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Early Events in the Signal Pathway for the Oxidative Burst in
Soybean Cells Exposed to Avirulent Pseudomonas
syringae
pv glycinea1
Vinagolu K. Rajasekhar2, *,
Chris Lamb3, and
Richard A. Dixon
Plant Biology Division, Samuel Roberts Noble Foundation, 2510 Sam
Noble Parkway, Ardmore, Oklahoma 73401 (V.K.R., R.A.D.); and Plant
Biology Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037 (C.L.)
Soybean
(Glycine max) cv Williams 82 suspension cultures exhibit
an oxidative burst approximately 3 h after challenge with Pseudomonas syringae pv glycinea
(Psg) harboring the avrA (avirulence) gene. Pretreatment with the tyrosine (Tyr) kinase inhibitor herbimycin A or the serine/threonine kinase inhibitor K252a abolished the burst and subsequent induction of glutathione
S-transferase. However, imposition of a 45-min rest
period between pathogen challenge and subsequent addition of the kinase
inhibitors resulted in escape from inhibition by herbimycin A, whereas
inhibition by K252a persisted. Suramin, a G-protein inhibitor,
inhibited the burst if added up to 90 min after pathogen challenge. The
burst was also induced by the ion channel generator amphotericin B, and
this induction was sensitive to suramin and K252a. Conversely, the ion
channel blocker anthracene-9-carboxylate inhibited the
Psg:avrA-induced burst.
Psg:avrA rapidly induced Tyr
phosphorylation of several proteins, and this was inhibited by
herbimycin A or anthracene 9-carboxylic acid. These data suggest that
the activation of ion channels is followed by an upstream Tyr kinase
before the serine/threonine kinase-dependent steps in the signal
pathway leading to the oxidative burst.
Psg:avrA-dependent induction of phenylalanine
ammonia-lyase was not inhibited by herbimycin or suramin, suggesting
the operation of different signal pathways for the oxidative burst and
phenylpropanoid-derived defense responses.
1
This work was supported by The Samuel Roberts
Noble Foundation.
2
Present address: Department of Molecular
Oncology, M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box
317, Houston, TX 77030.
3
Present address: Institute of Cell and Molecular
Biology, University of Edinburgh, Mayfield Road, Edinburgh EH9 3JH,
Scotland, UK.
*
Corresponding author; e-mail rajbvkrj{at}hotmail.com.
Plant Physiol. (1999) 120: 1137-1146
Copyright Clearance Center: 0032-0889/99/120//10
© 1999 American Society of Plant Physiologists
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