Role of dynamics of intracellular calcium in aluminium‐toxicity syndrome

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<jats:title>Summary</jats:title><jats:p>This review is concentrating on the role of aluminium (Al)‐calcium (Ca) interactions in Al toxicity syndrome in plants. Disruption of cytoplasmic Ca<jats:sup>2+</jats:sup> homeostasis has been suggested as a primary trigger of Al toxicity. Aluminium causes an increase in cytosolic Ca<jats:sup>2+</jats:sup> activity, potentially disrupting numerous biochemical and physiological processes, including those involved in the root growth. The source of Ca<jats:sup>2+</jats:sup> for the increase in cytosolic Ca<jats:sup>2+</jats:sup> activity under Al exposure is partly extracellular (likely to be due to the Al‐resistant portion of the flux through depolarization‐activated Ca<jats:sup>2+</jats:sup> channels and fluxes through Ca<jats:sup>2+</jats:sup>‐permeable nonselective cation channels in the plasma membrane) as well as intracellular (increased cytosolic Ca<jats:sup>2+</jats:sup> activity enhances the activity of Ca<jats:sup>2+</jats:sup> release channels in the tonoplast and the endoplasmic reticulum membrane). The effect on increased cytosolic Ca<jats:sup>2+</jats:sup> activity of possible Al‐related inhibition of the plasma membrane and endo‐membrane Ca<jats:sup>2+</jats:sup>‐ATPases and Ca<jats:sup>2+</jats:sup> exchangers (CaX) that sequester Ca<jats:sup>2+</jats:sup> out of the cytosol is insufficiently documented at present. The relationship between Al toxicity, cytoplasmic Ca<jats:sup>2+</jats:sup> homeostasis and cytoplasmic pH needs to be elucidated. Technical improvements that would allow measurements of cytosolic Ca<jats:sup>2+</jats:sup> activity within the short time after exposure to Al (seconds or shorter) are eagerly awaited. <jats:table-wrap position="anchor"> <jats:table frame="void"> <jats:col /> <jats:col /> <jats:col /> <jats:thead> <jats:tr> <jats:th /> <jats:th>Contents</jats:th> <jats:th /> </jats:tr> </jats:thead> <jats:tbody> <jats:tr> <jats:td>I.</jats:td> <jats:td><jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="#ss3">Introduction</jats:ext-link></jats:td> <jats:td>296</jats:td> </jats:tr> <jats:tr> <jats:td>II.</jats:td> <jats:td><jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="#ss4">Symptoms of aluminium toxicity</jats:ext-link></jats:td> <jats:td>296</jats:td> </jats:tr> <jats:tr> <jats:td>III.</jats:td> <jats:td><jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="#ss5">Calcium – aluminium interactions</jats:ext-link></jats:td> <jats:td>297</jats:td> </jats:tr> <jats:tr> <jats:td>IV.</jats:td> <jats:td><jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="#ss20">The role of electrical properties of the plasma membrane in calcium–aluminium interactions</jats:ext-link></jats:td> <jats:td>306</jats:td> </jats:tr> <jats:tr> <jats:td>V.</jats:td> <jats:td><jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="#ss23">Oxidative stress</jats:ext-link></jats:td> <jats:td>307</jats:td> </jats:tr> <jats:tr> <jats:td>VI.</jats:td> <jats:td><jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="#ss24">Callose</jats:ext-link></jats:td> <jats:td>308</jats:td> </jats:tr> <jats:tr> <jats:td>VII.</jats:td> <jats:td><jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="#ss25">Cytoskeleton</jats:ext-link></jats:td> <jats:td>308</jats:td> </jats:tr> <jats:tr> <jats:td>VIII.</jats:td> <jats:td><jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="#ss26">Conclusions</jats:ext-link></jats:td> <jats:td>309</jats:td> </jats:tr> <jats:tr> <jats:td /> <jats:td><jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="#ss27">Acknowledgements</jats:ext-link></jats:td> <jats:td>309</jats:td> </jats:tr> <jats:tr> <jats:td /> <jats:td><jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="#ss28">References</jats:ext-link></jats:td> <jats:td>309</jats:td> </jats:tr> </jats:tbody> </jats:table> </jats:table-wrap> </jats:p>

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