Role of dynamics of intracellular calcium in aluminium-toxicity syndrome

This review is concentrating on the role of aluminium (Al)-calcium (Ca) interactions in Al toxicity syndrome in plants. Disruption of cytoplasmic Ca2+ homeostasis has been suggested as a primary trigger of Al toxicity. Aluminium causes an increase in cytosolic Ca2+ activity, potentially disrupting numerous biochemical and physiological processes, including those involved in the root growth. The source of Ca2+ for the increase in cytosolic Ca2+ activity under Al exposure is partly extracellular (likely to be due to the Al-resistant portion of the flux through depolarization-activated Ca2+ channels and fluxes through Ca2+ -permeable nonselective cation channels in the plasma membrane) as well as intracellular (increased cytosolic Ca2+ activity enhances the activity of Ca2+ release channels in the tonoplast and the endoplasmic reticulum membrane). The effect on increased cytosolic Ca2+ activity of possible Al-related inhibition of the plasma membrane and endo-membrane Ca2+ -ATPases and Ca2+ exchangers (CaX) that sequester Ca2+ out of the cytosol is insufficiently documented at present. The relationship between Al toxicity, cytoplasmic Ca2+ homeostasis and cytoplasmic pH needs to be elucidated. Technical improvements that would allow measurements of cytosolic Ca2+ activity within the short time after exposure to Al (seconds or shorter) are eagerly awaited.