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Horn removal through gene editing is a win-win both for the animal and for the farmer, says Muir, who did not take part in this research. "These findings show that you can take highly desirable genes from animals and move them to other members of their species," he told Popular Science. "One could achieve the same results with natural breeding, but gene editing greatly speeds up the process, reducing the time it takes to accomplish the goal from centuries to years."

hose who would much rather prefer to burn the midnight oil than get up early in the morning can find solace in a new research that suggests they might be genetically predisposed to being nocturnal. It is your genes that allow you to be more productive at night-time instead of the day. Researchers from the University of Leicester in the UK have identified about 80 genes that are closely linked to a preference for either morningness or eveningness. Though these genes were identified in fruit flies and appear unrelated to your own body clock, most of these buggers are found in us mammals as well.

The researchers concluded that genetics - or perhaps other factors, such as environmental influences - play a larger role than practice in certain aspects of musical talent such as recognizing pitch and rhythms. Mosey and her colleagues made another interesting finding: Genes may determine a person's motivation to practice. The majority of participants who reported practicing a lot also shared a high percentage of the same genes. "The association between practice and skill was largely due to the same genes, suggesting that practice will not necessarily make you perfect, but it certainly will enhance your skills," Mosey said.

Why does a snake have 25 or more rows of ribs, whereas a mouse has only 13? The answer, according to a new study, may lie in "junk DNA," large chunks of an animal's genome that were once thought to be useless. The findings could help explain how dramatic changes in body shape have occurred over evolutionary history. Scientists began discovering junk DNA sequences in the 1960s. These stretches of the genome-also known as noncoding DNA-contain the same genetic alphabet found in genes, but they don't code for the proteins that make us who we are. As a result, many researchers long believed this mysterious genetic material was simply DNA debris accumulated over the course of evolution. But over the past couple decades, geneticists have discovered that this so-called junk is anything but. It has important functions, such as switching genes on and off and setting the timing for changes in gene activity. 

A genetic "crystal ball" can predict whether certain people will respond effectively to the flu vaccine. Nine genes are associated with a strong immune response to the flu vaccine in those aged 35 and under, a new study finds. If these genes were highly active before vaccination, an individual would generate a high level of antibodies after vaccination, no matter the flu strain in the vaccine, researchers report online August 25 in Science Immunology. This response can help a person avoid getting the flu.

Learn to use Online Mendelian Inheritance in Man®, or OMIM®, a catalog of human genes and genetic conditions. OMIM is a foundational resource in genomics and is valuable for clinicians and biomedical researchers. OMIM links and data are found at sites all around the bioinformatics sphere, but understanding the full scope of OMIM's data and resources enable the most comprehensive understanding of human phenotypes and disease. OMIM contains full-text summaries of information from the scientific literature, and provides extensive links to the literature resources and other genomic resource tools as well. Use OMIM as a comprehensive first stop to find important information and gene links for human Mendelian disorders.

A single genetic mutation causes resistance to DDT and pyrethroids (an insecticide class used in mosquito nets), new research concludes. With the continuing rise of resistance, the research is key as scientists say that this knowledge could help improve malaria control strategies. The researchers used a wide range of methods to narrow down how the resistance works, finding a single mutation in the GSTe2 gene, which makes insects break down DDT so it's no longer toxic. They have also shown that this gene makes insects resistant to pyrethroids raising the concern that GSTe2 gene could protect mosquitoes against the major insecticides used in public health.

Now, scientists at the Salk Institute for Biological Studies in La Jolla, Calif., have pinpointed a gene linked to these disorders that seems to be crucial for normal brain structure in prenatal development. The findings, which appear in an open-access article in the Jan. 14 issue of Cell Reports, shed new light on the mechanistic workings of a gene called MDGA1, previously implicated in autism, schizophrenia and bipolar disorder.

In 2007, researchers discovered that people with a common variant of FTO tend to be heavier than those without it. Since then, studies have repeatedly confirmed the link. On average, one copy of the risky variant adds up to 3.5 extra pounds of weight. Two copies of the gene bring 7 extra pounds - and increase a person's risk of becoming obese by 50 percent.

The external environment's effects upon genes can influence disease, and some of these effects can be inherited in humans. Studies investigating how environmental factors impact the genetics of an individual's offspring are difficult to design. However, in certain parts of the world in which social systems are highly centralized, environmental information that might have influenced families can be obtained. For example, Swedish scientists recently conducted investigations examining whether nutrition affected the death rate associated with cardiovascular disease and diabetes and whether these effects were passed from parents to their children and grandchildren (Kaati et al., 2002). These researchers estimated how much access individuals had to food by examining records of annual harvests and food prices in Sweden across three generations of families, starting as far back as the 1890s. These researchers found that if a father did not have enough food available to him during a critical period in his development just before puberty, his sons were less likely to die from cardiovascular disease. Remarkably, death related to diabetes increased for children if food was plentiful during this critical period for the paternal grandfather, but it decreased when excess food was available to the father. These findings suggest that diet can cause changes to genes that are passed down though generations by the males in a family, and that these alterations can affect susceptibility to certain diseases. But what are these changes, and how are they remembered? The answers to questions such as these lie in the concept of epigenetics.

Dogs are excellent models for studying genetics, especially disease genetics. Work done in the last 20 years has shown that dogs share many gene-related disorders with people. Each breed is a closed reproductive population with distinct rates of heritable diseases, which dramatically increases the odds of finding disease-related loci. In creating new dog breeds, we reduce the gene pool within those populations, and fix many alleles. This homogeneous background makes it much easier to map QTLs and perform linkage analyses

This video excerpt from NOVA examines the promise and realities of developing drugs designed to treat genetic disorders. The video presents the story of one patient, Michael McCarrick, whose lungs were devastated from years of suffering from cystic fibrosis. After researchers identified the gene involved in cystic fibrosis, it took decades to find ways to fortify the faulty protein responsible for the serious illness. While two drugs, including one called Kalydeco, offer a small number of patients hope that they will not have to endure a lung transplant, it may be years and several hundred million more development dollars before effective drugs are available for a wider population.

Find out how researchers identify genetic diseases and determine possible treatments. short film, genes as medicine click and learn, central dogma scientists at work, the search for a mutated gene central dogma card activity animation, CF mechanism and treatment click and learn. CRISPR-Cas9

Medical researchers have discovered a gene that increases the risk of schizophrenia, a mental illness that affects more than 2 million Americans, sometimes causing delusions and hallucinations. The finding was first reported this week in the scientific journal "Nature".

This case study follows a young cystic fibrosis (CF) patient named Lucas. Through Lucas's story and interactions between his parents and pediatrician, students learn about the scientific background and basis of CF. By reviewing email correspondence between Lucas's parents and various doctors, students gain an overview of CF research. CF has become a model disease in certain undergraduate biology classrooms due to its relatively clear mechanism and genetic basis. This case asks students to come up with their own ideas to improve on an existing line of research - gene therapy - in treating CF. During the process, students will gain a better appreciation of the innovative nature of science and develop research skills such as finding, understanding and analyzing primary literature. The activity was originally designed for first- and second-year students as part of an extracurricular case competition, but may be used for any undergraduate biology level. The case assumes basic (high school level) knowledge of genetics, biochemistry, cell biology and physiology.

At about 3 billion letters long, reading and finding anything meaningful in the human genome is a daunting task. But that's just what genome researchers do. This interactive feature provides a microscopic view of some of what they've found on our 24 chromosomes, including the locations of about 200 different genes, especially those that have been associated with disease.

The early stages of embryonic development shape our cells and tissues for life. It is during this time that our newly formed cells are transformed into heart, skin, nerve or other cell types. Scientists are finding that this process is largely controlled not by the genome, but by the epigenome, chemical markers on DNA that tell cells when to turn genes on and off. Now, studying zebrafish embryos, researchers at Washington University School of Medicine in St. Louis have shown that the epigenome plays a significant part in guiding development in the first 24 hours after fertilization.

As the leader of a project called Finding of Rare Disease Genes (FORGE) in Canada, Kym Boycott is one of the top experts in the world in the application of exome sequencing to solve rare disorders. The Canadian project involves a network of doctors and scientists all across the country looking to identify patients with rare childhood conditions and refer them when appropriate for sequencing and analysis.

When scientists first made contact with an isolated village of Yanomami hunter-gatherers in the remote mountains of the Amazon jungle of Venezuela in 2009, they marveled at the chance to study the health of people who had never been exposed to Western medicine or diets. But much to their surprise, these Yanomami's gut bacteria have already evolved a diverse array of antibiotic-resistance genes, according to a new study, even though these mountain people had never ingested antibiotics or animals raised with drugs. The find suggests that microbes have long evolved the capability to fight toxins, including antibiotics, and that preventing drug resistance may be harder than scientists thought.

Bipolar disorder is a common, complex genetic disorder, but the mode of transmission remains to be discovered. Many researchers assume that common genomic variants carry some risk for manifesting the disease. The research community has celebrated the first genome-wide significant associations between common single nucleotide polymorphisms (SNPs) and bipolar disorder. Currently, attempts are under way to translate these findings into clinical practice, genetic counseling, and predictive testing. However, some experts remain cautious. After all, common variants explain only a very small percentage of the genetic risk, and functional consequences of the discovered SNPs are inconclusive. Furthermore, the associated SNPs are not disease specific, and the majority of individuals with a "risk" allele are healthy. On the other hand, population-based genome-wide studies in psychiatric disorders have rediscovered rare structural variants and mutations in genes, which were previously known to cause genetic syndromes and monogenic Mendelian disorders.