Abstract
Organisms adapt to environmental changes in order to survive. Mothers exposed to nutritional stresses can induce an adaptive response in their offspring. However, the molecular mechanisms behind such inheritable links are not clear. Here we report that in Drosophila, starvation of mothers primes the progeny against subsequent nutritional stress. We found that RpL10Ab represses TOR pathway activity by genetically interacting with TOR pathway components TSC2 and Rheb. In addition, starved mothers produce offspring with lower levels of RpL10Ab in the germline, which results in higher TOR pathway activity, conferring greater resistance to starvation-induced oocyte loss. The RpL10Ab locus encodes for the RpL10Ab mRNA and a stable intronic sequence RNA (sisR-8), which collectively repress RpL10Ab pre-mRNA splicing in a negative feedback mechanism. During starvation, an increase in maternally deposited RpL10Ab and sisR-8 transcripts leads to the reduction of RpL10Ab expression in the offspring. Our study suggests that the maternally deposited RpL10Ab and sisR-8 transcripts trigger a negative feedback loop that mediates intergenerational adaptation to nutritional stress as a starvation response.
Highlights
Studies in various organisms have suggested an adaptive function for maternal effects [1]
Mothers who are exposed to nutritional stresses are known to produce offspring which are preconditioned to adapt to the mothers’ environment
We show that Drosophila mothers exposed to starvation produce offspring which are more resistant to starvation during oogenesis
Summary
Studies in various organisms have suggested an adaptive function for maternal effects [1]. Important is the effect of epigenetic modification of the oocyte DNA that can serve as a memory of maternal experience [2]. In Caenorhabditis elegans (C. elegans), maternal environmental factors such as nutrient availability and osmotic conditions lead to changes in the maternal inheritance of small RNA, insulin signalling, vitellogenin and sugars, which protect the progeny against subsequent stressful conditions [3,4,5,6,7]. Starvation of the mothers had been proposed to lead to inappropriate adaptation, which subsequently resulted in a higher incidence of metabolic syndrome such as diabetes and obesity in the generation [8]. The molecular mechanisms behind such an inheritable link are generally unknown
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