Viral Perturbation of Alternative Splicing of a Host Transcript Benefits Infection
Viral Perturbation of Alternative Splicing of a Host Transcript Benefits Infection
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宿主转录本选择性剪接的病毒扰动有利于感染
DOI：
10.1104/pp.20.00903
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发表时间：
2020-11-01
期刊：
影响因子：
7.4
通讯作者：
Zhou, Tao
中科院分区：
文献类型：
--
作者：
Du, Kaitong;Jiang, Tong;Zhou, Tao
病原体干扰受感染真核宿主的选择性剪接模式。然而，在植物中，它是未知的，如果这是偶然的感染或代表病原体诱导的宿主基因表达的重塑需要支持感染。在这里，我们比较了转录和蛋白质积累的变化，在玉米（玉米）感染全球重要的病原体甘蔗花叶病毒（SCMV）的转录剪接模式的变化。我们的研究结果表明，选择性剪接的变化在确定病毒诱导的蛋白质组学变化中起着重要作用。集中在玉米八氢番茄红素脱氢酶1（ZmPSY 1），它编码类胡萝卜素生物合成的关键调控酶，我们发现，虽然SCMV感染减少总ZmPSY 1转录积累，剪接变体T001的比例增加后期感染阶段，使ZmPSY 1蛋白水平得以维持。我们确定ZmPSY 1具有两个叶特异性转录物T001和T003，其区别在于各自的3 '非翻译区（UTR）之间的差异。T001的较短的3 '-UTR使其成为更有效的mRNA。无义ZmPSY 1突变体或病毒诱导的ZmPSY 1表达沉默抑制SCMV积累，减轻症状，并减少叶绿体损伤。因此，ZmPSY 1作为病毒积累和致病所需的前病毒宿主因子。总而言之，我们的研究结果表明，SCMV感染调节的选择性剪接确保ZmPSY 1合成在感染期间持续，这支持有效的病毒感染。
Pathogens disturb alternative splicing patterns of infected eukaryotic hosts. However, in plants it is unknown if this is incidental to infection or represents a pathogen-induced remodeling of host gene expression needed to support infection. Here, we compared changes in transcription and protein accumulation with changes in transcript splicing patterns in maize (Zea mays) infected with the globally important pathogen sugarcane mosaic virus (SCMV). Our results suggested that changes in alternative splicing play a major role in determining virus-induced proteomic changes. Focusing on maize phytoene synthase1 (ZmPSY1), which encodes the key regulatory enzyme in carotenoid biosynthesis, we found that although SCMV infection decreases total ZmPSY1 transcript accumulation, the proportion of splice variant T001 increases by later infection stages so that ZmPSY1 protein levels are maintained. We determined that ZmPSY1 has two leaf-specific transcripts, T001 and T003, distinguished by differences between the respective 3 '-untranslated regions (UTRs). The shorter 3 '-UTR of T001 makes it the more efficient mRNA. Nonsense ZmPSY1 mutants or virus-induced silencing of ZmPSY1 expression suppressed SCMV accumulation, attenuated symptoms, and decreased chloroplast damage. Thus, ZmPSY1 acts as a proviral host factor that is required for virus accumulation and pathogenesis. Taken together, our findings reveal that SCMV infection-modulated alternative splicing ensures that ZmPSY1 synthesis is sustained during infection, which supports efficient virus infection.