“…Moreover, different molecular players have been identified in the past two decades that mediate Mit mutants' longevity: a handful of transcription factors [7,[17][18][19][20][21][22], autophagy-and apoptosis-regulatory genes [7,14,18,23,24], some kinases [25][26][27], as well as some mitochondrial metabolites [28] and chromatin remodeling genes [29,30]. Nonetheless, whether the same molecular mechanisms underlie the different Mit-mutant's phenotypic features is largely unknown [14,31,32]. The C. elegans p53 ortholog, cep-1, specifies many of the Mitmutant phenotypes, including animal's reduced fertility and germline size [14,17,18,33], and mediates germ-cell apoptosis in response to genotoxic stress [34,35].…”