MAP1S protein regulates the phagocytosis of bacteria and toll-like receptor (TLR) signaling

Ming Shi, Yifan Zhang, Leyuan Liu, Tingting Zhang, Fang Han, Joseph Cleveland, Fen Wang, Wallace L. McKeehan, Yu Li, Dekai Zhang

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

Phagocytosis is a critical cellular process for innate immune defense against microbial infection. The regulation of phagocytosis process is complex and has not been well defined. An intracellular molecule might regulate cell surface-initiated phagocytosis, but the underlying molecular mechanism is poorly understood (1). In this study, we found that microtubule-associated protein 1S (MAP1S), a protein identified recently that is involved in autophagy (2), is expressed primarily in macrophages. MAP1S-deficient macrophages are impaired in the phagocytosis of bacteria. Furthermore, we demonstrate that MAP1Sinteracts directly with MyD88, a key adaptor of Toll-like receptors (TLRs), upon TLR activation and affects the TLR signaling pathway. Intriguingly, we also observe that, upon TLR activation, MyD88 participates in autophagy processing in a MAP1S-dependent manner by co-localizing with MAP1 light chain 3 (MAP1-LC3 or LC3). Therefore, we reveal that an intracellular autophagy-related molecule of MAP1S controls bacterial phagocytosis through TLR signaling.

Original languageEnglish (US)
Pages (from-to)1243-1250
Number of pages8
JournalJournal of Biological Chemistry
Volume291
Issue number3
DOIs
StatePublished - Jan 15 2016
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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