Abstract
The theory that ageing evolves because of competitive resource allocation between the soma and the germline has been challenged by studies showing that somatic maintenance can be improved without impairing reproduction. However, it has been suggested that cost‐free improvement in somatic maintenance is possible only under a narrow range of benign conditions. Here, we show that experimental downregulation of insulin/IGF‐1 signaling (IIS) in C. elegans nematodes, a robustly reproducible life span‐ and health span‐extending treatment, reduces fitness in a complex variable environment when initiated during development but does not reduce fitness when initiated in adulthood. Thus, our results show that the costs and benefits of reduced IIS can be uncoupled when organisms inhabit variable environments, and, therefore, do not provide support for the resource allocation theory. Our findings support the theory that the force of natural selection on gene expression in evolutionarily conserved signaling pathways that shape life‐history traits declines after the onset of reproduction resulting in organismal senescence.
Highlights
Ageing, or senescence, is a physiological deterioration of an organism resulting in reduced health, impaired reproduction, and increased probability of death with advancing age (Partridge and Barton 1993; Flatt and Partridge 2018)
The ELIT predicts that the costs and the benefits of insulin/IGF-1 signaling (IIS) downregulation can be separated along the life course of an organism, such that postdevelopment downregulation can improve the soma without a cost to reproduction by abolishing “early-life inertia” in the level of IIS signaling
We directly test the predictions derived from the disposable soma” theory (DST) and the E-LIT by downregulating IIS signaling in Caenorhabditis elegans nematodes using daf-2 RNA interference (RNAi) approach, starting either in early development or after reproductive maturity in a variable environment
Summary
Senescence, is a physiological deterioration of an organism resulting in reduced health, impaired reproduction, and increased probability of death with advancing age (Partridge and Barton 1993; Flatt and Partridge 2018). Mutations in key elements of these pathways can result in life span increases (Kenyon 2010; Kenyon 2011), sometimes up to 100−500% (Chen et al 2013), but are often associated with costs to other life-history traits such as impaired development and reduced reproductive performance (Briga and Verhulst 2015; Maklakov et al 2017)
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