• It is critically important for plants to control the trade‐off between normal growth and pathogen immunity. However, the underlying molecular mechanism remains largely unknown. Here we report such a mechanism controlled by WRKY70 and its partner CHYR1 in Arabidopsis.
• We found that both levels of the WRKY70 target gene SARD1 and the phosphorylated forms of WRKY70 were increased in WRKY70OE plants upon Pst DC3000 infection. Mechanistically, phosphorylation of WRKY70 at Thr22 and Ser34 occurs, which then activates SARD1 expression through binding to a WT box.
• Phosphorylated WRKY70 is degraded by 26S proteasome via CHYR1 when resuming normal growth after infection. In addition, nonphosphorylated WRKY70 represses SARD1 expression by binding to both W (inhibitory activity site) and WT (active activity site) boxes.
• The binding of WRKY70 to alternative cis‐elements of SARD1 through a phosphorylation‐mediated switch controlled by CHYR1 contributes to modulating the balance between immunity and growth.

中文翻译：

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CHYR1泛素化磷酸化的WRKY70以降解以平衡拟南芥的免疫力

• 对于植物而言，控制正常生长与病原体免疫力之间的权衡至关重要。但是，基本的分子机制仍然是未知的。在这里，我们报告了由WRKY70及其合作伙伴CHYR1在拟南芥中控制的这种机制。
• 我们发现在Pst DC3000感染后，WRKY70OE植物中WRKY70目标基因SARD1的水平和磷酸化形式的WRKY70均增加。从机制上讲，WRKY70在Thr22和Ser34发生磷酸化，然后通过与WT盒结合而激活SARD1表达。
• 当感染后恢复正常生长时，磷酸化的WRKY70被经由CHYR1的26S蛋白酶体降解。此外，非磷酸化的WRKY70通过结合W（抑制活性位点）和WT（活性活性位点）框来抑制SARD1表达。
• WRKY70的替代结合顺式的-elements SARD1通过CHYR1有助于控制以调节免疫和生长之间的平衡磷酸化介导的开关。