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RXLR effector diversity in Phytophthora infestans isolates determines recognition by potato resistance proteins; the case study AVR1 and R1
Studies in Mycology ( IF 14.1 ) Pub Date : 2018-02-07 , DOI: 10.1016/j.simyco.2018.01.003
Y. Du , R. Weide , Z. Zhao , P. Msimuko , F. Govers , K. Bouwmeester

Late blight disease caused by the plant pathogenic oomycete pathogen Phytophthora infestans is one of the most limiting factors in potato production. P. infestans is able to overcome introgressed late blight resistance by adaptation of effector genes. AVR1 is an RXLR effector that triggers immune responses when recognized by the potato resistance protein R1. P. infestans isolates avirulent on R1 plants were found to have AVR1 variants that are recognized by R1. Virulent isolates though, lack AVR1 but do contain a close homologue of AVR1, named A-L, of which all variants escape recognition by R1. Co-expression of AVR1 and R1 in Nicotiana benthamiana results in a hypersensitive response (HR). In contrast, HR is not activated when A-L is co-expressed with R1. AVR1 and A-L are highly similar in structure. They share two W motifs and one Y motif in the C-terminal part but differ in the T-region, a 38 amino acid extension at the carboxyl-terminal tail of AVR1 lacking in A-L. To pinpoint what determines R1-mediated recognition of AVR1 we tested elicitor activity of AVR1 and A-L chimeric and deletion constructs by co-expression with R1. The T-region is important as it enables R1-mediated recognition of A-L, not only when fused to A-L but also via trans-complementation. Yet, AVR1 lacking the T-region is still active as an elicitor of HR, but this activity is lost when certain motifs are swapped with A-L. These data show that A-L circumvents R1 recognition not only because it lacks the T-region, but also because of differences in the conserved C-terminal effector motifs.



中文翻译:

疫霉疫霉菌分离物中的RXLR效应子多样性决定了马铃薯抗性蛋白的识别。案例研究AVR1和R1

由植物病原性卵菌病原体致病疫霉引起的晚疫病是马铃薯生产中的最大限制因素之一。致病疫霉能够通过调节效应基因来克服渗入的晚疫病抗性。AVR1是一种RXLR效应子,当被马铃薯抗性蛋白R1识别时会触发免疫反应。发现在R1植物上无毒的致病疫霉分离株具有R1识别的AVR1变体。尽管有毒力的分离株缺乏AVR1,但确实包含一个名为AL的AVR1的近源同源物,其中的所有变体都逃避了R1的识别。AVR1R1本氏烟草中的共表达导致过敏反应(HR)。相反,当ALR1共表达时,HR未激活。AVR1和AL在结构上非常相似。它们在C端部分共有两个W基元和一个Y基元,但在T区不同,在AL中,AVR1的羧基端尾部有38个氨基酸延伸。为了查明是什么决定了R1介导的对AVR1的识别,我们通过与R1共表达来测试AVR1和AL嵌合和缺失构建体的激发子活性。T区非常重要,因为它不仅可以融合到AL,而且还可以通过反补体实现R1介导的AL识别。然而,缺少T区的AVR1仍然是激活HR的诱因,但是当某些基序与AL交换时,这种活性就会丢失。这些数据表明,AL绕开R1识别不仅是因为它缺少T区域,而且还因为保守的C末端效应子基元存在差异。

更新日期:2018-02-07
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