NPR1
生物
受体
细胞生物学
水杨酸
抑制因子
转录调控
激活剂(遗传学)
免疫
功能(生物学)
转录因子
基因
免疫系统
生物化学
遗传学
内科学
利钠肽
医学
心力衰竭
作者
Yuli Ding,Tongjun Sun,Kevin Ao,Yujun Peng,Yaxi Zhang,Xin Li,Yuelin Zhang
出处
期刊:Cell
[Elsevier]
日期:2018-04-12
卷期号:173 (6): 1454-1467.e15
被引量:546
标识
DOI:10.1016/j.cell.2018.03.044
摘要
Salicylic acid (SA) is a plant defense hormone required for immunity. Arabidopsis NPR1 and NPR3/NPR4 were previously shown to bind SA and all three proteins were proposed as SA receptors. NPR1 functions as a transcriptional co-activator, whereas NPR3/NPR4 were suggested to function as E3 ligases that promote NPR1 degradation. Here we report that NPR3/NPR4 function as transcriptional co-repressors and SA inhibits their activities to promote the expression of downstream immune regulators. npr4-4D, a gain-of-function npr4 allele that renders NPR4 unable to bind SA, constitutively represses SA-induced immune responses. In contrast, the equivalent mutation in NPR1 abolishes its ability to bind SA and promote SA-induced defense gene expression. Further analysis revealed that NPR3/NPR4 and NPR1 function independently to regulate SA-induced immune responses. Our study indicates that both NPR1 and NPR3/NPR4 are bona fide SA receptors, but play opposite roles in transcriptional regulation of SA-induced defense gene expression.
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