Ethylene signaling is required for the acceleration of cell death induced by the activation of AtMEK5 in Arabidopsis.

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.Cell Research (2008) 18:422–432. doi: 10.1038/cr.2008.29; published online 12 February 2008 [ABSTRACT FROM AUTHOR]