CHARACTERIZATION OF A MAJOR OBESITY LOCUS

肥胖症在美国正达到流行病的比例，超过60%的美国人要么肥胖，要么 超重。肥胖有很强的遗传成分，然而，人们对肥胖的了解相对较少 影响肥胖的常见等位基因的特异性。描述自然遗传变异的特征 影响肥胖我建议研究BCQ-HG/HG同源株。BC9-HG/HG小鼠具有同源基因 C57B-6J-HG/HG背景上的CAST/EIJ染色体9等位基因BC9-HG/HG女性占57%，男性 比对照组小鼠肥胖30%，HG是小鼠10号染色体上的一个缺失，导致30%-50%的肥胖 体型的增加和证据表明，BCQ-HG/HG小鼠的肥胖需要HG。为了更好地 了解BCQ-HG/HG肥胖的本质我概述了三个具体目标。目标1衡量 年龄和饮食对BCQ-HG/HG肥胖的影响，并将决定肥胖是否依赖于HG的存在。目标2 使用同源基因衍生的F2群体来缩小携带肥胖QTL的基因组间隔。最后，目标 3使用遗传基因组学方法定位同源基因区间内基因的eQTL。来自这些网站的数据 AIMS将加强我们对肥胖的遗传学和生理学的理解。

Obesity is reaching epidemic proportions in the U.S. with over 60% of Americans being either obese or overweight. Obesity has a strong genetic component, however, relatively little is known regarding the specific identity of genes with common alleles influencing obesity. To characterize natural genetic variation influencing obesity I propose to study the BCQ-hg/hg congenic strain. BC9-hg/hg mice are congenic for CAST/EiJ chromosome 9 alleles on a C57B\/6J-hg/hg background. BC9-hg/hg females are 57% and males are 30% more obese than control mice, hg is a deletion on mouse chromosome 10 leading to a 30-50% increase in body size and evidence suggests that hg is required for obesity in BCQ-hg/hg mice. To better understand the nature of BCQ-hg/hg obesity I have outlined three specific aims. Aim 1 measures the effect o age and diet on BCQ-hg/hg obesity and will determine if obesity is dependent on the presence of hg. Aim 2 uses a congenic-derived F2 population to narrow the genomic interval harboring the obesity QTL. Lastly, aim 3 uses a genetical genomics approach to map eQTL for genes within the congenic interval. Data from these aims will enhance our understanding of the genetics and physiology of obesity.