Effects of Phenylacetic Acid on Abaxial and Adaxial Stomatal Movements and Its Interaction With Abscisic Acid

Abstract

SUMMARY The effects of varying concentrations of phenylacetic acid (PAA), alone and in combination with abscisic acid (ABA), on abaxial and adaxial stomatal movements were examined on isolated epidermis of Commelina communis. Increasing PAA concentration progressively suppressed abaxial opening, while up to 5 mol m−3 PAA produced remarkably wide adaxial apertures but higher concentrations caused closure; the stomatal K.+ changed accordingly. PAA, like the K+ ionophore benzo‐18‐crown‐6, showed strong antagonistic interactions with ABA. The results are interpreted by postulating that PAA, like benzo‐18‐crown‐6, increases the membrane permeability to K+. The normal abaxial permeability allows a net K+ gain required for opening, but the PAA‐induced increase in permeability causes a net K+ loss leading to closure, because the efflux down a concentration gradient outweighs the influx coupled with proton extrusion. In contrast, the normal K+ content is much less in adaxial than in abaxial guard cells, clear evidence of an inherent restriction to K+ fluxes; this is attributed to restricted membrane permeability to K+, which PAA is postulated to alleviate progressively with increasing concentration. Thus, an increase in permeability up to a critical limit favours a net K+ gain and promotes opening, but any further increase leads to a net K+ loss and causes closure, as in abaxial guard cells. This interpretation is substantiated by both the progressive reduction of PAA‐induced closure with increasing KC1 in the medium and the close similarity of the effects of PAA and benzo‐18‐crown‐6, alone and in antagonism with ABA, on abaxial and adaxial stomata.

Sodium Ions Can Eliminate the Normal Disparity in Abaxial and Adaxial Stomatal Opening on Isolated Epidermes

“…The ability of fusicoccin (Pemadasa, 1981a), IAA (Pemadasa, 1982a), phenylacetic acid (Pemadasa, 1982b) and benzo-18-crown-6 (Pemadasa, 1983), in antagonism with ABA, to eliminate the normal differences in opening as well as K+ accumulation between ahaxial and adaxial stomatal cells is suggestive of a specific link between the two phenomena. If this were so, alternative cations such as Na""" should be able to modify the disparity in abaxial and adaxial opening.…”

“…The well-known disparity in opening between abaxial and adaxial stomata (Turner, 1979) is closely associated with differential starch hydrolysis, malate synthesis and K* accumulation in the guard cells (Pemadasa, 1979a(Pemadasa, , 1981a(Pemadasa, , 1982a(Pemadasa, , b,c, 1983, but the primary cause is still an enigma. The ability of fusicoccin (Pemadasa, 1981a), IAA (Pemadasa, 1982a), phenylacetic acid (Pemadasa, 1982b) and benzo-18-crown-6 (Pemadasa, 1983), in antagonism with ABA, to eliminate the normal differences in opening as well as K+ accumulation between ahaxial and adaxial stomatal cells is suggestive of a specific link between the two phenomena. If this were so, alternative cations such as Na""" should be able to modify the disparity in abaxial and adaxial opening.…”