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 () and Boyoun Park ()
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Eun A. Ra: College of Life Science and Biotechnology, Yonsei University
Taeyun A. Lee: College of Life Science and Biotechnology, Yonsei University
Seung Won Kim: Yonsei University College of Medicine
Areum Park: College of Life Science and Biotechnology, Yonsei University
Hyun jin Choi: College of Life Science and Biotechnology, Yonsei University
Insook Jang: Yonsei University
Sujin Kang: College of Life Science and Biotechnology, Yonsei University
Jae Hee Cheon: Yonsei University College of Medicine
Jin Won Cho: Yonsei University
Ji Eun Lee: Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University
Sungwook Lee: College of Life Science and Biotechnology, Yonsei University
Boyoun Park: College of Life Science and Biotechnology, Yonsei University

Nature Communications, 2016, vol. 7, issue 1, 1-15

Abstract: 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 of intestinal 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 against intestinal pathogenic bacterial infection.

Date: 2016
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DOI: 10.1038/ncomms11726

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