Abstract: | Signalling process of water stress‐induced abscisic acid (ABA) accumulation was investigated in maize (Zea mays L.) leaf and root tissues. Potent free‐radical scavengers and reducing agents, N‐acetyl cysteine (NAC) and cystein (Cys), significantly inhibited or nearly completely blocked dehydration‐induced ABA accumulation. Dithiothreitol (DTT), a reducing agent but not a free‐radical scavenger, also significantly inhibited such accumulation whereas solely free‐radical scavengers, dimethyl sulphoxide (DMSO) and melatonin (Mela), had no effects. Moreover, water stress‐induced ABA accumulation was not affected either by free radicals, such as superoxide anion and hydrogen peroxide, or by oxidants such as KIO4. These observations suggest that the blocking of water stress‐induced ABA accumulation resulted from the reducing effect, rather than from anything associated with free radicals. The disulphide bond might be crucial to the reactivity of some signal element(s) in the signalling process of water stress‐induced ABA accumulation. To test the hypothesis, we used a sulfhydryl modifier, iodoacetamide (IOA), and found that it nearly totally blocked the water stress‐induced ABA accumulation. Furthermore, an impermeable sulfhydryl modifier, p‐chloromercuriphenylsulphonic acid (PCMBS), could also inhibit the water stress‐induced ABA accumulation in the leaf tissues. These results indicate that water stress‐perception protein(s) or receptor(s) may be located on the plasmalemma and a sulfhydryl group in the extracellular domain is critical to the reactivity of the speculated water stress receptors. Cys, DTT and IOA did not lead to a decrease of the baseline ABA level, i.e. in non‐stressed roots. Result indicates that their blocking of water stress‐induced ABA accumulation occurred upstream of the ABA biosynthesis pathway, i.e. in the signalling process that initiates such accumulation. |