During macroautophagy, the human WIPI (WD-repeat protein interacting with phosphoinositides) proteins (WIPI14) function as phosphatidylinositol 3-phosphate effectors at the nascent autophagosome. Likewise, the two WIPI homologues in <i>Caenorhabditis elegans</i>, ATG-18 and EPG-6, play important roles in autophagy, whereby ATG-18 is considered to act upstream of EPG-6 at the onset of autophagy. Due to its essential role in autophagy, ATG-18 was found to be also essential for lifespan extension in <i>Caenorhabditis elegans</i>; however, this has not yet been addressed with regard to EPG-6. Here, we wished to address this point and generated mutant strains that expressed the autophagy marker GFP::LGG-1 (GFP-LC3 in mammals) and harbored functional deletions of either <i>
atg-18</i> (<i>
atg18(gk378)</i>), <i>
epg-6</i> (<i>
epg-6(
bp242)</i>) or both (<i>
atg-18(
gk378);
epg-6(
bp242)</i>). Using quantitative fluorescence microscopy, Western blotting, and lifespan assessments, we provide evidence that in the absence of either ATG-18 or EPG-6 autophagy was impaired, and while <i>
atg-18</i> mutant animals showed a short-lived phenotype, lifespan was significantly increased in <i>
epg-6</i> mutant animals. We speculate that the long-lived phenotype of <i>
epg-6</i> mutant animals points towards an autophagy-independent function of EPG-6 in lifespan control that warrants further mechanistic investigations in future studies.