A role for salicylic acid and NPR1 in regulating cell growth in Arabidopsis.

A role for salicylic acid and NPR1 in regulating cell growth in Arabidopsis.
复制标题

水杨酸和 NPR1 在调节拟南芥细胞生长中的作用。

DOI:
10.1046/j.1365-313x.2001.01158.x
复制
发表时间:
2001
期刊:
The Plant journal : for cell and molecular biology
影响因子:
--
通讯作者:
Greenberg,JT
Greenberg,JT
中科院分区:
--
文献类型:
--
作者:
Vanacker,H;Lu,H;Rate,DN;Greenberg,JT

文献摘要

被引文献

相似文献

水杨酸(SA)在植物与病原体相互作用过程中激活防御和细胞死亡中发挥着关键作用。针对某些病原体,SA 还限制了细胞死亡的程度,这表明它的作用取决于宿主与病原体的相互作用,是积极的还是消极的。此外,我们之前表明SA影响拟南芥防御相关突变体的细胞生长,加速细胞死亡6-1(acd6-1)和异常生长和死亡2(agd2)。利用acd6-1,agd2和其他两个防御相关突变体,病变模拟疾病6(lsd6),SA不敏感抑制子(ssi1),我们在这里详细表明SA调节 通过特异性影响细胞增大、核内复制和/或细胞分裂来促进细胞生长。我们发现 SA 可以积极或消极地调节细胞生长,具体取决于信号传导发生的环境。此外,PR 1 非表达蛋白 (NPR1) 是一种对调节防御和细胞死亡很重要的关键 SA 信号蛋白,也可在叶子发育过程中促进细胞分裂和/或抑制核内复制。我们认为 SA 与多种受体或信号通路相互作用,以控制正常发育、病原体攻击和/或应激情况下的细胞变化。我们认为 SA 和 NPR1 在细胞命运控制中发挥的作用比以前所理解的更广泛。
Salicylic acid (SA) plays a key role in activating defenses and cell death during plant–pathogen interactions. In response to some pathogens, SA also limits the extent of cell death, indicating that it acts positively or negatively depending on the host–pathogen interaction. In addition, we previously showed that SA affects cell growth in the Arabidopsis defense‐related mutantsaccelerated cell death 6–1(acd6–1) andaberrant growth and death 2(agd2).Usingacd6–1,agd2and two other defense‐related mutants,lesion simulating disease 6(lsd6),suppressor of SA‐insensitivity(ssi1), we show here in detail that SA regulates cell growth by specifically affecting cell enlargement, endoreduplication and/or cell division. We find that SA can act either positively or negatively to regulate cell growth depending on the context in which signaling occurs. Additionally, Nonexpressor of PR 1 (NPR1), a key SA signaling protein important for regulating defenses and cell death, also acts to promote cell division and/or suppress endoreduplication during leaf development. We propose that SA interacts with multiple receptors or signaling pathways to control cellular alterations during normal development, pathogen attack and/or stress situations. We suggest that SA and NPR1 play broader roles in cell fate control than has previously been understood.