U-box E3 ubiquitin ligase PUB17 acts in the nucleus to promote specific immune pathways triggered by Phytophthora infestans.

Ubiquitin E3 ligase PUB17 functions in the nucleus to regulate transcriptional responses positively in PAMP-triggered immunity and programmed cell death following perception of specific elicitors at the plant cell surface. Ubiquitination regulates many processes in plants, including immunity. The E3 ubiquitin ligase PUB17 is a positive regulator of programmed cell death (PCD) triggered by resistance proteins CF4/9 in tomato. Its role in immunity to the potato late blight pathogen, Phytophthora infestans, was investigated here. Silencing StPUB17 in potato by RNAi and NbPUB17 in Nicotiana benthamiana by virus-induced gene silencing (VIGS) each enhanced P. infestans leaf colonization. PAMP-triggered immunity (PTI) transcriptional responses activated by flg22, and CF4/Avr4-mediated PCD were attenuated by silencing PUB17. However, silencing PUB17 did not compromise PCD triggered by P. infestans PAMP INF1, or co-expression of R3a/AVR3a, demonstrating that not all PTI- and PCD-associated responses require PUB17. PUB17 localizes to the plant nucleus and especially in the nucleolus. Transient over-expression of a dominant-negative StPUB17V314I,V316I mutant, which retained nucleolar localization, suppressed CF4-mediated cell death and enhanced P. infestans colonization. Exclusion of the StPUB17V314I,V316I mutant from the nucleus abolished its dominant-negative activity, demonstrating that StPUB17 functions in the nucleus. PUB17 is a positive regulator of immunity to late blight that acts in the nucleus to promote specific PTI and PCD pathways.

泛素E3连接酶PUB17在细胞核中发挥作用，在植物细胞表面感知特定激发子后，正向调节病原相关分子模式触发的免疫（PTI）中的转录反应以及程序性细胞死亡。 泛素化调节植物中的许多过程，包括免疫。E3泛素连接酶PUB17是番茄中由抗性蛋白CF4/9触发的程序性细胞死亡（PCD）的正调节因子。在此研究了它在对马铃薯晚疫病菌（Phytophthora infestans）免疫中的作用。通过RNA干扰使马铃薯中的StPUB17沉默以及通过病毒诱导的基因沉默（VIGS）使本氏烟（Nicotiana benthamiana）中的NbPUB17沉默，均增强了晚疫病菌在叶片上的定殖。由flg22激活的病原相关分子模式触发的免疫（PTI）转录反应以及由CF4/Avr4介导的PCD因PUB17沉默而减弱。然而，PUB17沉默并不影响由晚疫病菌病原相关分子模式INF1触发的PCD，或R3a/AVR3a的共表达，这表明并非所有与PTI和PCD相关的反应都需要PUB17。PUB17定位于植物细胞核，尤其在核仁中。显性负性的StPUB17V314I，V316I突变体（其保留核仁定位）的瞬时过表达抑制了CF4介导的细胞死亡并增强了晚疫病菌的定殖。将StPUB17V314I，V316I突变体排除在细胞核外消除了其显性负性活性，表明StPUB17在细胞核中发挥作用。PUB17是对晚疫病免疫的正调节因子，它在细胞核中起作用以促进特定的PTI和PCD途径。