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Two Redundant Receptor-Like Cytoplasmic Kinases Function Downstream of Pattern Recognition Receptors to Regulate Activation of SA Biosynthesis

机译:两个冗余受体样细胞质激酶功能的下游模式识别受体调节SA生物合成的激活。

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摘要

Salicylic acid () serves as a critical signaling molecule in plant defense. Two transcription factors, SARD1 and CBP60g, control biosynthesis through regulating pathogen-induced expression of Isochorismate Synthase1, which encodes a key enzyme for biosynthesis. Here, we report that Pattern-Triggered Immunity Compromised Receptor-like Cytoplasmic Kinase1 (PCRK1) and PCRK2 function as key regulators of biosynthesis. In the pcrk1 pcrk2 double mutant, pathogen-induced expression of SARD1, CBP60g, and ICS1 is greatly reduced. The pcrk1 pcrk2 double mutant, but neither of the single mutants, exhibits reduced accumulation of and enhanced disease susceptibility to bacterial pathogens. Both PCRK1 and PCRK2 interact with the pattern recognition receptor FLS2, and treatment with pathogen-associated molecular patterns leads to rapid phosphorylation of PCRK2. Our data suggest that PCRK1 and PCRK2 function downstream of pattern recognition receptor in a signal relay leading to the activation of biosynthesis.
机译:水杨酸()是植物防御中的关键信号分子。 SARD1和CBP60g这两个转录因子通过调节病原体诱导的等渗线合成酶1(Isochoorismate Synthase1)的表达来控制生物合成,该编码酶是生物合成的关键酶。在这里,我们报告模式触发的免疫受损的受体样细胞质激酶1(PCRK1)和PCRK2充当生物合成的关键调节剂。在pcrk1 pcrk2双突变体中,病原体诱导的SARD1,CBP60g和ICS1的表达大大降低。 pcrk1 pcrk2双突变体,但单个突变体均未显示,减少了细菌病原体的积累并增强了其对细菌病原体的敏感性。 PCRK1和PCRK2都与模式识别受体FLS2相互作用,并且病原体相关分子模式的处理导致PCRK2的快速磷酸化。我们的数据表明,PCRK1和PCRK2在信号中继中模式识别受体的下游起作用,从而导致生物合成的激活。

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