Genetic and molecular analysis of wild-derived arrhythmic mice.
Genetic and molecular analysis of wild-derived arrhythmic mice.
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DOI：
10.1371/journal.pone.0004301
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发表时间：
2009
期刊：
影响因子：
3.7
通讯作者：
Ebihara S
中科院分区：
文献类型：
--
作者：
Watanabe T;Suzuki T;Ishikawa A;Yokota Y;Ueda HR;Yamada RG;Tei H;Imai S;Tomida S;Kobayashi J;Naito E;Yasuo S;Nakao N;Namikawa T;Yoshimura T;Ebihara S
A new circadian variant was isolated by screening the intercross offspring of wild-caught mice (Mus musculus castaneus). This variant was characterized by an initial maintenance of damped oscillations and subsequent loss of rhythmicity after being transferred from light-dark (LD) cycles to constant darkness (DD). To map the genes responsible for the persistence of rhythmicity (circadian ratio) and the length of free-running period (τ), quantitative trait locus (QTL) analysis was performed using F2 mice obtained from an F1 cross between the circadian variant and C57BL/6J mice. As a result, a significant QTL with a main effect for circadian ratio (Arrhythmicity; Arrh-1) was mapped on Chromosome (Chr) 8. For τ, four significant QTLs, Short free-running period (Sfp-1) (Chr 1), Sfp-2 (Chr 6), Sfp-3 (Chr 8), Sfp-4 (Chr 11) were determined. An epistatic interaction was detected between Chr 3 (Arrh-2) and Chr 5 (Arrh-3). An in situ hybridization study of clock genes and mouse Period1::luciferase (mPer1::luc) real-time monitoring analysis in the suprachiasmatic nucleus (SCN) suggested that arrhythmicity in this variant might not be attributed to core circadian mechanisms in the SCN neurons. Our strategy using wild-derived variant mice may provide a novel opportunity to evaluate circadian and its related disorders in human that arise from the interaction between multiple variant genes.
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影响因子：
64.8
作者：
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通讯作者：
Zhou, QY
影响因子：
30.8
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2.5
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作者：
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通讯作者：
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