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MdVQ12 confers resistance to Valsa mali by regulating MdHDA19 expression in apple
Molecular Plant Pathology ( IF 4.9 ) Pub Date : 2023-12-10 , DOI: 10.1111/mpp.13411
Pengliang Han 1 , Ruotong Zhang 1 , Rui Li 1 , Fudong Li 1 , Jiajun Nie 1 , Ming Xu 1 , Chengli Wang 1 , Lili Huang 1
Affiliation  

Valine-glutamine (VQ) motif-containing proteins play a crucial role in plant biotic stress responses. Apple Valsa canker, caused by the ascomycete Valsa mali, stands as one of the most severe diseases affecting apple trees. Nonetheless, the underlying resistance mechanism of VQ proteins against this disease has remained largely unexplored. This study reports MdVQ12, a VQ motif-containing protein, as a positive regulator of apple Valsa canker resistance. Genetic transformation experiments demonstrated that MdVQ12 overexpression increased resistance to V. mali, while gene silencing lines exhibited significantly reduced resistance. MdVQ12 interacted with the transcription factor MdWRKY23, which bound to the promoter of the histone deacetylase gene MdHDA19, activating its expression. MdHDA19 enhanced apple resistance to V. mali by participating in the jasmonic acid (JA) and ethylene (ET) signalling pathways. Additionally, MdVQ12 promoted the transcriptional activity of MdWRKY23 towards MdHDA19. Our findings reveal that MdVQ12 enhances apple resistance to V. mali by regulating MdHDA19 expression and thereby regulating the JA and ET signalling pathways, offering potential candidate gene resources for breeding apple Valsa canker-resistant germplasm.

中文翻译:

MdVQ12 通过调节苹果中 MdHDA19 的表达赋予苹果腐烂病抗性

含有缬氨酸-谷氨酰胺(VQ)基序的蛋白质在植物生物胁迫反应中发挥着至关重要的作用。苹果腐烂病是由子囊菌苹果腐烂病引起的,是影响苹果树的最严重的疾病之一。尽管如此,VQ 蛋白对抗这种疾病的潜在抵抗机制在很大程度上仍未被探索。这项研究报告称 MdVQ12(一种含有 VQ 基序的蛋白质)是苹果 Valsa 溃疡病抗性的正调节因子。遗传转化实验表明,MdVQ12过表达增加了对苹果弧菌的抗性,而基因沉默株系则表现出显着降低的抗性。MdVQ12 与转录因子 MdWRKY23 相互作用,后者与组蛋白脱乙酰酶基因MdHDA19的启动子结合,激活其表达。MdHDA19通过参与茉莉酸 (JA) 和乙烯 (ET) 信号通路增强苹果对苹果弧菌的抗性。此外,MdVQ12促进 MdWRKY23 对MdHDA19的转录活性。我们的研究结果表明,MdVQ12通过调节MdHDA19的表达进而调节JA和ET信号通路来增强苹果对V. mali的抗性,为培育苹果抗Valsa溃疡病种质提供潜在的候选基因资源。
更新日期:2023-12-10
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