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Loss of a callose synthase results in salicylic acid-dependent disease resistance

机译:愈伤组织合酶的丧失导致水杨酸依赖性疾病抗性

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Plants attacked by pathogens rapidly deposit callose, a beta-1,3-glucan, at wound sites. Traditionally, this deposition is thought to reinforce the cell wall and is regarded as a defense response. Surprisingly, here we found that powdery mildew resistant 4 (pmr4), a mutant lacking pathogen-induced callose, became resistant to pathogens, rather than more susceptible. This resistance was due to mutation of a callose synthase, resulting in a loss of the induced callose response. Double-mutant analysis indicated that blocking the salicylic acid ( SA) defense signaling pathway was sufficient to restore susceptibility to pmr4 mutants. Thus, callose or callose synthase negatively regulates the SA pathway. [References: 21]
机译:受病原体攻击的植物在伤口处迅速沉积deposit,即β-1,3-葡聚糖。传统上,这种沉积被认为可以增强细胞壁,并被认为是防御反应。令人惊讶的是,在这里我们发现白粉病抗性4(pmr4)是一种缺乏病原体诱导的call的突变体,对病原体具有抗性,而不是更易感。这种抗性是由于a质合酶的突变,导致诱导的call质反应的丧失。双突变分析表明,阻断水杨酸(SA)防御信号传导途径足以恢复对pmr4突变体的敏感性。因此,call质或ose质合酶负调节SA途径。 [参考:21]

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