Genetically prolonged lifespan has been reported to be associated with better capability to resist to environmental stresses. In the previous fly work, we found a long-lived mutant with up-regulation of diacylglycerol lipase (DAGL) gene, inaE, and the DAGL transgenic fly displayed enhanced lifespan. Yet the role of DAGL in C. elegans lifespan remains unknown. Here, I demonstrated that the transgenic worm overexpressing F42G9.6, the DAGL orthologous gene, increases lifespan and RNA-interfered expression of DAGL decreases lifespan in C. elegans. On the other hand, the DAGL mutants exhibit decreased lifespan and lowered resistance to oxidative stress. The longevity and stress resistance of daf-2 partially depends on the function of DAGL and DAGL may be a target of DAF-16 which regulates the transcript expression level of DAGL. The knocking-down either DAG kinase or oligopeptide-transporter-2, which both genes are involved in TOR pathway, rescue the short-lived defect of the DAGL mutants. In summary, we propose that F42G9.6 is likely to catalyze the hydrolysis of DAG and overexpression of F42G9.6 plays an important function in TOR signaling to retard aging of C. elegans.