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Regulation of Caenorhabditis elegans vitellogenesis by DAF-2/IIS through separable transcriptional and posttranscriptional mechanisms

DOI: 10.1186/1472-6793-11-11

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Abstract:

In order to identify mechanisms that suppress vitellogenesis under prolongevity conditions, we studied factors regulating vitellogenesis in C. elegans nematodes. In C. elegans, vitellogenesis is depressed in the absence of insulin-like signaling (IIS). We found that the C. elegans daf-2/IIS pathway regulates vitellogenesis through two mechanisms. vit-2 transcript levels in daf-2 mutants were indirectly regulated through a germline-dependent signal, and could be rescued by introduction of daf-2(+) sperm. However, yolk protein (YP) levels in daf-2 mutants were also regulated by germline-independent posttranscriptional mechanisms.C. elegans vitellogenesis is regulated transcriptionally and posttranscriptionally in response to environmental and reproductive cues. The daf-2 pathway suppressed vitellogenesis through transcriptional mechanisms reflecting reproductive phenotypes, as well as distinct posttranscriptional mechanisms. This study reveals that pleiotropic effects of IIS pathway mutations can converge on a common downstream target, vitellogenesis, as a mechanism to modulate longevity.According to evolutionary theories of aging, lifespan evolves as a trade-off between the metabolic costs of somatic maintenance with those of reproduction. Reproductive processes such as egg production and progeny rearing are energy-intense and drain resources away from processes that promote somatic maintenance. Studies have provided evidence for a trade-off between reproduction and survival. For example, experimentally increased egg production in wild seabirds is associated with lower rates of postmigratory return to breeding grounds [1,2]. One mechanism by which organisms can regulate the relative burdens of reproduction and somatic maintenance in response to environmental conditions is through phenotypic plasticity of life-history traits, such as growth and reproduction [3]. Plasticity in life-history traits can affect lifespan directly, such as to delay reproduction until environ

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