Recruitment of LC3 by Campylobacter jejuni to bacterial invasion site on host cells via the Rac1-mediated signaling pathway

• Material Type: 博士論文
• ISSN: 2235-2988
• Title: Recruitment of LC3 by Campylobacter jejuni to bacterial invasion site on host cells via the Rac1-mediated signaling pathway
• Volume: 12
• Author/Editor: Fukushima, Shiho; Shimohata, Takaaki; Inoue, Yuri; Kido, Junko; Uebanso, Takashi; Mawatari, Kazuaki; Takahashi, Akira
• Author Heading: Fukushima, Shiho; Shimohata, Takaaki; Inoue, Yuri; Kido, Junko; Uebanso, Takashi; Mawatari, Kazuaki; Takahashi, Akira
• Publication, Distribution, etc.: Frontiers Media S.A.
• Publication Date: 2022-03-03
• Publication Date (W3CDTF): 2022-03-03
• Alternative Title: Rac1シグナル伝達経路を介したカンピロバクター・ジェジュニの宿主細胞侵入部位へのLC3動員; New Function of Autophagy in C. jejuni Invasion
• Periodical title: Frontiers in Cellular and Infection Microbiology
• Degree grantor/type: 徳島大学
• Date Granted: 2022-03-23
• Date Granted (W3CDTF): 2022-03-23
• Dissertation Number: 甲第3601号
• Degree Type: 博士（栄養学）
• Conferring No. (Dissertation): 甲第3601号
• Text Language Code: eng
• Subject Heading: Campylobacter jejuni; autophagy; LC3; Rac1; invasion
• Target Audience: 一般
• Note (General): Campylobacter jejuni is a leading cause of food-borne disease worldwide. The pathogenicity of C. jejuni is closely associated with the internalization process in host epithelial cells, which is related to a host immune response. Autophagy indicates a key role in the innate immune system of the host to exclude invasive pathogens. Most bacteria are captured by autophagosomes and degraded by autophagosome-lysosome fusion in host cells. However, several pathogens, such as Salmonella and Shigella, avoid and/or escape autophagic degradation to establish infection. But autophagy involvement as a host immune response to C. jejuni infection has not been clarified. This study revealed autophagy association in C. jejuni infection. During infection, C. jejuni activated the Rho family small GTPase Rac1 signaling pathway, which modulates actin remodeling and promotes the internalization of this pathogen. In this study, we found the LC3 contribution to C. jejuni invasion signaling via the Rac1 signaling pathway. Interestingly, during C. jejuni invasion, LC3 was recruited to bacterial entry site depending on Rac1 GTPase activation just at the early step of the infection. C. jejuni infection induced LC3-II conversion, and autophagy induction facilitated C. jejuni internalization. Also, autophagy inhibition attenuated C. jejuni invasion step. Moreover, Rac1 recruited LC3 to the cellular membrane, activating the invasion of C. jejuni. Altogether, our findings provide insights into the new function of LC3 in bacterial invasion. We found the interaction between the Rho family small GTPase, Rac1, and autophagy-associated protein, LC3.
• DOI: info:doi/10.3389/fcimb.2022.829682; https://doi.org/info:doi/10.3389/fcimb.2022.829682
• Persistent ID (NDL): info:ndljp/pid/12296657; https://dl.ndl.go.jp/pid/12296657
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2022-06-05T18:01:14+09:00
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://repo.lib.tokushima-u.ac.jp/117002
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp