Signals controlling the expression of cytosolic ascorbate peroxidase during pathogen-induced programmed cell death in tobacco

被引:86
作者
Mittler, R [1 ]
Lam, E
Shulaev, V
Cohen, M
机构
[1] Hebrew Univ Jerusalem, Dept Plant Sci, IL-91904 Jerusalem, Israel
[2] Rutgers State Univ, Cook Coll, Biotech Ctr, New Brunswick, NJ 08903 USA
关键词
ascorbate peroxidase; hypersensitive response; programmed cell death; reactive oxygen species;
D O I
10.1023/A:1006110223774
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In plants ascorbate peroxidase (APX) is an important H2O2-detoxifying enzyme. The expression of APX is rapidly induced in response to stresses that result in the accumulation of reactive oxygen species (ROS). We have recently reported that the steady-state level of transcripts encoding cytosolic APX (cAPX) is dramatically induced during the hypersensitive response (HR) of tobacco plants infected with tobacco mosaic virus (TMV). Because cAPX expression is closely linked to the production of ROS in plant cells, studying the regulation cAPX mRNA can reveal some of the signal transduction events associated with ROS metabolism during the HR. Analysis of cAPX mRNA induction during the HR suggested that the expression of cAPX is under the control of the HR signal transduction pathway. The activation of cAPX expression followed signaling events such as changes in protein phosphorylation and induction of ion fluxes. Expression of cAPX was suppressed under conditions of low oxygen pressure, and could only be mimicked by enhancing the intracellular generation of ROS. Interestingly, salicylic acid (SA), which is thought to be involved in ROS metabolism during the HR, did not affect the induction of cAPX mRNA during TMV-induced KR. Using cAPX expression as a marker for the production of ROS, it is suggested that SA may not be involved in the formation of ROS during the HR of tobacco to TMV, and that ROS may not be involved in the induction of the pathogenesis-related protein, PR-1, during this process.
引用
收藏
页码:1025 / 1035
页数:11
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