Calcium Involvement In the IAA-induced Leaflet Opening ofCassia fasciculata

Abstract

Opening of Cassia fasciculata leaflets was induced in darkness after application of indole-3-acetic acid (IAA). This movement was obtained with concentrations from 10−6 M to 10−4 M, after a corresponding time-lag ranging from 120 to 30 min. IAA (5×10−5 M) allowed leaflet opening at all the pH values tested (from 3·5 to 7·5), the largest aperture being obtained at pH 60 in MES 2·5 mM. Our data suggest a functional involvement of calcium in the regulation of the turgor variations occurring in the pulvinar motor cells during IAA-induced leaflet opening which occurs in darkness: indeed, this movement was inhibited by the Ca2+ chelator EGTA (this inhibition was reversed by CaCl2) or by antagonists (LaCl3, TMB-8); on the contrary, the IAA-opening was enhanced by ionophore A 23187. Calcium mobilization through specific channels was tested using antagonists such as verapamil and nifedipine: at physiological doses, these compounds did not significantly affect leaflet response. The possibility that calcium could originate from internal stores was checked using lithium chloride which is known to block the phosphatidylinositol cycle in animal cells. This compound hindered auxin-induced opening for concentrations higher than 5×10−4 M. The calcium-binding protein calmodulin was shown to be implicated in the IAA-induced response since opening was inhibited in a concentration-dependent manner after treatment with compound 48/80 and with W-7.