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首页> 外文期刊>Quarterly Journal of the Royal Meteorological Society >Botrytis cinerea B05.10 promotes disease development in Arabidopsis by suppressing WRKY33-mediated host immunity
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Botrytis cinerea B05.10 promotes disease development in Arabidopsis by suppressing WRKY33-mediated host immunity

机译:Botrytis cinerea b05.10通过抑制Wrky33介导的宿主免疫来促进拟南芥中的疾病发展

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The large WRKY transcription factor family is mainly involved in regulating plant immune responses. Arabidopsis WRKY33 is a key transcriptional regulator of hormonal and metabolic processes towards Botrytis cinerea strain 2100 infection and is essential for resistance. In contrast to B. cinerea strain 2100, the strain B05.10 is virulent on wild-type (WT) Col-0 Arabidopsis plants highlighting the genetic diversity within this pathogen species. We analysed how early WRKY33-dependent responses are affected upon infection with strain B05.10 and found that most of these responses were strongly dampened during this interaction. Ectopic expression of WRKY33 resulted in complete resistance towards this strain indicating that virulence of B05.10, at least partly, depends on suppressing WRKY33 expression/protein accumulation. As a consequence, the expression levels of direct WRKY33 target genes, including those involved in the biosynthesis of camalexin, were also reduced upon infection. Concomitantly, elevated levels of the phytohormone abscisic acid (ABA) were observed. Molecular and genetic studies revealed that ABA negatively influences defence to B05.10 and effects jasmonic acid/ethylene (JA/ET) and salicylic acid (SA) levels. Susceptibility/resistance was determined by the antagonistic effect of ABA on JA, and this crosstalk required suppressing WRKY33 functions at early infection stages. This indicates that B. cinerea B05.10 promotes disease by suppressing WRKY33-mediated host defences.
机译:大型腕形转录因子家族主要参与调节植物免疫应答。 Arabidopsis Wrky33是对Botrytis Cinerea菌株2100感染的激素和代谢过程的关键转录调节因子,对抗性至关重要。与B.灰质菌株2100相反,菌株B05.10是野生型(WT)COL-0拟南芥植物的毒力,突出了该病原体物种内的遗传多样性。我们分析了Wrky33依赖性如何对菌株B05.10感染的影响如何影响,发现大多数这些反应在这种相互作用期间受到强烈抑制。 Wrky33的异位表达导致朝向该菌株的完全抗性,表明B05.10的毒力至少部分地取决于抑制Wrky33表达/蛋白质积累。因此,在感染后,也减少了涉及Camalexin的生物合成中的直接Wrky33靶基因的表达水平。同时,观察到植物激素脱落酸(ABA)的升高。分子和遗传研究表明,ABA对B05.10产生负面影响,并影响茉莉酸/乙烯(JA / ET)和水杨酸(SA)水平。通过ABA对JA的拮抗作用决定了敏感性/抵抗力,并且这种串扰在早期感染阶段需要抑制WRKY33功能。这表明B. Cinerea B05.10通过抑制Wrky33介导的宿主防御来促进疾病。

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