MAP1S Protein Regulates the Phagocytosis of Bacteria and Toll-like Receptor (TLR) Signaling

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

来源：JOURNAL OF BIOLOGICAL CHEMISTRY, 2016, 291(3): 1243-1250.

DOI：10.1074/jbc.M115.687376

• INNATE IMMUNITY
• STIMULATED PHAGOCYTOSIS
• PHAGOSOME MATURATION
• AUTOPHAGY
• ACTIVATION
• MICROTUBULE
• RECOGNITION
• PATHWAY
• CELLS
• INFECTION

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 MAP1S interacts 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.

• 出版日期2016-1-15
• 单位哈尔滨工业大学