Plant and Cell Physiology Advance Access originally published online on March 7, 2005
Plant and Cell Physiology 2005 46(4):638-648; doi:10.1093/pcp/pci069
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Plant Cell Growth and Ion Flux Responses to the Streptomycete Phytotoxin Thaxtomin A: Calcium and Hydrogen Flux Patterns Revealed by the Non-invasive MIFE Technique
1 Tasmanian Institute of Agricultural Research, New Town Research Laboratories, 13 St John’s Avenue, New Town, Tasmania 7008, Australia
2 School of Agricultural Science, University of Tasmania, Private Bag 54, Hobart, Tasmania 7001, Australia
3 Corresponding author: E-mail, Sergey.Shabala{at}utas.edu.au; Fax, +613-6226-2642.
Thaxtomin A, a key phytotoxin produced by plant pathogenic Streptomyces sp., is implicit in common scab disease expression in potato. Primary targets and modes of action of thaxtomin A toxicity in plant cells are not well understood. In this work, early signalling events associated with thaxtomin A toxicity were studied using the ion-selective microelectrode ion flux estimation (MIFE) technique. Thaxtomin A-induced changes in net ion fluxes were measured across the plasma membrane (PM) of root and pollen tube tissue in Arabidopsis thaliana and tomato. Within a minute after toxin application, a rapid and short-lived Ca2+ influx was observed. Well ahead of the marked inhibition of root growth, a significant shift towards net H+ efflux across the PM occurred in all tissues. Similar to root tissues, thaxtomin A significantly modified ion flux profiles from growing pollen tubes. Thaxtomin A was more effective in young, physiologically active tissues (root elongation zone or pollen tube apex), suggesting a higher density of thaxtomin A-binding sites in these regions. Overall, our data provide the first evidence that thaxtomin A triggers an early signalling cascade, which may be crucial in plant–pathogen interactions. It also suggests a possible interaction between thaxtomin A and PM auxin receptors, as revealed from experiments on the auxin-sensitive ucu2-2/gi2 A. thaliana mutant.
Received October 3, 2004; Accepted February 4, 2005
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