Abstract
The primary Al lesion is suggested to be blockage of the root plasma membrane Ca super(2+) channels. Resulting decrease in net Ca super(2+) uptake into the root tip cells leads to Ca super(2+) deficiency in the cytoplasm and disturbance of the cell Ca super(2+) homeostasis, effects that can deleteriously influence cell structure and function. Contribution of internal Ca super(2+) stores to maintaining cytoplasmic Ca super(2+) concentration at physiological levels is considered to be insufficient in meristematic cells at the root tip. It is suggested that differential blockage of Ca super(2+) channels may be at the core of differential tolerance to Al, opening up the possibility of manipulating Al tolerance at the molecular level. (DBO)