¹State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100094, China

Correspondence: Dongtao Ren Tel: 0086-10-62733794; Fax: 0086-10-62891332 E-mail: ren@cau.edu.cn

^*These two authors contributed equally to this work.

Received 4 June 2007; Revised 3 September 2007; Accepted 25 September 2007.

Abstract

Mitogen-activated protein kinases (MAPKs) are involved in the regulation of plant growth, development and responses to a wide variety of stimuli. In a conditional gain-of-function transgenic system, the activation of AtMEK5, a MAPK kinase, can in turn activate endogenous AtMAPK3 and AtMAPK6, and can lead to a striking increase in ethylene production and induce hypersensitive response (HR)-like cell death in Arabidopsis. However, the role of the increased ethylene production in regulating this HR-like cell death remains unknown. Using Arabidopsis transgenic plants that express AtMEK5^DD, an active mutant of AtMEK5 that is under the control of a steroid-inducible promoter, we tested the contribution of ethylene to cell death. We found that ethylene biosynthesis occurs before cell death. Cell death was delayed by inhibiting AtMEK5-induced ethylene production using inhibitors of ACC-synthases, ACC-oxidases or ethylene receptors. In the mutants AtMEK5^DD/etr1-1 and AtMEK5^DD/ein2-1, both of which showed insensitivity to ethylene, the expression of AtMEK5^DD protein, activity of AtMAPK3 and AtMAPK6, and ethylene production were the same as those seen in AtMEK5^DD transgenic plants, but cell death was also delayed. These data suggest that ethylene signaling perception is required to accelerate cell death that is induced by AtMEK5 activation.