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ATG-18 and EPG-6 are Both Required for Autophagy but Differentially Contribute to Lifespan Control in Caenorhabditis elegans

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Takacs,  Z       
IMPRS From Molecules to Organisms, Max Planck Institute for Developmental Biology, Max Planck Society;

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Sporbeck,  K       
IMPRS From Molecules to Organisms, Max Planck Institute for Developmental Biology, Max Planck Society;

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Proikas-Cezanne,  T       
IMPRS From Molecules to Organisms, Max Planck Institute for Developmental Biology, Max Planck Society;

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Citation

Takacs, Z., Sporbeck, K., Stoeckle, J., Prado Carvajal, M., Grimmel, M., & Proikas-Cezanne, T. (2019). ATG-18 and EPG-6 are Both Required for Autophagy but Differentially Contribute to Lifespan Control in Caenorhabditis elegans. Poster presented at GBM/DGZ Fall Conference 2019: Age-Related Human Diseases, Special Focus: Autophagy, Tübingen, Germany.


Cite as: https://hdl.handle.net/21.11116/0000-000C-1E3C-1
Abstract
During macroautophagy, the human WIPI (WD-repeat protein interacting with phosphoinositides) proteins (WIPI1–4) function as phosphatidylinositol 3-phosphate effectors at the nascent autophagosome. Likewise, the two WIPI homologues in Caenorhabditis elegans, 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 Caenorhabditis elegans; 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 atg-18 (atg18(gk378)), epg-6 (epg-6(bp242)) or both (atg-18(gk378);epg-6(bp242)). 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 atg-18 mutant animals showed a short-lived phenotype, lifespan was significantly increased in epg-6 mutant animals. We speculate that the long-lived phenotype of epg-6 mutant animals points towards an autophagy-independent function of EPG-6 in lifespan control that warrants further mechanistic investigations in future studies.