Among invertebrates, birds and mammals, experimental paradigms that limit reproductive investment also cause lifespan extension [232]. Hypothetically, the need for repairing and preventing damage to the germline dominates resource allocation strategies, while the somatic tissues age and deteriorate [112]. In support of such theories, modulations of reproduction that eliminate germ cells in C. elegans and D. melanogaster provide effective mechanisms for extending lifespan [232-234], phenotypes that may be caused by heightened resource availability and proteome stability within the post-mitotic soma [17, 235]. Inhibiting germline proliferation delays the onset of PolyQ-dependent aggregation and toxicity [235]. Proteasome activity and RPN-6 protein levels are increased in germline-lacking worms [17]. In these long-lived animals, increased proteasome activity, rpn-6 expression and longevity are modulated by DAF-16 [17]. Similar to these long-lived worms, FOXO4 is necessary for increased proteasome activity and PSMD11/Rpn6 levels in immortal hESCs [28, 236]. Interestingly, it has been recently reported that DNA damage in germ cells of C. elegans induce a systemic response that protects somatic tissues by increasing their proteasome activity [237].
Possibly slightly relevant