Title of article
Genome Sequencing Reveals Loci under Artificial Selection that Underlie Disease Phenotypes in the Laboratory Rat
Author/Authors
Santosh S. Atanur، نويسنده , , Ana Garcia Diaz، نويسنده , , Klio Maratou، نويسنده , , Allison Sarkis، نويسنده , , Maxime Rotival، نويسنده , , Laurence Game، نويسنده , , Michael R. Tschannen، نويسنده , , Pamela J. Kaisaki، نويسنده , , Georg W. Otto، نويسنده , , Man Chun John Ma، نويسنده , , Thomas M. Keane، نويسنده , , Oliver Hummel، نويسنده , , Kathrin Saar، نويسنده , , Wei Chen، نويسنده , , Victor Guryev، نويسنده , , Kathirvel Gopalakrishnan، نويسنده , , Michael R. Garrett، نويسنده , , Bina Joe، نويسنده , , Lorena Citterio، نويسنده , , Giuseppe Bianchi، نويسنده , , et al.، نويسنده ,
Issue Information
هفته نامه با شماره پیاپی سال 2013
Pages
13
From page
691
To page
703
Abstract
Large numbers of inbred laboratory rat strains have been developed for a range of complex disease phenotypes. To gain insights into the evolutionary pressures underlying selection for these phenotypes, we sequenced the genomes of 27 rat strains, including 11 models of hypertension, diabetes, and insulin resistance, along with their respective control strains. Altogether, we identified more than 13 million single-nucleotide variants, indels, and structural variants across these rat strains. Analysis of strain-specific selective sweeps and gene clusters implicated genes and pathways involved in cation transport, angiotensin production, and regulators of oxidative stress in the development of cardiovascular disease phenotypes in rats. Many of the rat loci that we identified overlap with previously mapped loci for related traits in humans, indicating the presence of shared pathways underlying these phenotypes in rats and humans. These data represent a step change in resources available for evolutionary analysis of complex traits in disease models.
Journal title
CELL
Serial Year
2013
Journal title
CELL
Record number
1021841
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