出囊,一种蛋白质复合物,在各种细胞功能中起着至关重要的作用,包括细胞极化,迁移,入侵,胞质分裂,和自噬。Sec3,称为Exoc1,是外囊复合物的关键亚基,可参与细胞存活和凋亡。在这项研究中,两种亚型的Sec3从斜纹石斑鱼中分离,是中国重要的海鱼。在新加坡石斑鱼虹彩病毒(SGIV)感染期间探索了E.coioidesSec3的作用,海鱼的一种重要病原体,可导致90%的死亡率。E.coioidesSec3序列显示出与其他物种的高度相似性,表明存在保守的Sec3超家族域。E.coioidesSec3mRNA可以在所有检查的组织中检测到,尽管表达水平不同。SGIV感染可以上调大肠杆菌Sec3mRNA。上调的Sec3显著促进SGIV诱导的CPE,以及病毒关键基因的表达。大肠杆菌Sec3可以抑制NF-κB和AP-1的激活,以及SGIV诱导的细胞凋亡。结果表明,大肠杆菌Sec3通过调节先天免疫应答促进SGIV感染。
Exocyst, a protein complex, plays a crucial role in various cellular functions, including cell polarization, migration, invasion, cytokinesis, and autophagy. Sec3, known as Exoc1, is a key subunit of the Exocyst complex and can be involved in cell survival and apoptosis. In this study, two subtypes of Sec3 were isolated from Epinephelus coioides, an important marine fish in
China. The role of E. coioides Sec3 was explored during Singapore grouper iridovirus (SGIV) infection, an important pathogen of marine fish which could induce 90 % mortality. E. coioides Sec3 sequences showed a high similarity with that from other species, indicating the presence of a conserved Sec3 superfamily domain. E. coioides Sec3 mRNA could be detected in all examined tissues, albeit at varying expression levels. SGIV infection could upregulate E. coioides Sec3 mRNA. Upregulated Sec3 significantly promoted SGIV-induced CPE, and the expressions of viral key genes. E. coioides Sec3 could inhibit the activation of NF-κB and AP-1, as well as SGIV-induced cell apoptosis. The results illustrated that E. coioides Sec3 promotes SGIV infection by regulating the innate immune response.