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Reported differences in the flg22 response of the null mutation of AtRGS1 correlates with fixed genetic variation in the background of Col-0 isolates

机译:报道了ATRGS1的NULL突变的FLG22响应的差异与COL-0隔离株背景下的固定遗传变异相关

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摘要

A role for the heterotrimeric G protein complex in the induction of a transient burst of reactive oxygen species (ROS) by the Microbial-Associated Molecular Pattern, flg22, a 22-amino acid peptide derived from bacterial flagella, is well established. However, the evidence for a negative or positive role for one component of the Arabidopsis G protein complex, namely, Regulator of G Signaling 1 (AtRGS1) leads to opposing conclusions. We show that the reason for this difference is due to the isolate of Col-0 ecotype used as the wildtype control in flg22-induced ROS and our data further support the idea that AtRGS1 is a negative regulator of the flg22-induced ROS response. Whole-genome genotyping led to the identification and validation of polymorphism in five genes between two Col-0 isolates that are candidates for the different ROS response relative to the rgs1 null mutant.
机译:异源三聚体G蛋白复合物通过微生物相关分子模式flg22(一种来源于细菌鞭毛的22个氨基酸的肽)在诱导活性氧物种(ROS)短暂爆发中的作用已得到充分证实。然而,有证据表明拟南芥G蛋白复合物的一个组成部分,即G信号调节因子1(AtRGS1)起到了消极或积极的作用,从而得出了相反的结论。我们发现,造成这种差异的原因是,在flg22诱导的活性氧反应中,Col-0生态型作为野生型对照被分离出来,我们的数据进一步支持AtRGS1是flg22诱导的活性氧反应的负调节因子的观点。全基因组基因分型导致了两个Col-0分离株之间五个基因多态性的鉴定和验证,这两个分离株是相对于rgs1空突变体的不同ROS反应的候选株。

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