a dominant x-linked qtl regulating pubertal timing in mice found by whole genome scanning and modified interval-specific congenic strain analysis主导和x染色体相关qtl调节发育期时机在老鼠身上发现的全基因组扫描和修改interval-specific同类品系分析.pdfVIP

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a dominant x-linked qtl regulating pubertal timing in mice found by whole genome scanning and modified interval-specific congenic strain analysis主导和x染色体相关qtl调节发育期时机在老鼠身上发现的全基因组扫描和修改interval-specific同类品系分析.pdf

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a dominant x-linked qtl regulating pubertal timing in mice found by whole genome scanning and modified interval-specific congenic strain analysis主导和x染色体相关qtl调节发育期时机在老鼠身上发现的全基因组扫描和修改interval-specific同类品系分析

A Dominant X-Linked QTL Regulating Pubertal Timing in Mice Found by Whole Genome Scanning and Modified Interval-Specific Congenic Strain Analysis Wangsheng Zhu1,2., Zhongpeng Fan1,2., Chao Zhang1,2, Zhengxia Guo1,2, Ying Zhao1,2,3, Yuxun Zhou1,2, Kai Li1,2, Zhenghong Xing2,3, Guoqiang Chen2,3, Yinming Liang1,2, Li Jin2,4, Junhua Xiao1,2* 1 College of Chemistry, Chemical Engineering Biotechnology, Donghua University, Shanghai Songjiang, People’s Republic of China, 2 Joint Laboratory for Model Animal Biodiversity, Shanghai Pudong, People’s Republic of China, 3 Shanghai British SIPPR/BK Lab Animal Ltd, Shanghai, People’s Republic of China, 4 School of Life Science, Fudan University, Shanghai, People’s Republic of China Abstract Background: Pubertal timing in mammals is triggered by reactivation of the hypothalamic-pituitary-gonadal (HPG) axis and modulated by both genetic and environmental factors. Strain-dependent differences in vaginal opening among inbred mouse strains suggest that genetic background contribute significantly to the puberty timing, although the exact mechanism remains unknown. Methodology/Principal Findings: We performed a genome-wide scanning for linkage in reciprocal crosses between two strains, C3H/HeJ (C3H) and C57BL6/J (B6), which differed significantly in the pubertal timing. Vaginal opening (VO) was used to characterize pubertal timing in female mice, and the age at VO of all female mice (two parental strains, F1 and F2 progeny) was recorded. A genome-wide search was performed in 260 phenotypically extreme F2 mice out of 464 female progeny of the F1 intercrosses to identify quantitative trait loci (QTLs) controlling this trait. A QTL significantly associated was mapped to the DXMit166 marker (15.5 cM, LOD = 3.86, p,0.01) in the reciprocal cross population (C3HB6F2). This QTL contributed 2.1 days