Lysosomal control of proteostasis and reproductive capacity by conserved LMD-3 protein in <i>C. elegans</i>.

ABSTRACT: Human female fertility declines markedly with age, a pattern mirrored in C. elegans fecundity. This shared vulnerability stems from evolutionarily conserved molecular pathways. A growing body of evidence links impaired proteostasis-the cell's ability to manage its proteins-to this age-related fertility drop in both species, although the underlying mechanisms are not fully understood. Here, we identify that LMD-3, a LysM domain protein, is a critical regulator of proteostasis and reproductive capacity in C. elegans. Deficiency of lmd-3 leads to notable defects in oxidation resistance and constitutively high cellular stress responses. We demonstrate that LMD-3, localized to the lysosome, interacts with vitellogenin and a proton-pumping V-type ATPase via its TLDc domain t

SUBMITTER: Zhai Y 

PROVIDER: S-EPMC12652258 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature