Quantitative proteomics analysis of Caenorhabditis elegans upon germ cell loss

The abrogation of the germ cells in Caenorhabditis elegans (C. elegans) by either genetic means or cell ablation results in about 60% increase of longevity. Upon the inhibition of germline stem cell proliferation, certain signaling molecules inhibit the target of rapamycin (TOR), activate the transcription factors including DAF-16, DAF-12, and PHA-4, leading to altered fatty acid lipolysis, autophagy, stress resistance, and the extended lifespan. But the exact cascades and interactions of those signaling pathways are still obscure. To understand how the reproductive system affects aging at the protein level, we determined the protein expression profile of the long-lived temperature-sensitive mutant glp-1(e2141) and wild-type N2 using isobaric tags for relative and absolute quantitation (iTRAQ) technology. Our results showed that the abundance of proteins relevant to transcription, RNA processing, translation, protein folding, and proteolytic process were decreased, while collagen proteins and proteins involved in detoxification and innate immune responses were increased in C. elegans glp-1 mutant, these alterations of protein abundance might attenuate protein metabolism and enhance immune response and stress resistance, and finally contribute to germline-mediated longevity.

This study provides an overview of the altered protein expression upon germline ablation. Germ-cell loss results in decreased abundance of proteins involved in protein synthesis and breakdown, and increased abundance of proteins involved in detoxification and immune response, suggesting that protein synthesis and metabolism might be attenuated, while detoxification and immune responses might be increased. The altered protein abundance might result in physiological adaptations that contribute to extended longevity in germline-deficient C. elegans. This study brings new light on the role of reproductive control of lifespan.