UMMS Affiliation

Program in Molecular Medicine

Publication Date

2-1-2017

Document Type

Article

Disciplines

Cell Biology | Cellular and Molecular Physiology

Abstract

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.

Keywords

C. elegans, HLH-30/TFEB, autophagy, effector triggered immunity (ETI), intrinsic cellular defense (INCED), pore-forming toxin (PFT), surveillance immunity

Rights and Permissions

Copyright © 2017 The Author(s). Published with license by Taylor and Francis.

DOI of Published Version

10.1080/15548627.2016.1256933

Source

Autophagy. 2017 Feb;13(2):371-385. doi: 10.1080/15548627.2016.1256933. Epub 2016 Nov 22. Link to article on publisher's site

Journal/Book/Conference Title

Autophagy

Comments

Full author list omitted for brevity. For full list of authors see article.

Related Resources

Link to Article in PubMed

PubMed ID

27875098

Creative Commons License

Creative Commons Attribution-Noncommercial 3.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial 3.0 License

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