Identification and functional characterization of an endoplasmic reticulum oxidoreductin 1-α gene in Litopenaeus vannamei. (April 2016)

• Record Type: Journal Article
• Authors: Zhang, Ze-Zhi; Yuan, Kai; Yue, Hai-Tao; Yuan, Feng-Hua; Bi, Hai-Tao; Weng, Shao-Ping; He, Jian-Guo; Chen, Yi-Hong
• Is Part Of: Developmental and comparative immunology. Volume 57(2016)
• Page Start: 10
• Page End: 19
• Publication Date: 2016-04
• Subjects: Litopenaeus vannamei -- White spot syndrome virus -- Endoplasmic reticulum stress -- Unfolded protein response -- Apoptosis -- ERO1-α; Immunology -- Periodicals; Developmental immunology -- Periodicals; 616.079
• DOI: 10.1016/j.dci.2015.11.013
• Languages: English
• ISSNs: 0145-305X

Abstract

Abstract: In the current study, full-length sequence of endoplasmic reticulum oxidoreductin 1-α ( LvERO1-α ) was cloned from Litopenaeus vannamei . Real-time RT-PCR results showed that LvERO1-α was highly expressed in hemocytes, gills, and intestines. White spot syndrome virus (WSSV) challenge was performed, and the expression of LvERO1-α and two other downstream genes of the double-stranded RNA-activated protein kinase-like ER kinase-eIF2α (PERK-α) pathway, namely, homocysteine-induced endoplasmic reticulum protein ( LvHERP ) and acylamino-acid-releasing enzyme ( LvAARE ), strongly increased in the hemocytes. Flow cytometry assay results indicated that the apoptosis rate of L . vannamei hemocytes in the LvERO1-α knockdown group was significantly lower than that of the controls. Moreover, shrimps with knockdown expression of LvERO1-α exhibited decreased cumulative mortality upon WSSV infection. Downregulation of L . vannamei immunoglobulin-binding protein ( LvBip ), which had been proven to induce unfolded protein response (UPR) in L . vannamei, did not only upregulate LvERO1-α, LvHERP, and LvAARE in hemocytes, but also increased their apoptosis rate, as well as the shrimp cumulative mortality. Furthermore, reporter gene assay results showed that the promoter of LvERO1-α was activated by L . vannamei activating transcription factor 4, thereby confirming that LvERO1-α was regulated by the PERK-eIF2α pathway. These results suggested that LvERO1-α plays a critical role in WSSV-induced apoptosis, which likely occurs through the WSSV-activated PERK-eIF2α pathway. Highlights: Identification and characterization of an ER oxidoreductin 1-α in Litopenaeus vannamei (designated as LvERO1-α ). Expression of LvERO1-α was upregulated by white spot syndrome virus (WSSV). LvERO1-α knocked-down decreased the apoptosis rate of hemocytes in WSSV infected L . vannamei. Promoter of LvERO1-α was activated by L. vannamei activating transcription factor 4.