Colloquium
Department of Physics, NCU
HLH-30-mediated autophagy functions cell-autonomously for intrinsic cellular defense against bacterial pore-forming toxin in C. elegans
Speaker
Prof. Chang-Shi Chen (陳昌熙)
Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University
Date 2016.05.24(Tue)
Time 14:00
Place S4-625
「歡迎大學部同學參加，可獲得中大護照認證2小時」
Abstract
Autophagy is an evolutionarily conserved intracellular system that maintains cellular homeostasis by degrading and recycling damaged cellular components. HLH-30-mediated autophagy has been reported to regulate tolerance to bacterial infection, but less is known about the bona fide bacterial effector that activates HLH-30 and autophagy. Today, I will show you that bacterial membrane pore-forming toxin (PFT) induces autophagy in an HLH-30-dependent manner in Caenorhabditis elegans. Moreover, autophagy controls the susceptibility of animals to PFT toxicity through xenophagic degradation of PFT and repairs the membrane-pore in a cell-autonomous fashion in PFT-targeted intestinal cells in C. elegans. These results demonstrate that autophagic pathways and autophagy are induced partly at the transcriptional level through HLH-30 activation and are required to protect metazoans upon PFT intoxication. Together, our data show a new and powerful connection between HLH-30-mediated autophagy and epithelial intrinsic cellular defense against the single most common mode of bacterial attack in vivo.