Bacterial spot, which is caused by several Xanthomonas species, is an economically important disease in tomato (Solanum lycopersicum). Great efforts have been made for the identification of resistant sources and the genetic analysis of resistance. However, the development of resistant commercial varieties is slow due to the existence of multiple species of the pathogen and a poor understanding of the resistance mechanism in tomato. The current study revealed that the Rx4 gene encodes a nucleotide‐binding leucine‐rich repeat protein in the wild tomato species Solanum pimpinellifolium and specifically recognizes and confers a hypersensitive response (HR) to Xanthomonas euvesicatoria pv. perforans race T3 expressing the AvrXv3 avirulence protein. Complementation of the Rx4 gene in the susceptible tomato line Ohio 88119 using a transgenic approach resulted in HR, whereas knockout of the gene through CRISPR/Cas9 editing in resistant lines Hawaii 7981 and PI 128216 led to non‐HR to race T3. Transcription of Rx4 was not induced by the presence of race T3. Furthermore, the Rx4 protein did not show physical interaction with AvrXv3 but interacted with SGT1‐1 and RAR1. Virus‐induced gene silencing of SGT1‐1 and RAR1 in the resistant line PI128216 suppressed the HR to race T3. Taken together, our study confirms Rx4 is the gene conferring the HR to bacterial spot race T3 and reveals the potential roles of SGT1‐1 and RAR1 as signals in the Rx4‐mediated HR. This discovery represents a step forward in our understanding of the mechanism of resistance to bacterial spot in tomato and may have important implications for understanding plant–bacterial interactions.

中文翻译：

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番茄蛋白 Rx4 介导对 Xanthomonas euvesicatoria pv 的过敏反应。穿孔比赛 T3

由几种黄单胞菌引起的细菌性斑点病是番茄 ( Solanum lycopersicum )经济上的重要病害。在抗性来源的识别和抗性的遗传分析方面做出了巨大努力。然而，由于该病原菌种类繁多，且对番茄的抗性机制了解不足，抗性商业品种的开发进展缓慢。目前的研究表明，Rx4基因编码野生番茄物种Solanum pimpinellifolium 中核苷酸结合的富含亮氨酸的重复蛋白，并特异性识别并赋予对Xanthomonas euvesicatoria pv的过敏反应 (HR) 。穿孔素表达 AvrXv3 无毒蛋白的种族 T3。使用转基因方法在易感番茄品系俄亥俄州 88119 中补充Rx4基因导致 HR，而在抗性品系夏威夷 7981 和 PI 128216 中通过 CRISPR/Cas9 编辑敲除该基因导致非 HR 到种族 T3。Rx4 的转录不是由种族 T3 的存在诱导的。此外，Rx4 蛋白不显示与 AvrXv3 的物理相互作用，但与 SGT1-1 和 RAR1 相互作用。在抗性品系 PI128216 中病毒诱导的SGT1-1和RAR1基因沉默抑制了 HR 到种族 T3。综上所述，我们的研究证实了Rx4是将 HR 赋予细菌斑点种族 T3 的基因，并揭示了 SGT1-1 和 RAR1 作为 Rx4 介导的 HR 中信号的潜在作用。这一发现代表着我们对番茄细菌性斑点病抗性机制的理解向前迈进了一步，可能对理解植物-细菌相互作用具有重要意义。