Zhou Shanshan, Mackay Trudy F C, Anholt Robert R H
Department of Biological Sciences, W, M, Keck Center for Behavioral Biology and Program in Genetics, Box 7614, North Carolina State University, Raleigh, NC 27695-7617, USA.
BMC Genomics. 2014 Oct 23;15(1):927. doi: 10.1186/1471-2164-15-927.
Phenotypic plasticity allows organisms to respond rapidly to changing environmental circumstances, and understanding its genomic basis can yield insights regarding the underlying genes and genetic networks affecting complex phenotypes. Female Drosophila melanogaster undergo dramatic physiological changes mediated by seminal fluid components transferred upon mating, including decreased longevity. Their physiological and behavioral effects have been well characterized, but little is known about resulting changes in regulation of gene expression or the extent to which mating-induced changes in gene expression are the same as those occurring during aging.
We assessed genome-wide mRNA, microRNA, and three common histone modifications implicated in gene activation for young and aged virgin and mated female D. melanogaster in a factorial design. We identified phenotypically plastic transcripts and epigenetic modifications associated with mating and aging. We used these data to derive phenotypically plastic regulatory networks associated with mating of young flies, and aging of virgin and mated flies. Many of the mRNAs, microRNAs and epigenetic modifications associated with mating of young flies also occur with age in virgin flies, which may reflect mating-induced accelerated aging. We functionally tested the plastic regulatory networks by overexpressing environmentally sensitive microRNAs. Overexpression resulted in altered expression of ~70% of candidate target genes, and in all cases affected oviposition.
Our results implicate microRNAs as mediators of phenotypic plasticity associated with mating and provide a comprehensive documentation of the genomic and epigenomic changes that accompany mating- and aging-induced physiological changes in female D. melanogaster.
表型可塑性使生物体能够对不断变化的环境状况迅速做出反应，了解其基因组基础有助于深入了解影响复杂表型的潜在基因和遗传网络。雌性黑腹果蝇在交配时会受到精液成分介导的显著生理变化，包括寿命缩短。它们的生理和行为效应已得到充分表征，但对于由此导致的基因表达调控变化，以及交配诱导的基因表达变化与衰老过程中发生的变化在多大程度上相同，人们了解甚少。
我们采用析因设计评估了年轻和年老的未交配及已交配雌性黑腹果蝇全基因组范围内的mRNA、微小RNA以及与基因激活相关的三种常见组蛋白修饰。我们鉴定出了与交配和衰老相关的表型可塑性转录本和表观遗传修饰。我们利用这些数据推导出与年轻果蝇交配以及未交配和已交配果蝇衰老相关的表型可塑性调控网络。许多与年轻果蝇交配相关的mRNA、微小RNA和表观遗传修饰在未交配果蝇衰老过程中也会出现，这可能反映了交配诱导的加速衰老。我们通过过表达对环境敏感的微小RNA对可塑性调控网络进行了功能测试。过表达导致约70%的候选靶基因表达改变，并且在所有情况下都影响产卵。
我们的结果表明微小RNA是与交配相关的表型可塑性的介导因子，并全面记录了雌性黑腹果蝇交配和衰老诱导的生理变化所伴随的基因组和表观基因组变化。
