Molecular characterization of a c-Jun NH2-terminal kinase (JNK)-interacting protein 4 (Lv-JIP4) in Litopenaeus vannamei and its potential role in the Lv-p38(MAPK) pathway in response to low temperature
文献类型: 外文期刊
第一作者: Zhong, Ping
作者: Zhong, Ping;Xu, Zhongneng;Huang, Wen;Zhong, Ping;Chen, Wei;Peng, Kai;Sun, Yuping;Wu, Xiaopeng;Sun, Huiming;Chen, Xiaoying;Huang, Wen;Wu, Xiaopeng;Huang, Wen;Luo, Peng;Li, Chaozheng;Huang, Wen;Li, Huo;Huang, Wen
作者机构:
关键词: Litopenaeus vannamei; C-Jun NH2-terminal kinase (JNK)-interacting proteins 4 (JIP4); Lv-p38(MAPK); Low-temperature stress
期刊名称:AQUACULTURE REPORTS ( 影响因子:3.385; 五年影响因子:3.645 )
ISSN: 2352-5134
年卷期: 2021 年 21 卷
页码:
收录情况: SCI
摘要: 9C-Jun NH2-terminal kinase (JNK)-interacting protein 4 (JIP4) is an essential molecule that organizes and links components of the mitogen-activated protein kinase (MAPK) pathway. In the present study, a novel JIP4 gene was identified in Litopenaeus vannamei and designated Lv-JIP4. The full-length Lv-JIP4 cDNA was 3923 bp in length and contained a 170-bp 5 '-untranslated region (UTR), a 72-bp 3 '-UTR, and a 3,681-bp open reading frame (ORF). The Lv-JIP4 protein contained three functional domains, including the Jnk-SapK_ap_N, JIP_LZII and WD40 domains. Lv-JIP4 mRNA was broadly distributed in all studied tissues, with the highest level in muscle. The in situ hybridization results showed that the Lv-JIP4 was scattered in muscle fibres and near the sarcolemma. Subcellular localization analysis indicated that Lv-JIP4 was located in the cytoplasm but not in the nucleus. The transcript levels of Lv-JIP4 in muscle were found to be significantly increased by low temperature, low pH, high salinity, poly(I:C), and LPS challenges, indicating that it might play a crucial role in responding to adverse stresses. The transcript levels of Lv-JIP4, Lv-p38a(MAPK9) and Lv-p38b(MAPK) in muscle were significantly upregulated after challenge with low temperature, suggesting that Lv-JIP4 may be the positive regulator of Lv-p38a(MAPK) and Lv-p38b(MAPK) under low temperature stress conditions. In addition, after knockdown of Lv-JIP4 expression, the protein levels of total Lv-p38(MAPK) and phospho-Lv-p38(MAPK) in the experimental dsRNA group were attenuated compared with those in the control group after 48 h (h), 60 h and 72 h of low-temperature stress, indicating that it might activate and phosphorylate the Lv-p38(MAPK) protein in response to cold stress. Here, we elucidated the molecular characteristics and the potential role of Lv-JIP4 and further refined the signal transduction mechanism of L. vannamei in response to low-temperature stress.
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