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

机译:U-box E3泛素连接酶PUB17在细胞核中起作用,以促进由疫霉疫霉引发的特异性免疫途径。

摘要

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.
机译:泛素化调节植物的许多过程,包括免疫力。 E3泛素连接酶PUB17是由番茄抗性蛋白CF4 / 9触发的程序性细胞死亡(PCD)的阳性调节剂。在此研究了其对马铃薯晚疫病病原体疫霉疫菌的免疫作用。通过病毒诱导的基因沉默(VIGS),通过RNAi沉默马铃薯中的StPUB17,并通过烟草诱导的本氏烟草中的NbPUB17沉默,均增强了致病疫霉的叶片定殖。 flg22和CF4 / Avr4介导的PCD激活的PAMP触发的免疫(PTI)转录反应通过沉默PUB17得以减弱。但是,沉默PUB17不会损害致病疫霉PAMP INF1触发的PCD或R3a / AVR3a的共表达,表明并非所有与PTI和PCD相关的反应都需要PUB17。 PUB17定位于植物核,尤其是在核仁中。暂时阴性的StPUB17V314I,V316I显性阴性突变体保留了核仁定位,抑制了CF4介导的细胞死亡并增强了P. infestans定植。从核中排除StPUB17V314I,V316I突变体消除了其显性负性活性,表明StPUB17在核中起作用。 PUB17是抗晚疫病的阳性调节剂,在核中起作用,以促进特定的PTI和PCD途径。

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