Plant virus infection-induced persistent host gene downregulation in systemically infected leaves
Plant virus infection-induced persistent host gene downregulation in systemically infected leaves
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DOI：
10.1111/j.1365-313x.2008.03501.x
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发表时间：
2008-07-01
期刊：
影响因子：
7.2
通讯作者：
Burgyan, Jozsef
中科院分区：
文献类型：
--
作者：
Havelda, Zoltan;Varallyay, Eva;Burgyan, Jozsef
了解病毒感染引起的宿主植物基因表达和代谢的改变导致病毒病症状的发展在科学和经济上都具有重要意义。在这里，我们表明，属于各种RNA病毒家族的病毒能够诱导有效的宿主基因mRNA下调（关闭）在系统感染的叶片。我们证明了宿主基因mRNA关闭与病毒占据的扇区在空间上重叠，表明病毒积累在这种现象中的直接作用。关闭的建立与活跃的病毒复制或RNA沉默机制没有直接联系。重要的是，诱导的关闭现象持续数周，导致感染植物中重要管家基因的mRNA严重缺乏。有趣的是，我们发现其他一些RNA病毒不诱导或仅轻微诱导同一组基因的关闭现象，这表明这一过程中存在遗传决定。核运行实验表明，植物病毒，类似于动物病毒，介导抑制宿主mRNA的合成在细胞核中。通过研究各种宿主-病毒相互作用，我们揭示了关闭现象的强度与疾病症状的严重程度之间的相关性。我们的数据表明，有效和持久的下调宿主基因可能是一个重要组成部分的症状发展在某些主机病毒的相互作用。
Understanding of virus infection-induced alterations in host plant gene expression and metabolism leading to the development of virus disease symptoms is both scientifically and economically important. Here, we show that viruses belonging to various RNA virus families are able to induce efficient host gene mRNA downregulation (shut-off) in systemically infected leaves. We demonstrate that the host gene mRNA shut-off overlaps spatially with virus-occupied sectors, indicating the direct role of virus accumulation in this phenomenon. The establishment of shut-off was not directly connected to active viral replication or the RNA-silencing machinery. Importantly, the induced shut-off phenomenon persisted for several weeks, resulting in severe deficiency of mRNA for important housekeeping genes in the infected plants. Interestingly, we found that some other RNA viruses do not induce or only slightly induce the shut-off phenomenon for the same set of genes, implicating genetic determination in this process. Nuclear run-on experiments suggest that plant viruses, similarly to animal viruses, mediate suppression of host mRNA synthesis in the nucleus. By investigating various host-virus interactions, we revealed a correlation between the intensity of the shut-off phenomenon and the severity of disease symptoms. Our data suggest that efficient and persistent downregulation of host genes may be an important component of symptom development in certain host-virus interactions.