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J Mol Biol. 2017 Jan 6;429(1):142-157. doi: 10.1016/j.jmb.2016.11.009. Epub 2016 Nov 19.

S100A10 Regulates ULK1 Localization to ER-Mitochondria Contact Sites in IFN-γ-Triggered Autophagy.

Author information

1
Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.
2
Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.
3
Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; Center of Infectious Disease and Signaling Research, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.
4
Center of Infectious Disease and Signaling Research, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; Department of Microbiology and Immunology, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.
5
Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; Center of Infectious Disease and Signaling Research, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; Department of Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.
6
Institute of Oral Medicine, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan.
7
Departments of Microbiology & Immunology and Pediatrics, and Canadian Center for Vaccinology, Dalhousie University, Halifax, Nova Scotia B3H 4R2, Canada.
8
Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan; Center of Infectious Disease and Signaling Research, College of Medicine, National Cheng Kung University, Tainan 701, Taiwan. Electronic address: yslin1@mail.ncku.edu.tw.

Abstract

During the process of autophagy, the autophagy-related proteins are translocated to autophagosome formation sites. Here, we demonstrate that S100A10 is required for ULK1 localization to autophagosome formation sites. Silencing of S100A10 reduces IFN-γ-induced autophagosome formation. We also determined the role of annexin A2 (ANXA2), a binding partner of S100A10, which has been reported to promote phagophore assembly. Silencing of ANXA2 reduced S100A10 expression. However, overexpression of S100A10 in ANXA2-silenced cells was still able to enhance autophagosome formation, suggesting that ANXA2 regulates IFN-γ-induced autophagy through S100A10. We also observed that S100A10 interacted with ULK1 after IFN-γ stimulation, and S100A10 knockdown prevented ULK1 localization to autophagosome formation sites. Finally, the release of high mobility group protein B1, one of the functions mediated by IFN-γ-induced autophagy, was inhibited in S100A10 knockdown cells. These results elucidate the importance of S100A10 in autophagosome formation and reveal the relationship between S100A10 and ULK1 in IFN-γ-induced autophagy.

KEYWORDS:

HMGB1; S100A10; ULK1 translocation; autophagosome formation; interferon-γ

PMID:
27871932
DOI:
10.1016/j.jmb.2016.11.009
[Indexed for MEDLINE]

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