Water stress-induced ABA accumulation is a cellular signaling process from
water stress perception to activation of genes encoding key
enzymes of ABA biosynthesis, of which the
water stress-signal perception by cells or triggering mechanism of the ABA accumulation is the center in the whole process of ABA related-stress signaling in plants. The cell biological mechanism for triggering of ABA accumulation under
water stress was studied in leaves of Vicia faba.
Mannitol at 890 mmol * kg(-1) osmotic concentration induced an increase of more than 5 times in ABA concentration in detached leaf tissues, but the same concentration of
mannitol only induced an increase of less than 40 % in ABA concentration in protoplasts. Like in detached leaf tissues, ABA concentration in isolated cells increased more than 10 times under the treatment of
mannitol at 890 mmol * kg(-1) concentration, suggesting that the interaction between plasmalemma and cell wall was essential to triggering of the
water stress-induced ABA accumulation. Neither Ca(2+)-
chelating agent EGTA nor Ca(2+)channel activator
A23187 nor the two cytoskeleton inhibitors,
colchicine and
cytochalasin B, had any effect on
water stress-induced ABA accumulation. Interestingly
water stress-induced ABA accumulation was effectively inhibited by a non-plasmalemma-permeable sulfhydryl-modifier
PCMBS (p-chloromercuriphenyl-
sulfonic acid), suggesting that plasmalemma
protein(s) may be involved in the triggering of
water stress-induced ABA accumulation, and the
protein may contain sulfhydryl group at its function domain.