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Systemic Immunity Requires SnRK2.8-Mediated Nuclear Import of NPR1 in Arabidopsis

机译:系统免疫需要拟南芥中SnRK2.8介导的NPR1的核输入。

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摘要

In plants, necrotic lesions occur at the site of pathogen infection through the hypersensitive response, which is followed by induction of systemic acquired resistance (SAR) in distal tissues. Salicylic acid (SA) induces SAR by activating NONEXPRESSER OF PATHOGENESIS-RELATED GENES1 (NPR1) through an oligomer-to-monomer reaction. However, SA biosynthesis is elevated only slightly in distal tissues during SAR, implying that SA-mediated induction of SAR requires additional factors. Here, we demonstrated that SA-independent systemic signals induce a gene encoding SNF1-RELATED PROTEIN KINASE 2.8 (SnRK2.8), which phosphorylates NPR1 during SAR. The SnRK2.8-mediated phosphorylation of NPR1 is necessary for its nuclear import. Notably, although SnRK2.8 transcription and SnRK2.8 activation are independent of SA signaling, the SnRK2.8-mediated induction of SAR requires SA. Together with the SA-mediated monomerization of NPR1, these observations indicate that SA signals and SnRK2.8-mediated phosphorylation coordinately function to activate NPR1 via a dual-step process in developing systemic immunity in Arabidopsis thaliana.
机译:在植物中,通过超敏反应在病原体感染部位发生坏死性病变,随后在远端组织中诱导全身获得性抗药性(SAR)。水杨酸(SA)通过低聚物与单体反应激活与光致病相关的GENES1(NPR1)的非表达子来诱导SAR。但是,SAR期间远端组织中SA的生物合成仅略有升高,这表明SA介导的SAR诱导需要其他因素。在这里,我们证明了SA独立的系统性信号诱导编码SNF1相关蛋白激酶2.8(SnRK2.8)的基因,该基因在SAR期间使NPR1磷酸化。 SnRK2.8介导的NPR1磷酸化是其核进口所必需的。值得注意的是,尽管SnRK2.8转录和SnRK2.8激活独立于SA信号传导,但SnRK2.8介导的SAR诱导仍需要SA。这些观察结果与SA介导的NPR1单体化反应一起表明,SA信号和SnRK2.8介导的磷酸化在拟南芥中发展系统性免疫的过程中通过双步过程协同激活NPR1。

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