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How does SA signaling link the Flg22 responses?

机译:SA信令如何链接Flg22响应?

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Slicylic acid (SA) has a central role inactivating plant resistance to patho-gens. SA levels increase in plant tissuefollowing pathogen infection and exoge-nous SA enhances resistance to a broadrange of pathogens. To study the rele-vance of the SA signaling in the flg22response, we investigated the responsesof SA-related mutants to flg22, a 22-amino acid peptide of the flagellin bacte-rial protein. We identified SA as animportant component of the flg22-trig-gered oxidative burst, a very early eventafter flg22 detection, and gene induction,an early event. SA acted partially byenhancing accumulation ofFLS2mRNA. We also provide new evidencethat NPR1 play a role in SA-inducedpriming event that enhances the flg22-triggered oxidative burst, which is corre-lated with enhancement of the flg22-induced callose deposition. Based onthese observations, we conclude that SAsignaling is required for early as well aslate flg22 responses.
机译:水杨酸(SA)在激活植物对病原体的抗性中起着重要作用。在病原体感染之后,植物组织中的SA水平升高,而过量的SA增强了对多种病原体的抗性。要研究flg22反应中SA信号的相关性,我们研究了SA相关突变体对flg22(鞭毛蛋白细菌蛋白的22个氨基酸肽)的反应。我们将SA鉴定为flg22-触发的氧化爆发的重要组成部分,这是flg22检测后的一个非常早期的事件,而基因诱导是一个早期的事件。 SA通过增强FLS2mRNA的积累来部分起作用。我们还提供了新的证据,即NPR1在SA诱导的引发事件中起作用,该事件增强了flg22触发的氧化爆发,这与flg22诱导的call糖沉积的增强相关。根据这些观察结果,我们得出结论,早期和后期flg22响应都需要SAsignaling。

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