The Polyadenylation Factor Subunit CLEAVAGE AND POLYADENYLATION SPECIFICITY FACTOR30: A Key Factor of Programmed Cell Death and a Regulator of Immunity in Arabidopsis

The Polyadenylation Factor Subunit CLEAVAGE AND POLYADENYLATION SPECIFICITY FACTOR30: A Key Factor of Programmed Cell Death and a Regulator of Immunity in Arabidopsis
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DOI:
10.1104/pp.114.236083
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发表时间:
2014-06-01
期刊:
影响因子:
7.4
通讯作者:
Delarue, Marianne
Delarue, Marianne
中科院分区:
生物学1区
文献类型:
--
作者:
Bruggeman, Quentin;Garmier, Marie;Delarue, Marianne

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细胞程序性死亡(PCD)是植物生命的几个方面,包括发育和胁迫反应所必需的。事实上,众所周知,不相容的植物-病原体相互作用会诱导过敏反应,即局部细胞死亡。突变分析已经确定了几个关键的PCD组件,我们最近确定了mips 1突变体的拟南芥(拟南芥),这是缺乏的关键酶催化肌醇合成的限制步骤。mips 1最显著的特征之一是由于水杨酸(SA)依赖的PCD,揭示肌醇或肌醇衍生物在PCD的调节中的作用,光依赖性的叶片上的病变的形成。在这里,我们确定了一个调节植物PCD的突变体,显示转录谱反对的mips 1突变体的筛选。我们的筛选鉴定了oxt 6突变体,该突变体先前已被描述为对氧化应激具有耐受性。在oxt 6突变体中,将转移DNA插入裂解和多聚腺苷酸化特异性因子30(CPSF 30)基因中,该基因编码多聚腺苷酸化因子亚基同源物。我们表明,CPSF 30是必需的损伤形成mips 1通过SA依赖性信号,CPSF 30的促死亡功能是不介导的谷胱甘肽状态的变化,和CPSF 30的活性所需的假单胞菌耐药。我们还表明,oxt 6突变抑制其他病变模拟突变体的细胞死亡,包括病变模拟疾病1,丝裂原活化蛋白激酶4,组成型表达的发病相关基因5,和过氧化氢酶2,这表明CPSF 30,因此,控制信使RNA 3'端加工,通过调节SA生产,是植物免疫反应的关键组成部分。
Programmed cell death (PCD) is essential for several aspects of plant life, including development and stress responses. Indeed, incompatible plant-pathogen interactions are well known to induce the hypersensitive response, a localized cell death. Mutational analyses have identified several key PCD components, and we recently identified the mips1 mutant of Arabidopsis (Arabidopsis thaliana), which is deficient for the key enzyme catalyzing the limiting step of myoinositol synthesis. One of the most striking features of mips1 is the light-dependent formation of lesions on leaves due to salicylic acid (SA)-dependent PCD, revealing roles for myoinositol or inositol derivatives in the regulation of PCD. Here, we identified a regulator of plant PCD by screening for mutants that display transcriptomic profiles opposing that of the mips1 mutant. Our screen identified the oxt6 mutant, which has been described previously as being tolerant to oxidative stress. In the oxt6 mutant, a transfer DNA is inserted in the CLEAVAGE AND POLYADENYLATION SPECIFICITY FACTOR30 (CPSF30) gene, which encodes a polyadenylation factor subunit homolog. We show that CPSF30 is required for lesion formation in mips1 via SA-dependent signaling, that the prodeath function of CPSF30 is not mediated by changes in the glutathione status, and that CPSF30 activity is required for Pseudomonas syringae resistance. We also show that the oxt6 mutation suppresses cell death in other lesion-mimic mutants, including lesion-simulating disease1, mitogen-activated protein kinase4, constitutive expressor of pathogenesis-related genes5, and catalase2, suggesting that CPSF30 and, thus, the control of messenger RNA 3' end processing, through the regulation of SA production, is a key component of plant immune responses.