Abstract：
Accurate nucleocytoplasmic transport of signal molecules is essential for plant growth and development. Multiple studies have confirmed that nucleocytoplasmic transport and receptors are involved in regulating plant disease resistance responses, however, little is known about the regulatory mechanism in plants. In this study, we showed that the mutant of the importin beta-like protein SAD2 exhibited a more susceptible phenotype than wild-type Col-0 after treatment with Pseudomonas syringae pv tomato DC3000 (Pst DC3000). Coimmunoprecipitation (Co-IP) and bimolecular fluorescence complementation (BiFC) experiments demonstrated that SAD2 interacts with the hypersensitive response (HR)-positive transcriptional regulator MYB30. Subcellular localization showed that MYB30 was not fully localized in the nucleus in sad2-5 mutants, and western-blot experiments further indicated that SAD2 was required for MYB30 nuclear trafficking during the pathogen infection process. A phenotypic test of pathogen inoculation demonstrated that MYB30 partially rescued the disease symptoms of sad2-5 caused by Pst DC3000, and that MYB30 worked downstream of SAD2 in plant pathogen defense. These results suggested that SAD2 might be involved in plant pathogen defense by mediating MYB30 nuclear trafficking. Taken together, our results revealed the important function of SAD2 in plant pathogen defense and enriched understanding of the mechanism of nucleocytoplasmic transport-mediated plant pathogen defense.
摘要：
信号分子的准确核质转运对于植物的生长和发育至关重要。多项研究证实，核质运输和受体参与调节植物抗病性反应，然而,对植物的调控机制知之甚少。在这项研究中,我们发现,在用丁香假单胞菌pv番茄DC3000(PstDC3000)处理后,与野生型Col-0相比,导入蛋白β样蛋白SAD2的突变体表现出更易感的表型.共免疫沉淀（Co-IP）和双分子荧光互补（BiFC）实验表明，SAD2与超敏反应（HR）-正转录调节因子MYB30相互作用。亚细胞定位表明，在sad2-5突变体中，MYB30未完全定位于细胞核中，蛋白质印迹实验进一步表明，在病原体感染过程中，MYB30核运输需要SAD2。病原体接种的表型测试表明，MYB30部分挽救了PstDC3000引起的sad2-5的疾病症状，并且MYB30在植物病原体防御中起SAD2的下游作用。这些结果表明，SAD2可能通过介导MYB30核运输参与植物病原体的防御。一起来看,我们的结果揭示了SAD2在植物病原体防御中的重要功能，并丰富了对核质运输介导的植物病原体防御机制的理解。
