Raffaele Sylvain, Rivas Susana, Roby Dominique
Laboratoire des Interactions Plantes-Microorganismes (LIPM), UMR CNRS/INRA 2594, Castanet-Tolosan, France.
FEBS Lett. 2006 Jun 12;580(14):3498-504. doi: 10.1016/j.febslet.2006.05.027. Epub 2006 May 15.
Salicylic acid (SA) plays a central role in resistance and defense induction in response to pathogen attack, but its role in the activation of the hypersensitive response (HR), a form of programmed cell death associated with resistance of plants, remains to be elucidated. AtMYB30, a R2R3-MYB transcriptional factor which acts as a positive regulator of the HR, is a good model for studying the role of SA in programmed cell death. Here, we demonstrate that AtMYB30 expression in response to an HR-inducing bacterial pathogen is dependent on SA accumulation, but NPR1-independent. Alterations of AtMYB30 expression (overexpression, depletion by antisense strategy, T-DNA insertion mutant) modulate SA levels and SA-associated gene expression. Additionally, mutants or transgenic lines altered in SA accumulation (nahG, sid1, sid2), but not those affected in SA signalling (npr1), abolish the accelerated cell death phenotype conferred by over-expression of AtMYB30. These results suggest that AtMYB30 is involved in an amplification loop or signalling cascade that modulates SA synthesis, which in turn modulates cell death.
水杨酸（SA）在植物响应病原体攻击的抗性和防御诱导中起着核心作用，但其在激活超敏反应（HR）中的作用仍有待阐明，超敏反应是一种与植物抗性相关的程序性细胞死亡形式。AtMYB30是一种R2R3-MYB转录因子，作为HR的正调控因子，是研究SA在程序性细胞死亡中作用的良好模型。在此，我们证明AtMYB30对诱导HR的细菌病原体的响应表达依赖于SA积累，但不依赖于NPR1。AtMYB30表达的改变（过表达、反义策略缺失、T-DNA插入突变体）调节SA水平和SA相关基因表达。此外，SA积累改变的突变体或转基因系（nahG、sid1、sid2），而非SA信号传导受影响的突变体或转基因系（npr1），消除了AtMYB30过表达赋予的加速细胞死亡表型。这些结果表明，AtMYB30参与了调节SA合成的放大环或信号级联反应，进而调节细胞死亡。
