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タイトル: | Bcl-xL affects group a streptococcus-induced autophagy directly, by inhibiting fusion between autophagosomes and lysosomes, and indirectly, by inhibiting bacterial internalization via interaction with beclin 1-UVRAG |
著者: | Nakajima, Shintaro Aikawa, Chihiro Nozawa, Takashi Minowa-Nozawa, Atsuko Toh, Hirotaka Nakagawa, Ichiro https://orcid.org/0000-0001-6552-1702 (unconfirmed) |
著者名の別形: | 相川, 知宏 野澤, 孝志 中川, 一路 |
発行日: | 13-Jan-2017 |
出版者: | Public Library of Science |
誌名: | PLOS ONE |
巻: | 12 |
号: | 1 |
論文番号: | e0170138 |
抄録: | Anti-apoptotic Bcl-2 and Bcl-xL are proposed to regulate starvation-induced autophagy by directly interacting with Beclin 1. Beclin 1 is also thought to be involved in multiple vesicle trafficking pathways such as endocytosis by binding to Atg14L and UVRAG. However, how the interaction of Bcl-2 family proteins and Beclin 1 regulates anti-bacterial autophagy (xenophagy) is still unclear. In this study, we analyzed these interactions using Group A Streptococcus (GAS; Streptococcus pyogenes) infection as a model. GAS is internalized into epithelial cells through endocytosis, while the intracellular fate of GAS is degradation by autophagy. Here, we found that Bcl-xL but not Bcl-2 regulates GAS-induced autophagy. Autophagosome-lysosome fusion and the internalization process during GAS infection were promoted in Bcl-xL knockout cells. In addition, knockout of Beclin 1 phenocopied the internalization defect of GAS. Furthermore, UVRAG interacts not only with Beclin 1 but also with Bcl-xL, and overexpression of UVRAG partially rescued the internalization defect of Beclin 1 knockout cells during GAS infection. Thus, our results indicate that Bcl-xL inhibits GASinduced autophagy directly by suppressing autophagosome-lysosome fusion and indirectly by suppressing GAS internalization via interaction with Beclin 1-UVRAG. |
著作権等: | © 2017 Nakajima et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
URI: | http://hdl.handle.net/2433/218028 |
DOI(出版社版): | 10.1371/journal.pone.0170138 |
PubMed ID: | 28085926 |
出現コレクション: | 学術雑誌掲載論文等 |
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