F56F11.4 Extends Healthspan by Regulation of TOR-Related Pathway in C. elegans

Aging has emerged as a significant issue in human society, warranting intensified research efforts. Despite this, there is a noticeable dearth of research on genetic factors that could potentially extend lifespan. The genetic role of TOR/let-363 and its interactome was delved into in the model organism C. elegans. Utilizing RNA interference (RNAi), the impact of predicted interactors within the TOR pathway were explored on aging, with a particular emphasis on healthspan. This was achieved through comprehensive lifespan and pumping rate assays. Of the 20 genes examined, only the knockdown of F56F11.4 resulted in a reduction in both lifespan and early-stage pumping rate. To elucidate the interplay between F56F11.4 and TOR/let-363, double knockdown and RT-qPCR assays were employed to reveal their intricate regulatory roles in the aging process. Additionally, the conserved nature of F56F11.4 and let-363 across five well-studied organisms (C. elegans, H. sapiens, M. musculus, R. norvegicus, and D. melanogaster) was identified using bioinformatics analyses. The discovery of the influence of F56F11.4 on healthspan through the modulation of TOR/let-363 signaling suggests a promising target for the development of novel therapeutic strategies aimed at enhancing healthy aging.