TAG: "Genetics"

UCLA awarded $7M to unravel mystery genetic diseases


One of six institutions chosen by NIH to help tackle the most difficult-to-solve medical cases.

The David Geffen School of Medicine at UCLA is one of six institutions nationwide chosen by the National Institutes of Health to join the agency’s efforts to tackle the most difficult-to-solve medical cases and develop ways to diagnose rare genetic disorders.

Part of a $120 million initiative called the Undiagnosed Diseases Network, the $7.2 million grant to UCLA will support comprehensive “bedside-to-bench” clinical research to aid physicians in their efforts to give long-sought answers to patients living with mystery diseases.

“Undiagnosed diseases take a huge toll on patients, their families and the health care system,” said Katrina Dipple, a co-principal investigator on the UCLA grant with Stanley Nelson, Christina Palmer and Eric Vilain. “This funding will accelerate and expand our clinical genomics program, enabling us to quickly give patients a firm diagnosis and clarify the best way to treat them.”

Despite extensive clinical testing by skilled physicians, some diseases remain unrecognized because they are extremely rare, underreported or atypical forms of more common diseases. An interdisciplinary team of geneticists at each Undiagnosed Diseases Network site will examine and study patients with prolonged undiagnosed diseases.

“A vast number of children and adults suffer from severe, often fatal, undiagnosed disorders,” Vilain said. “This program will enable us to discover new genes causing ultra-rare medical conditions and to identify environmental factors that lead to disease or that interact with genes to cause disease.”

Patients will undergo an intensive weeklong clinical assessment that includes a clinical evaluation, consultations with specialists, and medical tests, including genome sequencing to identify genetic mutations. The team will also evaluate the impact on patients and families of genetic counseling and genomic test results to develop best practices for conveying this information.

The Undiagnosed Diseases Network capitalizes on the strengths of UCLA’s genetic medicine program, particularly its Clinical Genomics Center, which utilizes powerful sequencing technology to diagnose rare genetic disorders. Using a simple blood sample from a patient and both parents, the center can perform a test that simultaneously searches 37 million base pairs in 20,000 genes to pinpoint the single DNA change responsible for causing a patient’s disease. To date, a specific genetic explanation has been identified in a quarter of the cases evaluated with this test, as have a number of novel disease-causing genes.

UCLA is the only facility in the western U.S. and one of only three nationwide with a laboratory that can perform genomic sequence directly usable for patient care, and the university’s Medical Genetics Clinic cares for more than 750 new patients a year and offers comprehensive pre- and post-test genetic counseling.

All patient studies will take place at UCLA’s Westwood campus, at the Clinical and Translational Research Center of the Clinical and Translational Science Institute. Network investigators will share genomic and clinical data gleaned from patients with their research colleagues nationwide to enhance the understanding of rare and unknown diseases.

Patients interested in participating in the Undiagnosed Diseases Network may learn more at www.rarediseases.info.nih.gov/undiagnosed. Applications will be accepted beginning in the fall.

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Families with an autistic child are a third less likely to have more kids


UCSF study has implications for studying the genetic basis and risk of the disorder.

Neil Risch, UC San Francisco

Parents who have a child with autism spectrum disorder (ASD) are about one-third less likely to have more children than families without an affected child, according to a study led by a UC San Francisco researcher.

The findings, which appear in today’s (June 18) issue of JAMA Psychiatry, stem from the largest study of its kind on further child bearing after a child has been diagnosed with the disorder. These are the first data to indicate that this is a reproductive decision. “While it has been postulated that parents who have a child with ASD may be reluctant to have more children, this is first time that anyone has analyzed the question with hard numbers,” said Neil Risch, Ph.D., a UCSF professor of epidemiology and biostatistics and director of the UCSF Institute for Human Genetics.

Most previous research into the heredity of autism has ignored a possible decision on the part of parents with affected children to reduce their subsequent child-bearing, a situation that occurs with some birth defects and has been termed “reproductive stoppage.” As a result, previous estimates of the odds of having a second child with the disorder may have made the risk appear lower than it actually is.

“This study is the first to provide convincing statistical evidence that reproductive stoppage exists and should be taken into account when calculating the risks for having a another child with ASD,” said Risch, who is senior author on the paper. “These findings have important implications for genetic counseling of affected families.”

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Your genes affect your betting behavior


Decisions influenced by variants of dopamine-regulating genes in a person’s brain.

Investors and gamblers take note: your betting decisions and strategy are determined, in part, by your genes.

University of California, Berkeley, and University of Illinois at Urbana-Champaign (UIUC) researchers have shown that betting decisions in a simple competitive game are influenced by the specific variants of dopamine-regulating genes in a person’s brain.

Dopamine is a neurotransmitter – a chemical released by brain cells to signal other brain cells – that is a key part of the brain’s reward and pleasure-seeking system. Dopamine deficiency leads to Parkinson’s disease, while disruption of the dopamine network is linked to numerous psychiatric and neurodegenerative disorders, including schizophrenia, depression and dementia.

While previous studies have shown the important role of the neurotransmitter dopamine in social interactions, this is the first study tying these interactions to specific genes that govern dopamine functioning.

“This study shows that genes influence complex social behavior, in this case strategic behavior,” said study leader Ming Hsu, an assistant professor of marketing in UC Berkeley’s Haas School of Business and a member of the Helen Wills Neuroscience Institute. “We now have some clues about the neural mechanisms through which our genes affect behavior.”

The implications for business are potentially vast but unclear, Hsu said, though one possibility is training workforces to be more strategic. But the findings could significantly affect our understanding of diseases involving dopamine, such as schizophrenia, as well as disorders of social interaction, such as autism.

“When people talk about dopamine dysfunction, schizophrenia is one of the first diseases that come to mind,” Hsu said, noting that the disease involves a very complex pattern of social and decision making deficits. “To the degree that we can better understand ubiquitous social interactions in strategic settings, it may help us understand how to characterize and eventually treat the social deficits that are symptoms of diseases like schizophrenia.”

Hsu, UIUC graduate student Eric Set and their colleagues, including Richard P. Ebstein and Soo Hong Chew from the National University of Singapore, will publish their findings the week of June 16 in the online early edition of the Proceedings of the National Academy of Sciences.

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Mexican genetics study reveals huge variation in ancestry


UCSF/Stanford team uncovers basis for health differences among Latinos.

In the most comprehensive genetic study of the Mexican population to date, researchers from UC San Francisco and Stanford University, along with Mexico’s National Institute of Genomic Medicine (INMEGEN), have identified tremendous genetic diversity, reflecting thousands of years of separation among local populations and shedding light on a range of confounding aspects of Latino health.

The study, which documented nearly 1 million genetic variants among more than 1,000 individuals, unveiled genetic differences as extensive as the variations between some Europeans and Asians, indicating populations that have been isolated for hundreds to thousands of years.

These differences offer an explanation for the wide variety of health factors among Latinos of Mexican descent, including differing rates of breast cancer and asthma, as well as therapeutic response. Results of the study, on which UCSF and Stanford shared both first and senior authors, appear in the June 13 online edition of the journal Science.

“Over thousands of years, there’s been a tremendous language and cultural diversity across Mexico, with large empires like the Aztec and Maya, as well as small, isolated populations,” said Christopher Gignoux, Ph.D., who was first author on the study with Andres Moreno-Estrada, M.D., Ph.D., first as a graduate student at UCSF and now as a postdoctoral fellow at Stanford. “Not only were we able to measure this diversity across the country, but we identified tremendous genetic diversity, with real disease implications based on where, precisely, your ancestors are from in Mexico.”

For decades, physicians have based a range of diagnoses on patients’ stated or perceived ethnic heritage, including baseline measurements for lung capacity, which are used to assess whether a patients’ lungs are damaged by disease or environmental factors. In that context, categories such as Latino or African-American, both of which reflect people of diverse combinations of genetic ancestry, can be dangerously misleading and cause both misdiagnoses and incorrect treatment.

While there have been numerous disease/gene studies since the Human Genome Project, they have primarily focused on European and European-American populations, the researchers said. As a result, there is very little knowledge of the genetic basis for health differences among diverse populations.

“In lung disease such as asthma or emphysema, we know that it matters what ancestry you have at specific locations on your genes,” said Esteban González Burchard, M.D., M.P.H., professor of bioengineering and therapeutic sciences, and of medicine, in the UCSF schools of pharmacy and medicine. Burchard is co-senior author of the paper with Carlos Bustamante, Ph.D., a professor of genetics at Stanford. “In this study, we realized that for disease classification it also matters what type of Native American ancestry you have. In terms of genetics, it’s the difference between a neighborhood and a precise street address.”

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Researchers discover new gene involved in Parkinson’s disease


UCLA finding may lead to new target for treatment.

Ming Guo, UCLA

In the past decade, scientists have identified a handful of genes connected with Parkinson’s disease. Now, a team of UCLA researchers has identified another gene involved in the neurological disorder. Their finding may provide a target for drugs that could one day prevent or even cure the debilitating illness.

Parkinson’s disease is the second most common neurodegenerative disorder, after Alzheimer’s disease, and it has no cure. About 60,000 Americans are diagnosed with Parkinson’s disease each year, and it is estimated that as many as 1 million Americans live with Parkinson’s disease – more than the number of people with multiple sclerosis, muscular dystrophy and Lou Gehrig’s disease combined.

In Parkinson’s disease, multiple neurons in the brain gradually break down or die, causing patients to experience tremors, rigidity, slowness in movement and difficulty walking, as well as depression, anxiety, sleeping difficulties and dementia, said Dr. Ming Guo, the study’s team leader, a UCLA associate professor of neurology and pharmacology.

In 2006, Guo’s team was one of two groups that first reported that two genes, PTEN-induced putative kinase 1 (PINK1) and Parkin, act together to maintain the health of mitochondria – which power the neurons that are important for maintaining brain health. Mutations in these genes lead to early-onset Parkinson’s disease.

Guo’s team also showed that when the PINK1 and Parkin genes are operating correctly, they help maintain the regular shape of healthy mitochondria and help cells eliminate damaged mitochondria. The accumulation of unhealthy or damaged mitochondria in neurons and muscles ultimately results in Parkinson’s disease.

In the new study, Guo and her colleagues found that a gene called MUL1 (also known as MULAN and MAPL) plays an important role in mediating the pathology of the PINK1 and Parkin. The study, performed in fruit flies and mice, showed that providing an extra amount of MUL1 helps reduce the amount of damage that mutated PINK/Parkin create in mitochondria, and that inhibiting MUL1 in mutant PINK1/Parkin exacerbates the damage to the mitochondria.  In addition, Guo and her collaborators found that removing MUL1 from mouse neurons of the Parkin disease model results in unhealthy mitochondria and degeneration of the neurons.

“We show that MUL1 dosage is key and optimizing its function is crucial for brain health and to ward off Parkinson’s disease,” said Guo, a practicing neurologist at UCLA. “Our work proves that mitochondrial health is of central importance to keep us from suffering from neurodegeneration. Further, finding a drug that can enhance MUL1 function would be of great benefit to patients with Parkinson’s disease.”

The five-year study was published June 4 in eLife, an open-access journal for biomedical and life sciences research.

“This finding is a major advance in Parkinson’s disease research,” Guo said. “There are several implications to this work, including that MUL1 appears to be a very promising drug target and that it may constitute a new pathway regulating the quality of mitochondria.”

Guo and her team plan to test their results in more complex organisms, hoping to understand more about how MUL1 works. Additionally, the team will work on identifying compounds that could specifically target MUL1 and examine whether mutations in MUL1 exist in some people with inherited forms of Parkinson’s.

The study was a collaboration between Guo’s lab and Dr. Zuhang Sheng of the National Institutes of Health, and was supported by the National Institute of Aging (R01, K02), the National Institute of Neurological Disorders and Stroke (EUREKA award), an Ellison Medical Foundation Senior Scholar Award, the McKnight Neuroscience Foundation, the Klingenstein Foundation, the American Parkinson’s Disease Association and the Glenn Family Foundation.

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Melanoma of the eye caused by two gene mutations


Therapeutic target identified for treatment.

Researchers at the UC San Diego School of Medicine have identified a therapeutic target for treating the most common form of eye cancer in adults. They have also, in experiments with mice, been able to slow eye tumor growth with an existing FDA-approved drug.

The findings are published online in today’s (May 29) issue of the journal Cancer Cell.

“The beauty of our study is its simplicity,” said Kun-Liang Guan, Ph.D., professor of pharmacology at UC San Diego Moores Cancer Center and co-author of the study. “The genetics of this cancer are very simple and our results have clear implications for therapeutic treatments for the disease.”

The researchers looked specifically at uveal melanoma. Uveal collectively refers to parts of the eye, notably the iris, that contain pigment cells. As with melanoma skin cancer, uveal melanoma is a malignancy of these melanin-producing cells.

Approximately 2,000 people in the United States are diagnosed with uveal melanoma each year. If the cancer is restricted to just the eye, the standard treatment is radiation and surgical removal of the eye. But uveal melanoma often spreads to the liver, and determining the metastatic status of the disease can be difficult. In cases of uveal melanoma metastasis, patients typically succumb within two to eight months after diagnosis.

Scientists have long suspected a genetic association with uveal melanoma because one of two gene mutations is present in approximately 70 percent of all tumors. Until this study, however, they had not identified a mechanism that could explain why and how these mutations actually caused tumors.

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Better cognition seen with gene variant carried by 1 in 5 people


Finding could have implications for treating age-related diseases like Alzheimer’s.

A scientific team led by the Gladstone Institutes and UC San Francisco has discovered that a common form of a gene already associated with long life also improves learning and memory, a finding that could have implications for treating age-related diseases like Alzheimer’s.

The researchers found that people who carry a single copy of the KL-VS variant of the KLOTHO gene perform better on a wide variety of cognitive tests. When the researchers modeled the effects in mice, they found it strengthened the connections between neurons that make learning possible – what is known as synaptic plasticity – by increasing the action of a cell receptor critical to forming memories.

The discovery is a major step toward understanding how genes improve cognitive ability and could open a new route to treating diseases like Alzheimer’s. Researchers have long suspected that some people may be protected from the disease because of their greater cognitive capacity, or reserve. Since elevated levels of the klotho protein appear to improve cognition throughout the lifespan, raising klotho levels could build cognitive reserve as a bulwark against the disease.

“As the world’s population ages, cognitive frailty is our biggest biomedical challenge,” said Dena Dubal, M.D., Ph.D., assistant professor of neurology, the David A. Coulter Endowed Chair in Aging and Neurodegeneration at UCSF and lead author of the study, published today in Cell Reports. “If we can understand how to enhance brain function, it would have a huge impact on people’s lives.”

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Detecting fetal chromosomal defects without risk


Noninvasive sequencing is faster, cheaper and safer for mother and fetus, say researchers.

Human karyotype

Chromosomal abnormalities that result in birth defects and genetic disorders like Down syndrome remain a significant health burden in the United States and throughout the world, with some current prenatal screening procedures invasive and a potential risk to mother and unborn child.

In a paper published online this week in the Early Edition of PNAS, a team of scientists at the UC San Diego School of Medicine and in China describe a new benchtop semiconductor sequencing procedure and newly developed bioinformatics software tools that are fast, accurate, portable, less expensive and can be completed without harm to mother or fetus.

“We believe this approach could become the standard of care for screening of prenatal chromosomal abnormalities,” said Kang Zhang, M.D., Ph.D., professor of ophthalmology, founding director of the Institute for Genomic Medicine at UC San Diego and a staff physician at the San Diego VA Healthcare System.

The incidence of chromosomal abnormalities – in numbers or structure – is one in 160 live births in the United States, higher in other countries. In China, for example, the rate is one in 60 live births. The effects of these abnormalities, known as aneuploidies, can be severe, from developmental delays and neurological disorders to infertility and death. The incidence rate rises with maternal age, most notably after age 35.

Current diagnoses of fetal aneuploidies often rely upon invasive tests that sample amniotic fluid or placental tissues for fetal DNA that can then be analyzed using a variety of complex and expensive methods, including full karyotyping in which the entire set of chromosomes is viewed microscopically. While highly reliable, these invasive tests may cause infections in the pregnant woman and pose as much as a 1 percent risk of miscarriage and fetal loss. Results are not available for one to two weeks, extending anxiety for families waiting for information.

The new method relies upon massively parallel sequencing of cell-free fetal DNA using a benchtop semiconductor sequencing platform (SSP) called an Ion Torrent sequencer developed by Life Technologies. Cell-free fetal DNA is genetic material from the fetus that circulates naturally and freely in the mother’s bloodstream. It can be obtained through an ordinary blood draw, with SSP analysis achieved in less than four days.

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Progressive neurodegenerative disorder linked to R-loop formation


UC Davis findings suggest R-loops may be potential targets for drug development.

Paul Hagerman, UC Davis

Researchers at UC Davis have identified a new feature of the genetic mutation responsible for the progressive neurodegenerative disorder fragile X-associated tremor/ataxia syndrome (FXTAS) — the formation of “R-loops,” which they believe may be associated with the disorder’s neurological symptoms, such as tremors, lack of balance, features of Parkinsonism and cognitive decline.

The finding suggests that the R-loops may be potential targets for drug development, said Paul Hagerman, senior study author, professor in the Department of Biochemistry and Molecular Medicine and director of the UC Davis NeuroTherapeutics Research Institute. The study, “Transcription-associated R-loop Formation across the Human FMR1 CGG-repeat Region,” is published today in the online journal PLoS Genetics.

An R-loop is formed when the messenger RNA being made at the gene reinserts itself into the DNA helix, displacing one strand of DNA, which creates the “loop.” Such loops are known to be prone to damage, which can in turn lead to loss of cell function, particularly in neurons.

Hagerman and his collaborators discovered the R-loops while investigating mutations in the gene that causes FXTAS and other conditions associated with the fragile X mental retardation gene 1 (FMR1). R-loops are not unique to FXTAS and can occur in the promoter regions of many genes.

“But in FXTAS, the R-loops are more numerous and much longer than they are in FMR1 genes that are not mutated,” said Hagerman, a researcher who also is affiliated with the UC Davis MIND Institute.

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Cleft palate discovery in dogs to aid in understanding human birth defect


UC Davis study also shows that dogs have multiple genetic causes of cleft palate.

This puppy is a Nova Scotia Duck Tolling Retriever, the breed with the newly discovered genetic mutation for cleft palate.

UC Davis School of Veterinary Medicine researchers have identified the genetic mutation responsible for a form of cleft palate in the dog breed Nova Scotia Duck Tolling Retrievers.

They hope that the discovery, which provides the first dog model for the craniofacial defect, will lead to a better understanding of cleft palate in humans. Although cleft palate is one of the most common birth defects in children, affecting approximately one in 1,500 live human births in the United States, it is not completely understood.

The findings appear this week online in the journal PLOS Genetics and are available online at https://tinyurl.com/knr8wb3.

“This discovery provides novel insight into the genetic cause of a form of cleft palate through the use of a less conventional animal model,” said professor Danika Bannasch, a veterinary geneticist who led the study. “It also demonstrates that dogs have multiple genetic causes of cleft palate that we anticipate will aid in the identification of additional candidate genes relevant to human cleft palate.”

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Tweaking potassium levels in brain could be a key to fighting Huntington’s


UCLA findings could point to new drug targets for treating the devastating disease.

Astrocytes in brain tissue

By boosting the ability of a specific type of cell to absorb potassium in the brain, UCLA researchers were able to improve walking and prolong survival in a mouse model of Huntington’s disease.

Their findings, published March 30 in the online edition of the journal Nature Neuroscience, could point to new drug targets for treating the devastating disease, which strikes one in every 20,000 Americans.

Huntington’s disease is passed from parent to child through a mutation in the huntingtin gene. By killing brain cells called neurons, the disorder gradually deprives patients of their ability to walk, speak, swallow, breathe and think clearly. No cure exists, and patients with aggressive cases can die in as little as 10 years.

The laboratories of Baljit Khakh, a UCLA professor of physiology and neurobiology, and Michael Sofroniew, a UCLA professor of neurobiology, teamed up at the David Geffen School of Medicine at UCLA to unravel the role that astrocytes — large, star-shaped cells found in the brain and spinal cord — play in Huntington’s.

“Astrocytes appear in the brain in equal numbers to neurons yet haven’t been closely studied,” Khakh said. “They enable neurons to signal each other by maintaining an optimal chemical environment outside the cells. We used two mouse models to explore whether astrocytes behave differently during Huntington’s disease.”

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Kaiser, UCSF add genetic, health information to NIH online database


Information is largest-ever genetic resource for researchers.

Catherine Schaefer

Researchers worldwide will now have access to genetic data linked to medical information on a diverse group of more than 78,000 people, enabling investigations into many diseases and conditions. The data have just been made available to qualified researchers through the database of Genotypes and Phenotypes (dbGaP), the online database of the National Institutes of Health (NIH). The announcement was made today (Feb. 26) at the National Advisory Council on Aging by Richard Hodes, director of the National Institute on Aging (NIA).

The data come from one of the nation’s largest and most diverse genomics projects — the Genetic Epidemiology Research on Adult Health and Aging (GERA) cohort — which was developed collaboratively by the Kaiser Permanente Research Program on Genes, Environment and Health (RPGEH) and UC San Francisco. The addition of the data to dbGaP was made possible with $24.9 million in support from the NIA and the National Institute of Mental Health at NIH, as well as from the Office of the NIH Director.

“Data from this immense and ethnically diverse population will be a tremendous resource for science,” said NIH Director Francis Collins. “It offers the opportunity to identify potential genetic risks and influences on a broad range of health conditions, particularly those related to aging.”

Neil Risch

The GERA cohort is part of the RPGEH, which includes more than 430,000 adult members of the Kaiser Permanente Northern California health plan who volunteered to participate in the research program. Data on this larger cohort include electronic medical records, behavioral and demographic information from surveys, and saliva or blood samples from 200,000 participants obtained with informed consent for genomic and other analyses.

This work was made possible with the investment of an $8.6 million grant from the Robert Wood Johnson Foundation, which saw the potential to build a resource that would transform genomic research. “This massive influx of new, high quality data will help scientists discover bigger breakthroughs faster,” said Nancy Barrand, the foundation’s senior adviser for Program Development. “Researchers used to have to go through the painstaking process of collecting and studying genomic samples on their own. Now researchers worldwide can find valuable clues for improving health by studying the genetic information from a cohort of 78,000 diverse individuals in dbGaP.”

Additional support for development of the RPGEH resource was provided by the Wayne and Gladys Valley Foundation, the Ellison Medical Foundation, and Kaiser Permanente.

The genetic information on more than 78,000 individuals translates into over 55 billion bits of genetic data for the cohort. The researchers conducted genome-wide genotyping using the newly developed Affymetrix Axiom Gene Titan system employed in the UCSF Institute for Human Genetics Genomics Core Facility to rapidly scan selected markers of genetic variation called single nucleotide polymorphisms (SNPs) in the genomes of the people in the GERA cohort. The RPGEH then combined the genetic data with information derived from Kaiser Permanente’s comprehensive longitudinal electronic medical records, as well as extensive survey data on participants’ health habits and backgrounds, providing researchers with an unparalleled research resource. These data form the basis of genome-wide association studies (GWAS) that can look at hundreds of thousands to millions of SNPs at the same time in relation to many different health conditions.

“The transfer of this data will greatly accelerate research on genetic influences on health, disease and aging,” said Catherine Schaefer, Ph.D., executive director of the Research Program on Genes, Environment and Health and co-principal investigator for GERA. “Making these data on such a large diverse cohort broadly available will enable many more scientists to work at a much greater scale that is likely to help answer important questions concerning health.”

“It’s all about time and money,” added Neil Risch, Ph.D., director of the UCSF Institute for Human Genetics and co-principal investigator for GERA. “Collecting large amounts of health data from people — and processing it — is labor intensive and expensive. With this data set, no one has to collect clinical information, take bio samples, safeguard and store them, or conduct genome-wide genotyping of their DNA. They can simply sit at a computer, ask questions of the data, and extract information.”

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