Experimentally reduced insulin/IGF-1 signaling in adulthood extends lifespan of parents and improves Darwinian fitness of their offspring. Issue 2 (1st April 2019)

• Record Type: Journal Article
• Authors: Lind, Martin I.; Ravindran, Sanjana; Sekajova, Zuzana; Carlsson, Hanne; Hinas, Andrea; Maklakov, Alexei A.
• Is Part Of: Evolution letters. Volume 3:Issue 2(2019)
• Page Start: 207
• Page End: 216
• Publication Date: 2019-04-01
• Subjects: Ageing -- antagonistic pleiotropy -- functional trade-offs -- hyperfunction -- IIS signaling -- parental effects -- senescence; Evolution (Biology) -- Periodicals; Evolution (Biology); Biological Evolution; Electronic journals; Fulltext; Internet Resources; Periodicals; Periodicals; Periodical; 576.8
• DOI: 10.1002/evl3.108
• Languages: English
• ISSNs: 2056-3744

Abstract

Abstract: Classical theory maintains that ageing evolves via energy trade-offs between reproduction and survival leading to accumulation of unrepaired cellular damage with age. In contrast, the emerging new theory postulates that ageing evolves because of deleterious late-life hyper-function of reproduction-promoting genes leading to excessive biosynthesis in late-life. The hyper-function theory uniquely predicts that optimizing nutrient-sensing molecular signaling in adulthood can simultaneously postpone ageing and increase Darwinian fitness. Here, we show that reducing evolutionarily conserved insulin/IGF-1 nutrient-sensing signaling via daf-2 RNA interference (RNAi) fulfils this prediction in Caenorhabditis elegans nematodes. Long-lived daf-2 RNAi parents showed normal fecundity as self-fertilizing hermaphrodites and improved late-life reproduction when mated to males. Remarkably, the offspring of daf-2 RNAi parents had higher Darwinian fitness across three different genotypes. Thus, reduced nutrient-sensing signaling in adulthood improves both parental longevity and offspring fitness supporting the emerging view that suboptimal gene expression in late-life lies at the heart of ageing.