Ilyas Muhammad, Hörger Anja C, Bozkurt Tolga O, van den Burg Harrold A, Kaschani Farnusch, Kaiser Markus, Belhaj Khaoula, Smoker Matthew, Joosten Matthieu H A J, Kamoun Sophien, van der Hoorn Renier A L
Plant Chemetics Laboratory, Max Planck Institute for Plant Breeding Research, Carl-von-Linné Weg 10, 50829 Cologne, Germany.
Plant Chemetics Laboratory, Department of Plant Sciences, University of Oxford, South Parks Road, OX1 3RB Oxford, UK; Plant Chemetics Laboratory, Max Planck Institute for Plant Breeding Research, Carl-von-Linné Weg 10, 50829 Cologne, Germany.
Curr Biol. 2015 Aug 31;25(17):2300-6. doi: 10.1016/j.cub.2015.07.030. Epub 2015 Aug 20.
Rcr3 and Pip1 are paralogous secreted papain-like proteases of tomato. Both proteases are inhibited by Avr2 from the fungal pathogen Cladosporium fulvum, but only Rcr3 acts as a co-receptor for Avr2 recognition by the tomato Cf-2 immune receptor. Here, we show that Pip1-depleted tomato plants are hyper-susceptible to fungal, bacterial, and oomycete plant pathogens, demonstrating that Pip1 is an important broad-range immune protease. By contrast, in the absence of Cf-2, Rcr3 depletion does not affect fungal and bacterial infection levels but causes increased susceptibility only to the oomycete pathogen Phytophthora infestans. Rcr3 and Pip1 reside on a genetic locus that evolved over 36 million years ago. These proteins differ in surface-exposed residues outside the substrate-binding groove, and Pip1 is 5- to 10-fold more abundant than Rcr3. We propose a model in which Rcr3 and Pip1 diverged functionally upon gene duplication, possibly driven by an arms race with pathogen-derived inhibitors or by coevolution with the Cf-2 immune receptor detecting inhibitors of Rcr3, but not of Pip1.
Rcr3和Pip1是番茄中同源的分泌型木瓜蛋白酶样蛋白酶。这两种蛋白酶都受到真菌病原体番茄叶霉病菌（Cladosporium fulvum）的Avr2抑制，但只有Rcr3作为番茄Cf-2免疫受体识别Avr2的共受体。在此，我们表明，缺失Pip1的番茄植株对真菌、细菌和卵菌植物病原体高度敏感，这表明Pip1是一种重要的广谱免疫蛋白酶。相比之下，在没有Cf-2的情况下，Rcr3缺失不会影响真菌和细菌的感染水平，但只会增加对卵菌病原体致病疫霉（Phytophthora infestans）的易感性。Rcr3和Pip1位于一个在3600多万年前进化而来的基因座上。这些蛋白质在底物结合槽外的表面暴露残基上有所不同，并且Pip1的丰度比Rcr3高5到10倍。我们提出了一个模型，其中Rcr3和Pip1在基因复制后功能发生分歧，这可能是由与病原体衍生抑制剂的军备竞赛或与检测Rcr3而非Pip1抑制剂的Cf-2免疫受体的共同进化驱动的。
