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dc.contributor.authorChen, Huan-Da
dc.contributor.authorAroian, Raffi V
dc.contributor.authorChen, Chang-Shi
dc.date2022-08-11T08:09:46.000
dc.date.accessioned2022-08-23T16:42:51Z
dc.date.available2022-08-23T16:42:51Z
dc.date.issued2017-02-01
dc.date.submitted2017-03-27
dc.identifier.citation<p>Autophagy. 2017 Feb;13(2):371-385. doi: 10.1080/15548627.2016.1256933. Epub 2016 Nov 22. <a href="https://doi.org/10.1080/15548627.2016.1256933">Link to article on publisher's site</a></p>
dc.identifier.issn1554-8627 (Linking)
dc.identifier.doi10.1080/15548627.2016.1256933
dc.identifier.pmid27875098
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40174
dc.description<p>Full author list omitted for brevity. For full list of authors see article.</p>
dc.description.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.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=27875098&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright © 2017 The Author(s). Published with license by Taylor and Francis.
dc.rights.urihttp://creativecommons.org/licenses/by-nc/3.0/
dc.subjectC. elegans
dc.subjectHLH-30/TFEB
dc.subjectautophagy
dc.subjecteffector triggered immunity (ETI)
dc.subjectintrinsic cellular defense (INCED)
dc.subjectpore-forming toxin (PFT)
dc.subjectsurveillance immunity
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.titleHLH-30/TFEB-mediated autophagy functions in a cell-autonomous manner for epithelium intrinsic cellular defense against bacterial pore-forming toxin in C. elegans
dc.typeJournal Article
dc.source.journaltitleAutophagy
dc.source.volume13
dc.source.issue2
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3977&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2972
dc.identifier.contextkey9928021
refterms.dateFOA2022-08-23T16:42:51Z
html.description.abstract<p>Autophagy 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.</p>
dc.identifier.submissionpathoapubs/2972
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages371-385


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Copyright © 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.