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JXB Advance Access originally published online on June 27, 2005
Journal of Experimental Botany 2005 56(418):2195-2201; doi:10.1093/jxb/eri219
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© The Author [2005]. Published by Oxford University Press [on behalf of the Society for Experimental Biology]. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org

RESEARCH PAPER

Overexpression of SIPK in tobacco enhances ozone-induced ethylene formation and blocks ozone-induced SA accumulation

Marcus A. Samuel1,*, Ankit Walia1, Shawn D. Mansfield2 and Brian E. Ellis1

1Michael Smith Laboratories, University of British Columbia, 2185 East Mall, Vancouver, BC, Canada V6T 1Z4
2Department of Wood Science, University of British Columbia, Canada

* Present address and to whom correspondence should be sent: Department of Botany, University of Toronto, Canada. Fax: +1 416 978 5878. E-mail: smarcus{at}interchange.ubc.ca

Ozone induces rapid activation of SIPK, a mitogen-activated protein kinase (MAPK) in tobacco. Through transgenic manipulation it has previously been shown that overexpression of SIPK leads to enhanced ozone-induced lesion formation with concomitant accumulation of ROS. In spite of this hypersensitive phenotype, the effect of this altered SIPK expression on the levels of various hormones that regulate ozone-induced cell death has remained unexplored. The response of both salicylate and ethylene, the major phytohormones that modulate ozone-induced cell death, have now been analysed in SIPK-OX tobacco plants. Ozone treatment strongly induced ethylene formation in the sensitive SIPK-OX plants at ozone concentrations that failed to elicit stress ethylene release in WT plants. By contrast, SIPK-overexpressing plants displayed no ozone-induced SA accumulation, whereas WT plants accumulated SA upon ozone exposure. Epistatic analysis of SIPK-OX function suggests that the ozone-induced cell death observed in SIPK-OX plants is either independent, or upstream, of SA accumulation.

Key words: Cell death, ethylene, ozone, ROS, SA, SIPK


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