Males induce premature demise of the opposite sex by multifaceted strategies.
Males induce premature demise of the opposite sex by multifaceted strategies.
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DOI:
10.1038/s43587-022-00276-y
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发表时间:
2022-09
期刊:
影响因子:
--
通讯作者:
Brunet, Anne
中科院分区:
文献类型:
--
作者:
Booth, Lauren N. N.;Shi, Cheng;Tantilert, Cindy;Yeo, Robin W. W.;Miklas, Jason W. W.;Hebestreit, Katja;Hollenhorst, Cecilia N. N.;Maures, Travis J. J.;Buckley, Matthew T. T.;Murphy, Coleen T. T.;Brunet, Anne
Interactions between the sexes negatively impact health in many species. In Caenorhabditis, males shorten the lifespan of the opposite sex—hermaphrodites or females. Here we use transcriptomic profiling and targeted screens to systematically uncover conserved genes involved in male-induced demise in C. elegans. Some genes (for example, delm-2, acbp-3), when knocked down, are specifically protective against male-induced demise. Others (for example, sri-40), when knocked down, extend lifespan with and without males, suggesting general mechanisms of protection. In contrast, many classical long-lived mutants are impacted more negatively than wild type by the presence of males, highlighting the importance of sexual environment for longevity. Interestingly, genes induced by males are triggered by specific male components (seminal fluid, sperm and pheromone), and manipulating these genes in combination in hermaphrodites induces stronger protection. One of these genes, the conserved ion channel delm-2, acts in the nervous system and intestine to regulate lipid metabolism. Our analysis reveals striking differences in longevity in single sex versus mixed sex environments and uncovers elaborate strategies elicited by sexual interactions that could extend to other species. Sexual interactions with males shorten the lifespan of the opposite sex in several species, including Caenorhabditis elegans, but the mechanisms are not fully understood. Here the authors use transcriptomic profiling in C. elegans to systematically identify the genetic pathways involved in male-induced demise, which include upregulation of a conserved ion channel that regulates fat metabolism.
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