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Leah C. Solberg William Valdar Dominique Gauguier Graciela Nunez Amy Taylor Stephanie Burnett Carmen Arboledas-Hita Polinka Hernandez-Pliego Stuart Davidson Peter Burns Shoumo Bhattacharya Tertius Hough Douglas Higgs Paul Klenerman William O. Cookson Youming Zhang Robert M. Deacon J. Nicholas P. Rawlins Richard Mott Jonathan Flint 《Mammalian genome》2006,17(2):129-146
Whole-genome genetic association studies in outbred mouse populations represent a novel approach to identifying the molecular
basis of naturally occurring genetic variants, the major source of quantitative variation between inbred strains of mice.
Measuring multiple phenotypes in parallel on each mouse would make the approach cost effective, but protocols for phenotyping
on a large enough scale have not been developed. In this article we describe the development and deployment of a protocol
to collect measures on three models of human disease (anxiety, type II diabetes, and asthma) as well as measures of mouse
blood biochemistry, immunology, and hematology. We report that the protocol delivers highly significant differences among
the eight inbred strains (A/J, AKR/J, BALBc/J, CBA/J, C3H/HeJ, C57BL/6 J, DBA/2 J, and LP/J), the progenitors of a genetically
heterogeneous stock (HS) of mice. We report the successful collection of multiple phenotypes from 2000 outbred HS animals.
The phenotypes measured in the protocol form the basis of a large-scale investigation into the genetic basis of complex traits
in mice designed to examine interactions between genes and between genes and environment, as well as the main effects of genetic
variants on phenotypes. 相似文献
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Benjamin Davies Anjali Gupta Hinch Alberto Cebrian-Serrano Samy Alghadban Philipp W Becker Daniel Biggs Polinka Hernandez-Pliego Chris Preece Daniela Moralli Gang Zhang Simon Myers Peter Donnelly 《Molecular biology and evolution》2021,38(12):5555
Sterility or subfertility of male hybrid offspring is commonly observed. This phenomenon contributes to reproductive barriers between the parental populations, an early step in the process of speciation. One frequent cause of such infertility is a failure of proper chromosome pairing during male meiosis. In subspecies of the house mouse, the likelihood of successful chromosome synapsis is improved by the binding of the histone methyltransferase PRDM9 to both chromosome homologs at matching positions. Using genetic manipulation, we altered PRDM9 binding to occur more often at matched sites, and find that chromosome pairing defects can be rescued, not only in an intersubspecific cross, but also between distinct species. Using different engineered variants, we demonstrate a quantitative link between the degree of matched homolog binding, chromosome synapsis, and rescue of fertility in hybrids between Mus musculus and Mus spretus. The resulting partial restoration of fertility reveals additional mechanisms at play that act to lock-in the reproductive isolation between these two species. 相似文献
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