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Genetic studies of human disease are more challenging to perform in sub-Saharan Africa because genetic diversity is greater than in other populations. This pilot will increase our understanding of African genome variation and enable the design of large-scale genetic association studies in the region. Studies into the genetic basis of disease in European populations have made major advances in the past few years, yet similar studies in sub-Saharan Africa have been slower to develop. The high level of genetic diversity that exists in populations from sub-Saharan Africa makes genetic associations with disease more difficult to identify. The African Genome Variation Project aims to collect essential information about the structure of African genomes to provide a basic framework for genetic disease studies in Africa.

Sub-Saharan Africa is the most genetically diverse region in the world." The rates of susceptibility and not only whether or not someone becomes ill, but also whether or not they live or die, or even display symptoms, varies widely. The genetics of both this deadly strain of Ebola itself, and of the populations living in the affected areas, are at the forefront of the efforts by Dr. Moses as she works with Dr.Pardis Sabeti at Harvard to provide samples for genome sequencing.

Genetic differences among ethnically diverse individuals are largely due to structural elements called copy number variants (CNVs), according to a study published today (August 6) in Science. Compared with other genomic features, such as single nucleotide variants (SNVs), CNVs have not previously been studied in as much detail because they are more difficult to sequence. Covering 125 distinct human populations around the world, geneticist Evan Eichler at the University of Washington in Seattle and an international team of colleagues studied the genomes of 236 people-analyzing both SNVs and CNVs. "The take-home message is that we continue to find a lot more genetic variation between humans than we appreciated previously," Eichler told The Scientist.

The mouse is the leading organism for disease research. A rich resource of genetic variation occurs naturally in inbred and special strains owing to spontaneous mutations. However, one can also obtain desired gene mutations by using the following processes: targeted mutations that eliminate function in the whole organism or in a specific tissue; forward genetic screens using chemicals or transposons; or the introduction of exogenous transgenes as DNAs, bacterial artificial chromosomes (BACs) or reporter constructs. The mouse is the only mammal that provides such a rich resource of genetic diversity coupled with the potential for extensive genome manipulation, and is therefore a powerful application for modeling human disease.

Over the past few decades, genetic research has revealed two deep truths about people. The first is that all humans are closely related-more closely related than all chimps, even though there are many more humans around today. Everyone has the same collection of genes, but with the exception of identical twins, everyone has slightly different versions of some of them. Studies of this genetic diversity have allowed scientists to reconstruct a kind of family tree of human populations. That has revealed the second deep truth: In a very real sense, all people alive today are Africans.

While genes determine most of our physical characteristics, the exact combination of genes we inherit, and thus our physical traits, is in part due to a process our chromosomes undergo, known as genetic recombination.

Existing mouse models of lethal Ebola virus infection do not reproduce hallmark symptoms of Ebola hemorrhagic fever, neither delayed blood coagulation and disseminated intravascular coagulation, nor death from shock, thus restricting pathogenesis studies to non-human primates. Here we show that mice from the Collaborative Cross exhibit distinct disease phenotypes following mouse-adapted Ebola virus infection. Phenotypes range from complete resistance to lethal disease to severe hemorrhagic fever characterized by prolonged coagulation times and 100% mortality. Inflammatory signaling was associated with vascular permeability and endothelial activation, and resistance to lethal infection arose by induction of lymphocyte differentiation and cellular adhesion, likely mediated by the susceptibility allele Tek. These data indicate that genetic background determines susceptibility to Ebola hemorrhagic fever.

Our planet's diverse, thriving ecosystems may seem like permanent fixtures, but they're actually vulnerable to collapse. Jungles can become deserts, and reefs can become lifeless rocks. What makes one ecosystem strong and another weak in the face of change? Kim Preshoff details why the answer, to a large extent, is biodiversity.

Why did you get the flu this winter, but your co-workers didn't? The answer, according to a new study of twins, may have less to do with your genes and more to do with your environment-including your past exposure to pathogens and vaccines. Our immune system is incredibly complex, with diverse armies of white blood cells and signal-sending proteins coursing through our veins, ready to mount an attack on would-be invaders. Everyone's immune system is slightly different-a unique mixture of hundreds of these cells and proteins. But the main driver of this variation is unclear. Although scientists know that our immune system can adapt to our environment-that's why vaccines work, for instance-it is also built by our genes.

The origin of viruses remains mysterious because of their diverse and patchy molecular and functional makeup. Although numerous hypotheses have attempted to explain viral origins, none is backed by substantive data. We take full advantage of the wealth of available protein structural and functional data to explore the evolution of the proteomic makeup of thousands of cells and viruses. Despite the extremely reduced nature of viral proteomes, we established an ancient origin of the "viral supergroup" and the existence of widespread episodes of horizontal transfer of genetic information. Viruses harboring different replicon types and infecting distantly related hosts shared many metabolic and informational protein structural domains of ancient origin that were also widespread in cellular proteomes. Phylogenomic analysis uncovered a universal tree of life and revealed that modern viruses reduced from multiple ancient cells that harbored segmented RNA genomes and coexisted with the ancestors of modern cells. The model for the origin and evolution of viruses and cells is backed by strong genomic and structural evidence and can be reconciled with existing models of viral evolution if one considers viruses to have originated from ancient cells and not from modern counterparts.

Article summarizing cell division with time lapse cell division video of 30hours pro vs eukaryotic division.