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Resistance gene N-mediated de novo synthesis and activation of a tobacco mitogen-activated protein kinase by tobacco mosaic virus infection

机译:抗性基因N介导的从头合成和烟草花叶病毒感染烟草丝裂原活化蛋白激酶的激活

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摘要

Salicylic acid-induced protein kinase (SIPK) and wounding-induced protein kinase (WIPK), two distinct members of the mitogen-activated protein (MAP) kinase family, are activated in tobacco resisting infection by tobacco mosaic virus (TMV). WIPK activation by TMV depends on the disease-resistance gene N because infection of susceptible tobacco not carrying the N gene failed to activate WIPK. Activation of WIPK required not only posttranslational phosphorylation but also a preceding rise in its mRNA and de novo synthesis of WIPK protein. The induction by TMV of WIPK mRNA and protein also occurred systemically. Its activation at the mRNA, protein, and enzyme levels was independent of salicylic acid. The regulation of WIPK at multiple levels by an N gene-mediated signal(s) suggests that this MAP kinase may be an important component upstream of salicylic acid in the signal-transduction pathway(s) leading to local and systemic resistance to TMV.
机译:水杨酸诱导的蛋白激酶(SIPK)和伤口诱导的蛋白激酶(WIPK)是丝裂原激活蛋白(MAP)激酶家族的两个不同成员,在抵抗烟草花叶病毒(TMV)感染的烟草中被激活。 TMV对WIPK的激活取决于抗病基因N,因为不携带N基因的易感烟草的感染未能激活WIPK。 WIPK的激活不仅需要翻译后磷酸化,还需要其mRNA的先前升高以及WIPK蛋白的从头合成。 TMV诱导WIPK mRNA和蛋白也全身发生。它在mRNA,蛋白质和酶水平上的激活与水杨酸无关。 N基因介导的信号在多个水平上对WIPK的调节表明,该MAP激酶可能是水杨酸上游信号传导途径中重要的组分,导致对TMV的局部和全身耐药。

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