Identification and characterization of a mitochondrial unfolded protein response transcription factor ATFS-1 in Litopenaeus vannamei. (July 2016)

• Record Type: Journal Article
• Authors: Chen, Yong-Gui; Yue, Hai-Tao; Zhang, Ze-Zhi; Yuan, Feng-Hua; Bi, Hai-Tao; Yuan, Kai; Weng, Shao-Ping; He, Jian-Guo; Chen, Yi-Hong
• Is Part Of: Fish & shellfish immunology. Volume 54(2016:Jul.)
• Page Start: 144
• Page End: 152
• Publication Date: 2016-07
• Subjects: Litopenaeus vannamei -- ATFS-1 -- ROS -- Innate immunity -- Mitochondrial unfolded protein response; Fishes -- Immunology -- Periodicals; Shellfish -- Immunology -- Periodicals; Poissons -- Immunologie -- Périodiques; Crustacés -- Immunologie -- Périodiques; 571.9617
• DOI: 10.1016/j.fsi.2015.10.019
• Languages: English
• ISSNs: 1050-4648

Abstract

Abstract: A mitochondrial specific stress response termed mitochondrial unfolded protein response (UPR mt ) is activated in responding to disturbance of protein homeostasis in mitochondria. The activating transcription factor associated with stress-1 (designated as ATFS-1 ) is the key regulator of UPR mt . To investigating the roles of ATFS-1 ( LvATFS-1 ) in Litopenaeus vannamei mitochondrial stress remission and immunity, it's full length cDNA was cloned. The open reading frame of LvATFS-1 was 1, 557 bp in length, deducing to a 268 amino acids protein. LvATFS-1 was highly expressed in muscle, hemocytes and eyestalk. Subcellular location assays showed that N-terminal of LvATFS-1 contained a mitochondrial targeting sequence, which could directed the fused EGFP located to mitochondria. And the C-terminal of LvATFS-1, which had a nuclear localization signal, expressed in nucleus. The in vitro experiments verified that LvATFS-1 could reduced the level of intracellular reactive oxygen species ( ROS ). And results of real-time RT-PCR indicated that LvATFS-1 might scavenge excess ROS via ROS-eliminating genes regulation. Reporter gene assays showed that LvATFS-1 could upregulated the expression of the antimicrobial peptide genes in Drosophila Schneider 2 cells. Results of real-time RT-PCR showed that Vibrio alginolyticus or white spot syndrome virus (WSSV) infection induced the expression of LvATFS-1 . And knocked-down LvATFS-1 by RNAi resulted in a higher cumulative mortality of L. vannamei upon V. alginolyticus or WSSV infection. These results suggested that LvATFS-1 not only rolled in mitochondrial specific stress responding, but also important for L. vannamei immunologic defence. Highlights: Cloning the activating transcription factor associated with stress-1 in Litopenaeus vannamei (designated as LvATFS-1). LvATFS-1 could reduced the level of intracellular reactive oxygen species. LvATFS-1 upregulated the expression of the antibacterial peptide genes in S2 cells. Knocked-down LvATFS-1 caused a higher cumulative mortality upon V. alginolyticus or WSSV infection in L. vannamei.