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Evol Lett. 2019 Mar 4;3(2):207-216. doi: 10.1002/evl3.108. eCollection 2019 Apr.

Experimentally reduced insulin/IGF-1 signaling in adulthood extends lifespan of parents and improves Darwinian fitness of their offspring.

Author information

1
Animal Ecology, Department of Ecology and Genetics Uppsala University Uppsala 752 36 Sweden.
2
School of Biological Sciences University of East Anglia Norwich NR4 7TJ United Kingdom.
3
Department of Cell and Molecular Biology Uppsala University Uppsala 751 24 Sweden.

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.

KEYWORDS:

Ageing; IIS signaling; antagonistic pleiotropy; functional trade‐offs; hyperfunction; parental effects; senescence

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