Induction of HSP70 and polyubiquitin expression associated with plant virus replication
Induction of HSP70 and polyubiquitin expression associated with plant virus replication
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DOI：
10.1073/pnas.93.26.15289
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发表时间：
1996-12-24
影响因子：
11.1
通讯作者：
Maule, AJ
中科院分区：
文献类型：
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作者：
Aranda, MA;Escaler, M;Maule, AJ
通过检查感染豌豆种传花叶病毒（PSbMV）的未成熟豌豆胚中的病毒入侵前沿，观察到不同宿主基因的选择性控制。根据我们的观察，对PSbMV复制的早期反应可分为三类：抑制宿主基因表达、诱导宿主基因表达和对正常宿主功能无影响。编码HSP70和多聚泛素的两个热诱导基因的表达与病毒复制的开始和多聚泛素的下调相协调地被诱导。另外两个编码脂氧合酶和热休克同源蛋白的基因，下调是宿主基因表达普遍抑制的一部分，可以通过宿主转录本的降解来实现，我们讨论了HSP70和多聚泛素基因的诱导是否代表病毒对各自蛋白质产物的需要，或者仅仅是其他宿主转录本耗尽的结果，前者是可行的，因为这两个基因的诱导确实导致HSP70和泛素积累增加，这还表明，与某些动物病毒感染相比，PSbMV 感染后宿主 mRNA 的翻译并没有普遍受到抑制。在胚胎的所有细胞类型中都观察到了宿主基因表达的这种选择性控制，并确定了可以作为症状表达触发因素的细胞破坏机制。
By examining the front of virus invasion in immature pea embryos infected with pea seed-borne mosaic virus (PSbMV), the selective control of different host genes has been observed, From our observations, the early responses to PSbMV replication can be grouped into three classes, inhibited host gene expression, induced host gene expression, and no effect on a normal host function, The expression of two heat-inducible genes encoding HSP70 and polyubiquitin was induced coordinately with the onset of virus replication and the down-regulation of two other genes encoding lipoxygenase and heat shock cognate protein, The down-regulation was part of a general suppression of host gene expression that mag be achieved through the degradation of host transcripts, We discuss the possibilities of whether the induction of HSP70 and polyubiquitin genes represents a requirement for the respective protein products by the virus or Is merely a consequence of the depletion of other host transcripts, The former is feasible, as the induction of both genes does result in increased HSP70 and ubiquitin accumulation, This also indicates that, in contrast to some animal virus infections, there is not a general inhibition of translation of host mRNAs following PSbMV infection, This selective control of host gene expression was observed in all cell types of the embryo and identifies mechanisms of cellular disruption that could act as triggers for symptom expression.