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TRIM31 promotes Atg5/Atg7-independent autophagy in intestinal cells.

Authors
 Eun A. Ra  ;  Taeyun A. Lee  ;  Seung Won Kim  ;  Areum Park  ;  Hyun jin Choi  ;  Insook Jang  ;  Sujin Kang  ;  Jae Hee Cheon  ;  Jin Won Cho  ;  Ji Eun Lee  ;  Sungwook Lee  ;  Boyoun Park 
Citation
 Nature Communications, Vol.7 : 11726-11726, 2016 
Journal Title
 Nature Communications 
Issue Date
2016
Abstract
Autophagy is responsible for the bulk degradation of cytosolic constituents and plays an essential role in the intestinal epithelium by controlling beneficial host-bacterial relationships. Atg5 and Atg7 are thought to be critical for autophagy. However, Atg5- or Atg7-deficient cells still form autophagosomes and autolysosomes, and are capable of removing proteins or bacteria. Here, we report that human TRIM31 (tripartite motif), an intestine-specific protein localized in mitochondria, is essential for promoting lipopolysaccharide-induced Atg5/Atg7-independent autophagy. TRIM31 directly interacts with phosphatidylethanolamine in a palmitoylation-dependent manner, leading to induction of autolysosome formation. Depletion of endogenous TRIM31 significantly increases the number ofintestinal epithelial cells containing invasive bacteria. Crohn's disease patients display TRIM31 downregulation. Human cytomegalovirus-infected intestinal cells show a decrease in TRIM31 expression as well as a significant increase in bacterial load, reversible by the introduction of wild-type TRIM31. We provide insight into an alternative autophagy pathway that protects againstintestinal pathogenic bacterial infection.
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DOI
10.1038/ncomms11726
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부)
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실)
Yonsei Authors
김승원(Kim, Seung Won)
천재희(Cheon, Jae Hee) ORCID logo https://orcid.org/0000-0002-2282-8904
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URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/146916
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