Abstract
We previously reported that the activity of agropine synthase gene promoter from Ri plasmid (Ri-ags promoter) was induced by wounding. The wound-induction was independent of jasmonic acid and did not require de novo protein synthesis, indicating that the induction might be a primary response to wounding. Furthermore, the induction was inhibited by extracellular EGTA or lanthanum ion (La3+) suggesting the involvement of calcium ion.
In this study, we investigated about involvement of the calcium ion in the wound induction of Ri-ags promoter pharmacologically. Verapamil, a blocker for L-type calcium channel, did not inhibit the wound induction, whereas gadolinium ion (Gd3+) did as effectively as La3+. These suggest the involvement of a calcium channel insensitive to verapamil. Furthermore, calmodulin antagonists W-7, trifluoperazine and chlorpromazine did not inhibit the wound induction, suggesting the noninvolvement of calmodulin in the pathway.
