Biochemical basis of aluminium tolerance in plant cells

To be considered in this treatise are recent developments on biochemical aspects of aluminium tolerance and toxicity. Advances in aluminium biochemistry are best illustrated by knowledge gained in the area of aluminium uptake across the plasma membrane and by the putative role of aluminium in transmembrane signalling pathways. Initial studies indicate that aluminium is taken up by endocytotic mechanisms, either via non-saturable, fluid-phase endocytosis or through saturable, membrane receptor-mediated endocytosis involving specific carriers. These uptake modes are respectively exemplified by aluminium internalization involving polysaccharides and carriers, perhaps present in the rhizosphere. Regarding aluminium interiorization, a working hypothesis can be formulated explaining endocytotic uptake followed by processing along intracellular pathways that in part determine aluminium's final destination. Given the complexity of endocytotic processes, genetic defects at the plasma membrane or at internal membranes probably lead to deficiencies in aluminium's uptake and intracellular routing, respectively. As to cellular communication, aluminium fluoride has been implicated in being a ligand for membrane-associated G proteins which function as intermediaries in signal transduction. G proteins in part control phosphoinositide hydrolysis which in turn is crucial for the release of second messenger molecules. Aluminium-related interaction with components of signalling pathways is expected to affect the cell's capability of processing sensory information. Findings are also presented on aluminium-enhanced membrane lipid peroxidation, aluminium interference with cytoskeletal elements, calmodulin, and the chromatin structure. The challenge will be to elucidate biochemical mechanisms of aluminium toxicity as a basis for designing aluminium tolerant plants.