Quantitative trait loci that control body weight in DDD/Sgn and C57BL/6J inbred mice.

Mamm Genome

Institute of Livestock and Grassland Science, National Agriculture and Food Research Organization (NARO), Tsukuba, Ibaraki, 305-0901, Japan.

Published: February 2017

AI Article Synopsis

  • Inbred DDD/Sgn mice are heavier than C57BL/6J mice, prompting a study on the genetic factors influencing body weight through QTL mapping.
  • Four significant QTL associated with body weight were identified on chromosomes 1, 2, 5, and 17, with the DDD/Sgn allele linked to higher weight at two QTL and lower weight at the others.
  • The study also explored testosterone levels, revealing a suggestive QTL on chromosome 5 that coincided with body weight, indicating a genetic connection between testosterone and weight regulation in male mice.

Article Abstract

Inbred DDD/Sgn mice are heavier than inbred C57BL/6J mice. In the present study, we performed quantitative trait loci (QTL) mapping for body weight using R/qtl in reciprocal F male populations between the two strains. We identified four significant QTL on Chrs 1, 2, 5, and 17 (proximal region). The DDD/Sgn allele was associated with increased body weight at QTL on Chrs 1 and 5, and the DDD/Sgn allele was associated with decreased body weight at QTL on Chrs 2 and 17. A multiple regression analysis indicated that the detected QTL explain 30.94 % of the body weight variation. Because DDD/Sgn male mice have extremely high levels of circulating testosterone relative to other inbred mouse strains, we performed QTL mapping for plasma testosterone level to examine the effect of testosterone levels on body weight. We identified one suggestive QTL on Chr 5, which overlapped with body weight QTL. The DDD/Sgn allele was associated with increased testosterone level. Thus, we confirmed that there was a genetic basis for the changes in body weight and testosterone levels in male mice. These findings provide insights into the genetic mechanism by which body weight is controlled in male mice.

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Source
http://dx.doi.org/10.1007/s00335-016-9666-3DOI Listing

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