The regulation of root development by aluminium in Zea mays L.

Abstract

This investigation confirmed that plant reaction to Al was directed through the disruption of intercellular co-ordination existing between the cell populations comprising the root meristem. The first detectable response to A1 in the root involved disruption of Golgi apparatus function in the cap periphery. Ultrastructural changes in the cap periphery coincided with the presence of A1 in these cells. Conspicuous physiological changes involving cell enlargement, cell metabolism and root elongation were identified in cells initially remote from the site(s) of A1 uptake. Communication between A1-damaged peripheral root cap cells and the cell populations of the cap and proximal meristems, quiescent centre and region of cell growth was therefore indicated. A decrease in amyloplast numbers in response to increasing AI concentration coincided with diminished Golgi apparatus activity in the peripheral cap. These changes preceded detectable reductions in mitotic activity, indicated by decreases in cap volume and root length, and it was consequently suggested that control of intercellular activities in the root meristem may be directed through polysaccharide metabolism. Low concentrations of A1 (≤ 1,25 mg dm ¯³) produced a positive growth response in the primary root. This coincided with an increase in mean cap volume and these events were interpreted as an A1-induced release of the proximal meristem from growth inhibition originating in the cap. Experiments which followed the effect of decapping on the morphology of quiescent centre cells in the presence and absence of A1 supported the existence of a Golgi apparatus-derived morphogen involved in the control of Golgi apparatus secretory activity and plastid differentiation. In contrast to the controls (0 ABA). treatment of decapped roots with 2 X 10[-4] and 5 X 10[-5] M abscisic acid inhibited the development of Golgi apparatus secretory activity and plastid differentiation. It is postulated therefore, that an early response to AI may involve inhibition of the basipetal movement of an endogenous growth inhibitor originating in the cap, which may be ABA. The presence of A1 in the nutrient solution caused an efflux of H[+] from the root. Some of the more adverse plant responses to AI were initiated at A1 concentrations where the molar ratio of charge between Ca[2+] and A1[3+] favoured A1. An hypothesis for an electrophysiological plant response to A1 involving membrane hyperpolarisation by Al ions is developed. Chemical analysis of plant fractions did not connect A1-induced nutrient disorders with the primary expression of A1 toxicity.