Department of Biological Sciences, Box 43131, Texas Tech University, Lubbock, TX 79409-3131, USA.
J Virol. 2011 Dec;85(24):13144-52. doi: 10.1128/JVI.05294-11. Epub 2011 Oct 12.
Apoptosis and inhibition of host gene expression are often associated with virus infections. Many viral polypeptides modulate apoptosis by direct interaction with highly conserved apoptotic pathways. Some viruses induce apoptosis during late stages of the infection cycle, while others inhibit apoptosis to facilitate replication or maintain persistent infection. In previous work, we showed that Chilo iridescent virus (CIV) or CIV virion protein extract induces apoptosis in spruce budworm and cotton boll weevil cell cultures. Here, we characterize the product of a CIV gene (iridovirus serine/threonine kinase; istk) with signature sequences for S/T kinase and ATP binding. ISTK appears to belong to the superfamily, vaccinia-related kinases (VRKs). The istk gene was expressed in Pichia pastoris vectors. Purified ISTK (48 kDa) exhibited S/T kinase activity. Treatment with ISTK induced apoptosis in budworm cells. A 35-kDa cleavage product of ISTK retaining key signature sequences was identified during purification. Pichia-expressed 35-kDa polypeptide, designated iridoptin, induced apoptosis and inhibition of host protein synthesis in budworm and boll weevil cells. A mutation in the ATP-binding site eliminated both kinase and apoptosis activity of iridoptin, suggesting that kinase activity is essential for induction of apoptosis. Analysis with custom antibody confirmed that ISTK is a structural component of CIV particles. This is the first demonstration of a viral kinase inducing apoptosis in any virus-host system and the first identification of a factor inducing apoptosis or host protein shutoff for the family Iridoviridae.
细胞凋亡和宿主基因表达抑制通常与病毒感染有关。许多病毒多肽通过与高度保守的凋亡途径直接相互作用来调节细胞凋亡。一些病毒在感染周期的晚期诱导细胞凋亡,而另一些病毒则抑制细胞凋亡以促进复制或维持持续性感染。在之前的工作中,我们表明,舞毒蛾虹彩病毒(CIV)或 CIV 病毒粒子蛋白提取物可诱导云杉芽虫和棉铃象鼻虫细胞培养物发生细胞凋亡。在这里,我们对 CIV 基因(虹彩病毒丝氨酸/苏氨酸激酶;istk)的产物进行了特征描述,该产物具有 S/T 激酶和 ATP 结合的特征序列。ISTK 似乎属于超级家族,即痘苗相关激酶(VRKs)。istk 基因在毕赤酵母载体中表达。纯化的 ISTK(48 kDa)表现出 S/T 激酶活性。用 ISTK 处理可诱导芽虫细胞发生细胞凋亡。在纯化过程中鉴定到保留关键特征序列的 ISTK 的 35 kDa 切割产物。在芽虫和象鼻虫细胞中,毕赤酵母表达的 35 kDa 多肽,命名为 iridoptin,可诱导细胞凋亡和宿主蛋白合成抑制。在 ATP 结合位点的突变消除了 iridoptin 的激酶和凋亡活性,表明激酶活性对于诱导细胞凋亡是必需的。用定制抗体进行的分析证实,ISTK 是 CIV 颗粒的结构成分。这是首次证明病毒激酶在任何病毒-宿主系统中诱导细胞凋亡,也是首次鉴定出诱导凋亡或家族虹彩病毒科宿主蛋白关闭的因子。