Guo Minglan, Wei Jingguang, Zhou Yongcan, Qin Qiwei
CAS Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou, 510301, PR China; CAS-HKUST Sanya Joint Laboratory of Marine Science Research, Key Laboratory of Tropical Marine Biotechnology of Hainan Province, Sanya Institute of Ocean Eco-Environmental Engineering, SCSIO, Sanya, 572000, PR China.
College of Marine Sciences, South China Agricultural University, Guangdong Laboratory for Lingnan Modern Agriculture, Guangzhou, 510642, PR China; Department of Biological Sciences, National University of Singapore, Singapore, 117543, Singapore.
Dev Comp Immunol. 2023 Jun;143:104674. doi: 10.1016/j.dci.2023.104674. Epub 2023 Mar 6.
Singapore grouper iridovirus (SGIV), with various mechanisms for evading and modulating host, has inflicted heavy economic losses in the grouper aquaculture. MAP kinase phosphatase 1 (MKP-1) regulates mitogen-activated protein kinases (MAPKs) to mediate the innate immune response. Here, we cloned EcMKP-1, an MKP-1 homolog from the orange-spotted grouper Epinephelus coioides, and investigated its role in the infection of SGIV. In juvenile grouper, EcMKP-1 was highly upregulated and peaked at different times after injection with lipopolysaccharide, polyriboinosinic polyribocytidylic acid and SGIV. EcMKP-1 expression in heterologous fathead minnow cells was able to suppress SGIV infection and replication. Furthermore, EcMKP-1 was a negative regulator of c-Jun N-terminal kinase (JNK) phosphorylation early in SGIV infection. EcMKP-1 decreased the apoptotic percentage and caspase-3 activity during the late stage of SGIV replication. Our results demonstrate critical functions of EcMKP-1 in antiviral immunity, JNK dephosphorylation and anti-apoptosis during SGIV infection.
新加坡石斑鱼虹彩病毒(SGIV)具有多种逃避和调节宿主的机制,给石斑鱼养殖业造成了巨大的经济损失。丝裂原活化蛋白激酶磷酸酶1(MKP-1)调节丝裂原活化蛋白激酶(MAPKs)以介导先天免疫反应。在此,我们克隆了橙色斑石斑鱼(Epinephelus coioides)的MKP-1同源物EcMKP-1,并研究了其在SGIV感染中的作用。在幼鱼中,注射脂多糖、聚肌苷酸-聚胞苷酸和SGIV后,EcMKP-1高度上调,并在不同时间达到峰值。异源黑头软口鲦细胞中EcMKP-1的表达能够抑制SGIV的感染和复制。此外,EcMKP-1是SGIV感染早期c-Jun氨基末端激酶(JNK)磷酸化的负调节因子。EcMKP-1在SGIV复制后期降低了凋亡百分比和半胱天冬酶-3活性。我们的结果证明了EcMKP-1在SGIV感染期间的抗病毒免疫、JNK去磷酸化和抗凋亡中的关键作用。