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Characterization and function analysis of Epinephelus coioides Hsp40 response to Vibrio alginolyticus and SGIV infection

Heat shock protein 40 (Hsp40), a member of Heat shock proteins (Hsps) family, plays a crucial role in regulation of cell proliferation, survival and apoptosis in mammals. In this study, Hsp40, EcHsp40, was identified from Epinephelus coioides, an economically important marine-cultured fish in China...

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Published in:Fish & shellfish immunology 2021-11, Vol.118, p.396-404
Main Authors: Chen, He-Jia, Li, Pin-Hong, Yang, Yun, Xin, Xiao-Hong, Ou, Yan, Wei, Jing-Guang, Huang, You-Hua, Huang, Xiao-Hong, Qin, Qi-Wei, Sun, Hong-Yan
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Language:English
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Summary:Heat shock protein 40 (Hsp40), a member of Heat shock proteins (Hsps) family, plays a crucial role in regulation of cell proliferation, survival and apoptosis in mammals. In this study, Hsp40, EcHsp40, was identified from Epinephelus coioides, an economically important marine-cultured fish in China and Southeast Asian counties. The full length of EcHsp40 was 2236 bp in length containing a 1026 bp open reading frame (ORF) encoding 341 amino acids, with a molecular mass of 37.88 kDa and a theoretical pI of 9.09. EcHsp40 has two conserved domains DnaJ and DnaJ_C. EcHsp40 mRNA was detected in all tissues examined, and the expression was significantly up-regulated response to challenged with Vibrio alginolyticus or Singapore grouper iridovirus (SGIV), one of the important pathogens of marine fish. EcHsp40 was distributed in both the cytoplasm and nucleus, over-expression of EcHsp40 can inhibit the activity of nuclear factor-κB (NF-κB) and activator protein-1 (AP-1), significantly promote SGIV-induced apoptosis, intracellular caspase-3 activity and viral replication, suggesting that the EcHsp40 may play an important role in pathogenic stimulation. •Heat shock protein 40 (Hsp40) was characterized from Epinephelus coioides.•EcHsp40 mRNA were detected in all tissues examined, and significantly up-regulated during SGIV or Vibrio alginolyticus infection.•EcHsp40 can affect the SGIV replication, the activity of NF-κB/AP-1 and SGIV-induced apoptosis.
ISSN:1050-4648
1095-9947
DOI:10.1016/j.fsi.2021.09.030