in genomics in such little time. Genetic improvement is absolutely vital for every segment of our industry because it helps promote multiple elements linked to sustainability. However, producers need to be mindful of the inevitable trade-off that comes with a rapidly accelerated discovery curve.

Decades ago, the push for performance was inadvertently tied to frame. Mature size and calving difficulties almost singlehandedly devastated the marketability of many breeds. Though unintended, the consequences were still significant. It is no different than the push for muscle cars with powerful stances and large throaty motors that also guzzled fuel by the gallon.

Oddly enough, we have corrected cow size, yet cow maintenance or input cost remains a common issue. If you install a high performance racing engine in a car, it will require a grade of fuel of equal magnitude to perform up to its potential. Cheap, poor quality fuels simply wont do. The same is true for your cowherd. If you continue to select for growth and milk genetics, be prepared to adjust the feed input requirements that will follow. Our push to discover that next elite genetic package is changing the beef herd from independent foragers to concentrate dependents.

There are other phenotypic systems that desperately need to catch up with a hastily advancing genotype population. Evidence of this can be seen in the national beef herd by simply looking at their feet. The push to discover cattle that can be marketed as the next top genetic package for extreme calving ease, growth and marbling, is creating a significant gap in animal soundness.

Unintended consequences, arise under the strain of scientific and economic achievement. It will take time and discipline to bring traits like soundness up to speed.

I am by no means making an argument against genetic advancement. On the contrary, I am a firm believer in improvement and making wise use of all genetic selection tools. I simply see the road to change is not straight and narrow. It winds and turns with plenty of peaks and valleys, as well as, the occasional switch back. As a breeder, you need to understand the trade-offs that come with accelerated genetic selection. Can you afford to add that next unit of performance or milk? Or, should you keep pace just behind the curve and capture value as the rest of the systems catch up?

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Jared Wareham; The Genetic Paradox - CattleNetwork.com

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BRIEF-Interleukin Genetics to explore strategic alternatives, reduce workforce - Reuters

When Daniel Benjamin was just beginning his PhD program in economics in 2001, he attended a conference with his graduate school advisers. They took in a presentation on neuroeconomics, a nascent field dealing with how the human brain goes about making decisions.

Afterward, as they took a stroll outside, they couldnt stop talking about what they had learned, how novel and intriguing it was. What would be next, they wondered. What would come after neuroeconomics?

The human genome project had just been completed, and we decided that even more fundamental than the brain would be genes, and that someday this was going to matter a lot for social science, said Benjamin, associate professor (research) of economics at the USC Dornsife College of Letters, Arts and Sciences Center for Economic and Social Research (CESR). Indeed, his excitement that day was the foundation of a visionary academic path.

Fast forward to today. Genoeconomics is now an emerging area of social science that incorporates genetic data into the work that economists do. Its based on the idea that a persons particular combination of genes is related to economic behavior and life outcomes such as educational attainment, fertility, obesity and subjective well-being.

Theres this rich new source of data that has only become available recently, said Benjamin, also co-director of the Social Science Genetic Association Consortium, which brings about cooperation among medical researchers, geneticists and social scientists.

Collecting genetic data and creating the large data sets used by economists and other social scientists have become increasingly affordable, and new analytical methods are getting more and more powerful as these data sets continue to grow. The big challenge, he said, is figuring out how scientists can leverage this new data to address a host of important policy questions.

Were ultimately interested in understanding how genes and environments interact to produce the kinds of outcomes people have in their lives, and then what kinds of policies can help people do better. That is really what economics is about and were trying to use genetics to do even better economics.

Only a handful of economists are working with genetics, but this brand of research is perfectly at home at CESR. The center, founded three years ago, was conceived as a place where visionary social science could thrive and where research could be done differently than in the past.

Being in a place where thats the shared vision is pretty rare, said econometrician Arie Kapteyn, professor (research) of economics and CESR director. Theres no restriction on which way you want to go or what you want to do. It doesnt mean that there are no restrictions on resources, but its the opportunity to think about your vision of whats really exciting in social science research. Then being able to actually implement it is absolutely fantastic.

The mission of CESR is discovering how people around the world live, think, interact, age and make important decisions. The centers researchers are dedicated to innovation and combining their analysis to deepen the understanding of human behavior in a variety of economic and social contexts.

What we try to do is mold a disciplinary science in a very broad sense, Kapteyn said. Because todays problems in society, theyre really all multidisciplinary.

Case in point: Benjamins work combining genetics and economics.

The flagship research effort for Benjamins CESR research group deals with genes and education. In a 2016 study, the team identified variants in 74 genes that are associated with educational attainment. In other words, people who carry more of these variants, on average, complete more years of formal schooling.

Benjamin hopes to use this data in a holistic way to create a predictive tool.

Were also creating methods for combining the information in a persons entire genome into a single variable that can be used to partially predict how much education a persons going to get.

Daniel Benjamin

Rather than just identifying specific genes, he said, were also creating methods for combining the information in a persons entire genome into a single variable that can be used to partially predict how much education a persons going to get.

The young field of genoeconomics is still somewhat controversial, and Benjamin is careful to point out that individual genes dont determine behavior or outcome.

The effect of any individual gene on behavior is extremely small, Benjamin explained, but the effects of all the genes combined on almost any behavior were interested in is much more substantial. Its the combined information of many genes that has predictive power, and that can be most useful for social scientists.

While the cohort of researchers actively using the available genome-wide data in this way is still somewhat limited, Benjamin says it is growing quickly.

I think across the social sciences, researchers are seeing the potential for the data, and people are starting to use it in their work and getting excited about it, but right now its still a small band of us trying to lay the foundations.

Were putting together huge data sets of hundreds of thousands of people approaching a million people in our ongoing work on educational attainment because you need those really big sample sizes to accurately detect the genetic influences.

As CESR works to improve social welfare by informing and influencing decision-making in the public and private sectors, big data such as Benjamins is a growing part of that process, according to Kapteyn.

What big data reflects is the fact that nowadays there are so many other ways in which we can learn about behavior, he said. As a result, I think well see many more breakthroughs and gain a much better understanding of whats going on in the world and in social science than in the past.

I think were really at the beginning of something pretty spectacular. What we are doing is really only scratching the surface theres so much more that can be done.

More stories about: Big Data, Economics, Research

Report comes as the university nears the opening of USC Village, the largest economic development project in the history of South Los Angeles.

The USC Dornsife Economics Department launches the USC Economics Review to spotlight students research.

The program at USC Dornsife offers tailored training in preparation for Fall Career Fair.

Conference covers methods of prompting change in human behavior for the public good.

Continued here:
Can genetics play a role in education and well-being? - USC News

TOKYO Japanese office equipment maker Konica Minolta Inc (4902.T) plans to acquire U.S. healthcare firm Ambry Genetics Corp to diversify its business, the Nikkei daily reported on Sunday.

The acquisition will likely cost around 100 billion yen ($890 million) and be Konica Minolta's most expensive, reflecting its ambition to branch out into healthcare as its printer business slows, the business daily reported without citing sources.

Konica Minolta will partner semi-government fund Innovation Network Corp of Japan (INCJ) to buy all shares of Ambry, a private firm that uses genetic data to screen for cancer, the Nikkei said.

Konica Minolta will own 60 percent of Ambry and INCJ the remainder, the newspaper reported.

Konica Minolta told Reuters nothing has been decided at this stage. INCJ did not respond to Reuters' requests for comment.

(Reporting by Leika Kihara; Editing by Christopher Cushing)

FRANKFURT German discount grocery chain Aldi North is planning to spend more than 5 billion euros ($5.71 billion) to revamp its stores around the world, which would be its biggest investment project ever, German weekly Bild am Sonntag reported, citing company sources.

JERUSALEM Flag carrier El Al Israel Airlines said on Sunday its board approved a plan by its Sun d'Or unit to buy smaller rival Israir from IDB Tourism.

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Japan's Konica Minolta plans to buy US cancer test firm: Nikkei - Reuters

Accelerated Genetics and Select Sires Inc. will be a merged cooperative.

According to a news release, the merger follows a June 22 vote by Accelerate Genetics officials. The vote green-lights an agreement recommended by both companies boards of directors. The smaller Accelerated Genetics has reported financial difficulty in the past. The larger Ohio-based Select Sires will acquire Accelerated Genetics assets, including a bull farm in Westby.

Both companies specialize in artificial insemination of cattle. The companies have an established working relationship that started in 2001 when the companies allied in international markets.

Accelerated Genetics has been searching for a partner who could enhance the business and move it forward, said Scott Dahlk, Accelerated Genetics Board chairman. Joining forces with Select Sires is a positive move for both the member-owners and producers worldwide.

The company said Accelerated Genetics assets, employees and sales representatives will be integrated into the organization. Both companies operate under the cooperative-business model and share similar structures, according to the company.

By working together we will be stronger, said David Thorbahn, Select Sires president and chief executive officer. The value and expertise gained by joining the people from both organizations allow us to offer our customers a broader genetics program in addition to an outstanding animal health product line. Its very exciting to work together, enabling our organizations the ability to expand genetic research, technical support, service, and programs with people who are passionate about the dairy and beef industries.

Link:
After vote, Accelerated Genetics slated to merge - La Crosse Tribune

Myriad Genetics, Inc.'s (NASDAQ: MYGN) strong run has caught investors attentions, however, JPMorgan analyst Tycho Peterson still doesn't see the stock being able to offset a decline in the hereditary cancer business.

Peterson maintained his Underweight rating and $16 price target.

While in the past, the esoteric LDT market was viewed as sitting at the nexus of the secular shift in healthcare towards personalized medicine, this vision has, in our view, run up against the reality that the LDT business model has a number of challenges, with many labs attempting to support a pharma model centered around heavy rep counts without the benefit of patent protection, Peterson said.

While Peterson expects the stock to fall to $16 - it trades around $25.60 per share - he noted the stock could still move in either direction.

Myriad represents, in our view, a significant opportunity, given near-term catalysts that could drive the stock meaningfully higher or lower, with the setting of FY18 guidance during F4Q earnings (including forward expectations for hereditary cancer) being the most significant upcoming event post-UNH renewal, he said.

However, with its core business in (arguably) structural decline and pipeline that could be long on potential, but short on near-term financial impact, Myriad is not an easy company to value. While we believe the pipeline is intriguing, we do not believe that it can offset what we expect to be a continued steady decline in the core hereditary cancer business.

View More Analyst Ratings for MYGN View the Latest Analyst Ratings

Posted-In: JPMorgan Tycho PetersonAnalyst Color Reiteration Analyst Ratings

2017 Benzinga.com. Benzinga does not provide investment advice. All rights reserved.

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JPMorgan Checks In On Myriad Genetics Following 30% Rally - Benzinga

June 28, 2017

While the definitive causes remain unclear, several genetic and environmental factors increase the likelihood of autism spectrum disorder, or ASD, a group of conditions covering a "spectrum" of symptoms, skills and levels of disability.

Taking advantage of advances in genetic technologies, researchers led by Alex Nord, assistant professor of neurobiology, physiology and behavior with the Center for Neuroscience at the University of California, Davis, are gaining a better understanding of the role played by a specific gene involved in autism. The collaborative work appears June 26 in the journal Nature Neuroscience.

"For years, the targets of drug discovery and treatment have been based on an unknown black box of what's happening in the brain," said Nord. "Now, using genetic approaches to study the impact of specific mutations found in cases, we're trying to build a cohesive model that links genetic control of brain development with behavior and brain function."

The Nord laboratory studies how the genome encodes brain development and function, with a particular interest in understanding the genetic basis of neurological disorders.

Mouse brain models

There is no known specific genetic cause for most cases of autism, but many different genes have been linked to the disorder. In rare, specific cases of people with ASD, one copy of a gene called CHD8 is mutated and loses function. The CHD8 gene encodes a protein responsible for packaging DNA in cells throughout the body. Packaging of DNA controls how genes are turned on and off in cells during development.

Because mice and humans share on average 85 percent of similarly coded genes, mice can be used as a model to study how genetic mutations impact brain development. Changes in mouse DNA mimic changes in human DNA and vice-versa. In addition, mice exhibit behaviors that can be used as models for exploring human behavior.

Nord's laboratory at UC Davis and his collaborators have been working to characterize changes in brain development and behavior of mice carrying a mutated copy of CHD8.

"Behavioral tests with mice give us information about sociability, anxiety and cognition. From there, we can examine changes at the anatomical and cellular level to find links across dimensions," said Nord. "This is critical to understanding the biology of disorders like autism."

By inducing mutation of the CHD8 gene in mice and studying their brain development, Nord and his team have established that the mice experience cognitive impairment and have increased brain volume. Both conditions are also present in individuals with a mutated CHD8 gene.

New implications for early and lifelong brain development

Analysis of data from mouse brains reveals that CHD8 gene expression peaks during the early stages of brain development. Mutations in CHD8 lead to excessive production of dividing cells in the brain, as well as megalencephaly, an enlarged brain condition common in individuals with ASD. These findings suggest the developmental causes of increased brain size.

More surprisingly, Nord also discovered that the pathological changes in gene expression in the brains of mice with a mutated CHD8 continued through the lifetime of the mice. Genes involved in critical biological processes like synapse function were impacted by the CHD8 mutation. This suggests that CHD8 plays a role in brain function throughout life and may affect more than early brain development in autistic individuals.

While Nord's research centers on severe ASD conditions, the lessons learned may eventually help explain many cases along the autism spectrum.

Collaborating to improve understanding

Nord's work bridges disciplines and has incorporated diverse collaborators. The genetic mouse model was developed at Lawrence Berkeley National Laboratory using CRISPR editing technology, and co-authors Jacqueline Crawley and Jill Silverman of the UC Davis MIND Institute evaluated mouse behavior to characterize social interactions and cognitive impairments.

Nord also partnered with co-author Konstantinos Zarbalis of the Institute for Pediatric Regenerative Medicine at UC Davis to examine changes in cell proliferation in the brains of mice with the CHD8 mutation, and with Jason Lerch from the Mouse Imaging Centre at the Hospital for Sick Children in Toronto, Canada, to conduct magnetic resonance imaging on mouse brains.

"It's the act of collaboration that I find really satisfying," Nord said. "The science gets a lot more interesting and powerful when we combine different approaches. Together we were able to show that mutation to CHD8 causes changes to brain development, which in turn alters brain anatomy, function and behavior."

In the future, Nord hopes to identify how CHD8 packages DNA in neural cells and to determine the specific impacts to early brain development and synaptic function. Nord hopes that deep exploration of CHD8 mutations will ultimately yield greater knowledge of the general factors contributing to ASD and intellectual disability.

Read more from the original source:
Mouse brain models reveal insights into genetics of autism - News-Medical.net

Martin Ogando and his 91-year-old grandmother, Delia Giovanola, flip through a stack of photos until they reach an image of a man Ogando never saw in life: his father.

The two share similar skin tone and blue eyes products of the same genetics that finally allowed Ogando to discover his birth identity through DNA tests in November 2015.

The tests showed that he's the biological son of Jorge Ogando and Stella Maris Montesano, a child born in captivity in a clandestine detention center and taken away from parents who were forcibly disappeared in 1976 during Argentina's dictatorship.

"I found out the truth about my life," Ogando said of the tests that also reunited him with his grandmother. "A beautiful, but heavy truth."

During the 1976-1983 dictatorship, Argentina's military rulers systematically stole babies born to political prisoners, most of whom were then killed. Some 30,000 people died or were disappeared for political reasons during the dictatorship, according to human rights groups.

The search for those children spearheaded by the Grandmothers of Plaza de Mayo human rights group, led to breakthrough advancements in DNA identification.

The group emerged from gatherings of grandmothers who marched every week in front of the main square in Buenos Aires to demand the missing children. They also traveled around the globe in search of experts to find out if it was possible to determine the parenthood of the stolen babies, perhaps from blood samples.

"What were we supposed to do?" said Giovanola, one of the founders of the Grandmothers group. "Blood from whom? First we needed to find the baby. And then, the problem was that we lacked the blood samples from the parents. That's why the whole family on the mother and the father's side began to give blood."

The Grandmothers turned for help to U.S. geneticist Mary-Claire King, who in 1984 worked with Argentine colleagues to identify by genetic analysis the first confirmed stolen child. She later developed a system using mitochondrial DNA, which is inherited only from mothers, to identify individuals.

That led officials in the post-dictatorship era with strong prodding from the Grandmothers to pass a law formally creating Argentina's National Genetics Bank, the first of its kind in the world, which is now celebrating its 30th anniversary.

The institution's head, Mariana Herrera, noted that the institution was created by the government to solve crimes committed by the state itself. "There's nowhere else where this has turned into a policy to repair human rights abuses," she said.

The bank contains a database of blood samples collected from families searching for kidnapped children as well as adults who suspect they might have been stolen as infants.

To date, 122 cases of stolen children have been resolved most by the Genetics Bank but several hundred remain unaccounted for.

The bank has become a world authority in the matter, helping Colombia, Peru and El Salvador find the disappeared from their own conflicts. It's also provided information to the group Bring Back Our Girls of Nigeria, which has been hunting for the children stolen by the militant Islamist group Boko Haram.

The 40-year-old Ogando, a Doral, Florida, resident who was known for most of his life as Diego Berestycki, contacted the Grandmothers and carried out the test after the man who raised him died.

"I would have loved to have met my parents. From what my grandma tells me, I looked a lot like my dad. I even walked like him," Ogando said.

Continued here:
Genetic bank that ID's Argentina's stolen babies turns 30 - ABC News - ABC News

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Researchers have known that genes contribute to autism since the 1970s, when a team found that identical twins often share the condition. Since then, scientists have been racking up potential genetic culprits in autism, a process that DNA-decoding technologies have accelerated in the past decade.

As this work has progressed, scientists have unearthed a variety of types of genetic changes that can underlie autism. The more scientists dig into DNA, the more intricate its contribution to autism seems to be.

Since the first autism twin study in 1977, several teams have compared autism rates in twins and shown that autism is highly heritable. When one identical twin has autism, there is about an 80 percent chance that the other twin has it too. The corresponding rate for fraternal twins is around 40 percent.

However, genetics clearly does not account for all autism risk. Environmental factors also contribute to the condition although researchers disagree on the relative contributions of genes and environment. Some environmental risk factors for autism, such as exposure to a maternal immune response in the womb or complications during birth, may work with genetic factors to produce autism or intensify its features.

Genetics in motion: The secret to understanding autism lies largely in our DNA.

Not really. There are several conditions associated with autism that stem from mutations in a single gene, including fragile X and Rett syndromes. But less than 1 percent of non-syndromic cases of autism stem from mutations in any single gene. So far, at least, there is no such thing as an autism gene meaning that no gene is consistently mutated in every person with autism. There also does not seem to be any gene that causes autism every time it is mutated.

Still, the list of genes implicated in autism is growing. Researchers have tallied 65 genes they consider strongly linked to autism, and more than 200 others that have weaker ties. Many of these genes are important for communication between neurons or control the expression of other genes.

Changes, or mutations, in the DNA of these genes can lead to autism. Some mutations affect a single DNA base pair, or letter. In fact, everyone has thousands of these genetic variants. A variant that is found in 1 percent or more of the population is considered common and is called a single nucleotide polymorphism, or SNP.

Common variants typically have subtle effects and may work together to contribute to autism. Rare variants, which are found in less than 1 percent of people, tend to have stronger effects. Many of the mutations linked to autism so far have been rare. It is significantly more difficult to find common variants for autism risk, although some studies are underway.

Other changes, known as copy number variations (CNVs), show up as deletions or duplications of long stretches of DNA and often include many genes.

But mutations that contribute to autism are probably not all in genes, which make up less than 2 percent of the genome. Researchers are trying to wade into the remaining 98 percent of the genome to look for irregularities associated with autism. So far, these regions are poorly understood.

No. At the molecular level, the effects of mutations may differ, even among SNPs. Mutations can be either harmful or benign, depending on how much they alter the corresponding proteins function. A missense mutation, for example, swaps one amino acid in the protein for another. If the substitution doesnt significantly change the protein, it is likely to be benign. A nonsense mutation, on the other hand, inserts a stop sign within a gene, causing protein production to halt prematurely. The resulting protein is too short and functions poorly, if at all.

Most mutations are inherited from parents, and they can be common or rare. Mutations can also arise spontaneously in an egg or sperm, and so are found only in the child and not in her parents. Researchers can find these rare de novo mutations by comparing the DNA sequences of people who have autism with those of their unaffected family members. Spontaneous mutations that arise after conception are usually mosaic, meaning they affect only some of the cells in the body.

Perhaps. Girls with autism seem to have more mutations than do boys with the condition. And boys with autism sometimes inherit their mutations from unaffected mothers. Together, these results suggest that girls may be somehow resistant to mutations that contribute to autism and need a bigger genetic hit to have the condition.

Clinicians routinely screen the chromosomes of a developing baby to identify large chromosomal abnormalities, including CNVs. There are prenatal genetic tests for some syndromes associated with autism, such as fragile X syndrome. But even if a developing baby has these rare mutations, there is no way to know for sure whether he will later be diagnosed with autism.

Read this article:
Autism genetics, explained - Spectrum

June 27, 2017 by David Slipher In this mouse cortex, a mutation in the CHD8 gene caused increased brain size, or megalencephaly, a condition also present in people with autism spectrum disorder. The colored sections correspond to different layers of the developing cortex. Credit: Alex Nord/UC Davis

While the definitive causes remain unclear, several genetic and environmental factors increase the likelihood of autism spectrum disorder, or ASD, a group of conditions covering a "spectrum" of symptoms, skills and levels of disability.

Taking advantage of advances in genetic technologies, researchers led by Alex Nord, assistant professor of neurobiology, physiology and behavior with the Center for Neuroscience at the University of California, Davis, are gaining a better understanding of the role played by a specific gene involved in autism. The collaborative work appears June 26 in the journal Nature Neuroscience.

"For years, the targets of drug discovery and treatment have been based on an unknown black box of what's happening in the brain," said Nord. "Now, using genetic approaches to study the impact of specific mutations found in cases, we're trying to build a cohesive model that links genetic control of brain development with behavior and brain function."

The Nord laboratory studies how the genome encodes brain development and function, with a particular interest in understanding the genetic basis of neurological disorders.

Mouse brain models

There is no known specific genetic cause for most cases of autism, but many different genes have been linked to the disorder. In rare, specific cases of people with ASD, one copy of a gene called CHD8 is mutated and loses function. The CHD8 gene encodes a protein responsible for packaging DNA in cells throughout the body. Packaging of DNA controls how genes are turned on and off in cells during development.

Because mice and humans share on average 85 percent of similarly coded genes, mice can be used as a model to study how genetic mutations impact brain development. Changes in mouse DNA mimic changes in human DNA and vice-versa. In addition, mice exhibit behaviors that can be used as models for exploring human behavior.

Nord's laboratory at UC Davis and his collaborators have been working to characterize changes in brain development and behavior of mice carrying a mutated copy of CHD8.

"Behavioral tests with mice give us information about sociability, anxiety and cognition. From there, we can examine changes at the anatomical and cellular level to find links across dimensions," said Nord. "This is critical to understanding the biology of disorders like autism."

By inducing mutation of the CHD8 gene in mice and studying their brain development, Nord and his team have established that the mice experience cognitive impairment and have increased brain volume. Both conditions are also present in individuals with a mutated CHD8 gene.

New implications for early and lifelong brain development

Analysis of data from mouse brains reveals that CHD8 gene expression peaks during the early stages of brain development. Mutations in CHD8 lead to excessive production of dividing cells in the brain, as well as megalencephaly, an enlarged brain condition common in individuals with ASD. These findings suggest the developmental causes of increased brain size.

More surprisingly, Nord also discovered that the pathological changes in gene expression in the brains of mice with a mutated CHD8 continued through the lifetime of the mice. Genes involved in critical biological processes like synapse function were impacted by the CHD8 mutation. This suggests that CHD8 plays a role in brain function throughout life and may affect more than early brain development in autistic individuals.

While Nord's research centers on severe ASD conditions, the lessons learned may eventually help explain many cases along the autism spectrum.

Collaborating to improve understanding

Nord's work bridges disciplines and has incorporated diverse collaborators. The genetic mouse model was developed at Lawrence Berkeley National Laboratory using CRISPR editing technology, and co-authors Jacqueline Crawley and Jill Silverman of the UC Davis MIND Institute evaluated mouse behavior to characterize social interactions and cognitive impairments.

Nord also partnered with co-author Konstantinos Zarbalis of the Institute for Pediatric Regenerative Medicine at UC Davis to examine changes in cell proliferation in the brains of mice with the CHD8 mutation, and with Jason Lerch from the Mouse Imaging Centre at the Hospital for Sick Children in Toronto, Canada, to conduct magnetic resonance imaging on mouse brains.

"It's the act of collaboration that I find really satisfying," Nord said. "The science gets a lot more interesting and powerful when we combine different approaches. Together we were able to show that mutation to CHD8 causes changes to brain development, which in turn alters brain anatomy, function and behavior."

In the future, Nord hopes to identify how CHD8 packages DNA in neural cells and to determine the specific impacts to early brain development and synaptic function. Nord hopes that deep exploration of CHD8 mutations will ultimately yield greater knowledge of the general factors contributing to ASD and intellectual disability.

Explore further: Study shows connection between key autism risk genes in the human brain

More information: Andrea L Gompers et al. Germline Chd8 haploinsufficiency alters brain development in mouse, Nature Neuroscience (2017). DOI: 10.1038/nn.4592

Journal reference: Nature Neuroscience

Provided by: UC Davis

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Mice provide insight into genetics of autism spectrum disorders - Medical Xpress