HLH-30/TFEB-mediated autophagy functions in a cell-autonomous manner for epithelium intrinsic cellular defense against bacterial pore-forming toxin in C. elegans
UMass Chan AffiliationsProgram in Molecular Medicine
Document TypeJournal Article
effector triggered immunity (ETI)
intrinsic cellular defense (INCED)
pore-forming toxin (PFT)
Cellular and Molecular Physiology
MetadataShow full item record
AbstractAutophagy is an evolutionarily conserved intracellular system that maintains cellular homeostasis by degrading and recycling damaged cellular components. The transcription factor HLH-30/TFEB-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. Here, we reveal 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 repair of membrane-pore cell-autonomously in the 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 metazoan upon PFT intoxication. Together, our data show a new and powerful connection between HLH-30-mediated autophagy and epithelium intrinsic cellular defense against the single most common mode of bacterial attack in vivo.
Autophagy. 2017 Feb;13(2):371-385. doi: 10.1080/15548627.2016.1256933. Epub 2016 Nov 22. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/40174
Full author list omitted for brevity. For full list of authors see article.
RightsCopyright © 2017 The Author(s). Published with license by Taylor and Francis.
Except where otherwise noted, this item's license is described as Copyright © 2017 The Author(s). Published with license by Taylor and Francis.