Streptococcus pneumoniae triggers hierarchical autophagy through reprogramming of LAPosome-like vesicles via NDP52-delocalization

Michinaga Ogawa, Naoki Takada, Sayaka Shizukuishi, Mikado Tomokiyo, Bin Chang, Mitsutaka Yoshida, Soichiro Kakuta, Isei Tanida, Akihide Ryo, Jun Lin Guan, Haruko Takeyama, Makoto Ohnishi

研究成果: Article

2 引用 (Scopus)

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In innate immunity, multiple autophagic processes eliminate intracellular pathogens, but it remains unclear whether noncanonical autophagy and xenophagy are coordinated, and whether they occur concomitantly or sequentially. Here, we show that Streptococcus pneumoniae, a causative of invasive pneumococcal disease, can trigger FIP200-, PI3P-, and ROS-independent pneumococcus-containing LC3-associated phagosome (LAPosome)-like vacuoles (PcLVs) in an early stage of infection, and that PcLVs are indispensable for subsequent formation of bactericidal pneumococcus-containing autophagic vacuoles (PcAVs). Specifically, we identified LC3- and NDP52-delocalized PcLV, which are intermediates between PcLV and PcAV. Atg14L, Beclin1, and FIP200 were responsible for delocalizing LC3 and NDP52 from PcLVs. Thus, multiple noncanonical and canonical autophagic processes are deployed sequentially against intracellular S. pneumoniae. The Atg16L1 WD domain, p62, NDP52, and poly-Ub contributed to PcLV formation. These findings reveal a previously unidentified hierarchical autophagy mechanism during bactericidal xenophagy against intracellular bacterial pathogens, and should improve our ability to control life-threating pneumococcal diseases.

元の言語English
記事番号25
ジャーナルCommunications Biology
3
発行部数1
DOI
出版物ステータスPublished - 2020 12 1

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)
  • Medicine (miscellaneous)

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    Ogawa, M., Takada, N., Shizukuishi, S., Tomokiyo, M., Chang, B., Yoshida, M., Kakuta, S., Tanida, I., Ryo, A., Guan, J. L., Takeyama, H., & Ohnishi, M. (2020). Streptococcus pneumoniae triggers hierarchical autophagy through reprogramming of LAPosome-like vesicles via NDP52-delocalization. Communications Biology, 3(1), [25]. https://doi.org/10.1038/s42003-020-0753-3