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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, 2016 
Journal Title
NATURE COMMUNICATIONS
Issue Date
2016
Abstract
Autophagyis responsible for the bulk degradation of cytosolic constituents and plays an essential role in theintestinalepithelium by controlling beneficial host-bacterial relationships.Atg5and Atg7 are thought to be critical forautophagy. However,Atg5- or Atg7-deficientcellsstill form autophagosomes and autolysosomes, and are capable of removing proteins or bacteria. Here, we report that humanTRIM31(tripartite motif), an intestine-specific protein localized in mitochondria, is essential for promoting lipopolysaccharide-inducedAtg5/Atg7-independentautophagy.TRIM31directly interacts with phosphatidylethanolamine in a palmitoylation-dependent manner, leading to induction of autolysosome formation. Depletion of endogenousTRIM31significantly increases the number ofintestinalepithelialcellscontaining invasive bacteria. Crohn's disease patients displayTRIM31downregulation. Human cytomegalovirus-infectedintestinalcellsshow a decrease inTRIM31expression as well as a significant increase in bacterial load, reversible by the introduction of wild-typeTRIM31. We provide insight into an alternativeautophagypathway that protects againstintestinalpathogenic bacterial infection.
Files in This Item:
T201601666.pdf Download
DOI
10.1038/ncomms11726
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Others (기타) > 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
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/146916
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