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

 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 
 Nature Communications, Vol.7 : 11726, 2016 
Journal Title
 Nature Communications 
Issue Date
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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1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Seung Won(김승원) ORCID logo https://orcid.org/0000-0002-1692-1192
Cheon, Jae Hee(천재희) ORCID logo https://orcid.org/0000-0002-2282-8904
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