In this way, our model is consistent with modern evolutionary models of aging, which explain animal lifespan diversity by evolution of different strategies for age-dependent investment in the maintenance of tissue architecture and function [ 28, 29, 65].
Is UPRmt activation sufficient to explain the lifespan extension of the nduf-7 (et19 ) mutant, as has been suggested for other long-lived mutants (Durieux et al. 2011; Houtkooper et al. 2013)?
In contrast, low doses of such cytotoxic agents can activate hormesis in several paradigms, and this may explain the lifespan-prolonging potential of autophagy inducers including resveratrol and caloric restriction.
Such correlations may explain aspects of lifespan evolution, and why loss-of-function mutants can result in lifespan extension.
For the two genes showing an association with lifespan (hep and Lim3), we address whether large differences in expression levels and/or amino acid differences could explain the observed lifespan differences.
The identification of genes under positive selection in this fish reveals potential candidates to explain its compressed lifespan.
Reduced granulomas in the lungs of Pycard−/− provide plausible mechanisms to explain the decreased lifespan observed in these animals during chronic Mtb infection.
Since AcCoA integrates various nutrition pathways, our findings may explain diet-dependent lifespan and autophagy regulation.
No model based on asymmetrical inheritance can explain increased male lifespan in response to inbreeding.
