Rate D N, Greenberg J T
Chemistry and Biochemistry Graduate Program, University of Colorado at Boulder, Boulder, CO 80309, USA.
Plant J. 2001 Aug;27(3):203-11. doi: 10.1046/j.0960-7412.2001.1075umedoc.x.
A novel Arabidopsis mutant has been identified with constitutive expression of GST1-GUS using plants with a pathogen-responsive reporter transgene containing the beta-glucuronidase (GUS) coding region driven by the GST1 promoter. The recessive mutant, called agd2 (aberrant growth and death2), has salicylic acid (SA)-dependent increased resistance to virulent and avirulent strains of the bacterial pathogen Pseudomonas syringae, elevated SA levels, a low level of spontaneous cell death, callose deposition, and enlarged cells in leaves. The enhanced resistance of agd2 to virulent P. syringae requires the SA signaling component NONEXPRESSOR OF PR1 (NPR1). However, agd2 renders the resistance response to P. syringae carrying avrRpt2 NPR1-independent. Thus agd2 affects both an SA- and NPR1-dependent general defense pathway and an SA-dependent, NPR1-independent pathway that is active during the recognition of avirulent P. syringae. agd2 plants also fail to show a hypersensitive cell death response (HR) unless NPR1 is removed. This novel function for NPR1 is also apparent in otherwise wild-type plants: npr1 mutants show a stronger HR, while NPR1-overproducing plants show a weaker HR when infected with P. syringae carrying the avrRpm1 gene. Spontaneous cell death in agd2 is partially suppressed by npr1, indicating that NPR1 can suppress or enhance cell death depending on the cellular context. agd2 plants depleted of SA show a dramatic exacerbation of the cell-growth phenotype and increased callose deposition, suggesting a role for SA in regulating growth and this cell-wall modification. AGD2 may function in cell death and/or growth control as well as the defense response, similarly to what has been described in animals for the functions of NFkappaB.
利用携带由谷胱甘肽S-转移酶1（GST1）启动子驱动的β-葡萄糖醛酸酶（GUS）编码区的病原体响应报告基因转基因的植物，已鉴定出一种新型拟南芥突变体，其GST1-GUS呈组成型表达。这种隐性突变体称为agd2（异常生长和死亡2），对细菌性病原菌丁香假单胞菌的致病和无毒菌株具有水杨酸（SA）依赖性增强抗性，SA水平升高，自发细胞死亡水平低，胼胝质沉积，且叶片细胞增大。agd2对致病丁香假单胞菌的增强抗性需要SA信号成分PR1非表达子（NPR1）。然而，agd2使对携带avrRpt2的丁香假单胞菌的抗性反应不依赖NPR1。因此，agd2影响SA和NPR1依赖性的一般防御途径以及在识别无毒丁香假单胞菌期间活跃的SA依赖性、NPR1非依赖性途径。除非去除NPR1，agd2植物也不会表现出超敏细胞死亡反应（HR）。NPR1的这种新功能在其他方面为野生型的植物中也很明显：npr1突变体表现出更强的HR，而过量产生NPR1的植物在感染携带avrRpm1基因的丁香假单胞菌时表现出较弱的HR。npr1部分抑制了agd2中的自发细胞死亡，表明NPR1可以根据细胞环境抑制或增强细胞死亡。缺乏SA的agd2植物表现出细胞生长表型的显著恶化和胼胝质沉积增加，表明SA在调节生长和这种细胞壁修饰中起作用。AGD2可能在细胞死亡和/或生长控制以及防御反应中发挥作用，类似于在动物中描述的NFκB的功能。
