State Key Laboratory Breeding Base of Marine Genetic Resources, Key Laboratory of Marine Genetic Resources of State Oceanic Administration, Third Institute of Oceanography, State Oceanic Administration, Fujian Key Laboratory of Marine Genetic Resources, South China Sea Bio-Resource Exploitation and Utilization Collaborative Innovation Center, Xiamen 361005, People's Republic of China.
State Key Laboratory Breeding Base of Marine Genetic Resources, Key Laboratory of Marine Genetic Resources of State Oceanic Administration, Third Institute of Oceanography, State Oceanic Administration, Fujian Key Laboratory of Marine Genetic Resources, South China Sea Bio-Resource Exploitation and Utilization Collaborative Innovation Center, Xiamen 361005, People's Republic of China; School of Life Science, Xiamen University, Xiamen 361005, People's Republic of China.
Fish Shellfish Immunol. 2018 Nov;82:220-228. doi: 10.1016/j.fsi.2018.08.032. Epub 2018 Aug 17.
GSK3β, a serine/threonine protein kinase, is a crucial regulator in several signaling pathway and plays a vital role in multiple cellular processes including cell proliferation, growth, apoptosis and immune response. In this study, a GSK3β homolog from L. vannamei, designed as LvGSK3β, was characterized. Sequence analysis showed that LvGSK3β possessed a highly similarity with GSK3β from other species, which contained a catalytic domain and serine/threonine phosphorylation sites. To analyze the role of LvGSK3β in the process of white spot syndrome virus (WSSV) infection, real-time quantitative PCR and western blot assays were performed. The results showed that the transcription and expression levels of LvGSK3β were inhibited upon WSSV challenge, accompanied with down-regulated phosphorylation levels. When LvGSK3β was silenced, the transcription of WSSV gene ie1 was inhibited, and the apoptosis of hemocytes induced by WSSV was up-regulated remarkably as well. In addition, inactivation of LvGSK3β could also depress virus infection that further validated the results. Conclusively, LvGSK3β was an important protein for shrimp immunomodulation, and shrimp might promote the apoptosis to restrain WSSV infection by inhibition of LvGSK3β. The study will be helpful for understanding the molecular mechanism of host-virus interaction.
GSK3β,一种丝氨酸/苏氨酸蛋白激酶,是几种信号通路的关键调节剂,在包括细胞增殖、生长、凋亡和免疫反应在内的多种细胞过程中发挥着重要作用。在这项研究中,鉴定了凡纳滨对虾的 GSK3β 同源物,命名为 LvGSK3β。序列分析表明,LvGSK3β与其他物种的 GSK3β具有高度相似性,包含一个催化结构域和丝氨酸/苏氨酸磷酸化位点。为了分析 LvGSK3β在白斑综合征病毒(WSSV)感染过程中的作用,进行了实时定量 PCR 和 Western blot 分析。结果表明,LvGSK3β的转录和表达水平在 WSSV 攻击后受到抑制,同时磷酸化水平也下调。当 LvGSK3β被沉默时,WSSV 的 ie1 基因转录受到抑制,WSSV 诱导的血细胞凋亡也显著上调。此外,LvGSK3β 的失活还能抑制病毒感染,进一步验证了上述结果。总之,LvGSK3β是虾类免疫调节的重要蛋白,虾类可能通过抑制 LvGSK3β 来促进细胞凋亡,从而抑制 WSSV 感染。该研究有助于理解宿主-病毒相互作用的分子机制。