State Key Laboratory of Crop Stress Biology in Arid Areas and College of Plant Protection, Northwest A&F University, Yangling, Shaanxi 712100, China.
Plant Physiol. 2023 Sep 22;193(2):1547-1560. doi: 10.1093/plphys/kiad404.
Phytophthora capsici deploys effector proteins to manipulate host immunity and facilitate its colonization. However, the underlying mechanisms remain largely unclear. In this study, we demonstrated that a Sne-like (Snel) RxLR effector gene PcSnel4 is highly expressed at the early stages of P. capsici infection in Nicotiana benthamiana. Knocking out both alleles of PcSnel4 attenuated the virulence of P. capsici, while expression of PcSnel4 promoted its colonization in N. benthamiana. PcSnel4B could suppress the hypersensitive reaction (HR) induced by Avr3a-R3a and RESISTANCE TO PSEUDOMONAS SYRINGAE 2 (AtRPS2), but it did not suppress cell death elicited by Phytophthora infestin 1 (INF1) and Crinkler 4 (CRN4). COP9 signalosome 5 (CSN5) in N. benthamiana was identified as a host target of PcSnel4. Silencing NbCSN5 compromised the cell death induced by AtRPS2. PcSnel4B impaired the interaction and colocalization of Cullin1 (CUL1) and CSN5 in vivo. Expression of AtCUL1 promoted the degradation of AtRPS2 and disrupted HR, while AtCSN5a stabilized AtRPS2 and promoted HR, regardless of the expression of AtCUL1. PcSnel4 counteracted the effect of AtCSN5 and enhanced the degradation of AtRPS2, resulting in HR suppression. This study deciphered the underlying mechanism of PcSnel4-mediated suppression of HR induced by AtRPS2.
辣椒疫霉菌分泌效应蛋白来操纵宿主免疫并促进其定植。然而，其潜在机制在很大程度上仍不清楚。在这项研究中，我们证明了一个 Sne 样（Snel）RxLR 效应基因 PcSnel4 在辣椒疫霉菌感染烟草原生质体的早期高度表达。敲除 PcSnel4 的两个等位基因会削弱辣椒疫霉菌的毒力，而表达 PcSnel4 则促进其在烟草原生质体上的定植。PcSnel4B 可以抑制 Avr3a-R3a 和 RESISTANCE TO PSEUDOMONAS SYRINGAE 2（AtRPS2）诱导的过敏反应（HR），但它不能抑制由 Phytophthora infestin 1（INF1）和 Crinkler 4（CRN4）引发的细胞死亡。在烟草原生质体中鉴定出 COP9 信号体 5（CSN5）是 PcSnel4 的宿主靶标。沉默 NbCSN5 会削弱 AtRPS2 诱导的细胞死亡。PcSnel4B 损害了 Cullin1（CUL1）和 CSN5 在体内的相互作用和共定位。表达 AtCUL1 促进了 AtRPS2 的降解并破坏了 HR，而 AtCSN5a 稳定了 AtRPS2 并促进了 HR，无论 AtCUL1 的表达情况如何。PcSnel4 抵消了 AtCSN5 的作用并增强了 AtRPS2 的降解，从而抑制了 HR。本研究阐明了 PcSnel4 介导的 AtRPS2 诱导的 HR 抑制的潜在机制。
