MAP1S Protein Regulates the Phagocytosis of Bacteria and Toll-like Receptor (TLR) Signaling. Academic Article uri icon

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 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.

published proceedings

  • J Biol Chem

altmetric score

  • 0.5

author list (cited authors)

  • Shi, M., Zhang, Y., Liu, L., Zhang, T., Han, F., Cleveland, J., ... Zhang, D

citation count

  • 13

complete list of authors

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

publication date

  • January 2016