Submitted to: Planta
Publication Type: Peer reviewed journal
Publication Acceptance Date: 9/1/1998
Publication Date: N/A
Citation: Interpretive Summary: Large areas of land within the U.S. and over 40% of the world s arable lands are acidic. In these acid soils, the phytotoxic aluminum (Al) ion, Al3+, is solubilized into soil solution and is toxic to root growth and function. Thus, Al toxicity is the primary factor limiting crop production on these acid soils. Understanding the cellular basis of aluminum toxicity is important in developing crop species that can tolerate Al toxicity and be cultivated on these acid soils. In this paper, we tested a hypothesis that has been frequently suggested in the literature that Al toxicity involves Al-induced disruption of the regulation of the concentration of free calcium ion in the cell. All living cells regulate their free calcium ion concentrations at very low levels, and rapid increases in cell calcium concentration are used as a cellular switch to control many processes. If this regulation is disrupted, cell death or impaired cell development results. In this study, we looked at the effect of Al exposure and other environmental stresses (oxidative stress, low oxygen, and mechanical stress) on cellular calcium concentrations in growing root hairs. It was found that Al exposure rapidly inhibited root hair growth and elicited significant increases in cellular calcium to levels that could impair cell function. However, these Al-induced increases in cell calcium occurred after root hair growth had ceased due to Al exposure, indicating the re- sponse was a symptom & not a cause of Al toxicity. It was also found that of the other environmental stresses studied, only oxidative stress caused a prolonged rise in cellular calcium, that also occurred after cell growth ceased. This study clearly indicates that Al-induced disruption of cellular calcium regulation is not a primary cause of Al toxicity in plants.
Technical Abstract: Aluminum inhibition of root growth is a major agricultural problem where the cause of toxicity has been linked to changes in cellular calcium homeostasis. Therefore, the effect of A1 and other stresses (mechanical, oxidative and anaerobic stress) on changes in cyto-plasmic calcium [Ca2+]c was followed in root hairs of wild-type, Al-sensitive & Al-resistant mutants of Arabidopsis thaliana. Generally, A1 exposure resulted in prolonged elevations in tip-localized [Ca2+]c & callose production in both wild type & Al-sensitive root hairs. However, these Al-induced increases in [Ca2+]c were not correlated with growth inhibition, occurring 5-10 min after A1 had induced growth to stop. In contrast, Al-resistant mutants showed little growth inhibition in response to A1 & produced no observable changes in [Ca2+]c. Oxidative, anaerobic & mechanical stress were applied to test whether a change in root hair [Ca2+]c was a specific response to A1. Only oxidative stress (H2O2, 10 uM) caused a prolonged rise in [Ca2+]c similar to that induced by A1, but again this occurred after growth had been inhibited. Application of mechanical stress did not cause measurable growth inhibition & did not lead to prolonged elevation in root hair [Ca2+]c. Anaerobic stress rapidly inhibited root hair growth but failed to cause increases in [Ca2+]c until 10 min of exposure, at which point the root hairs burst at the tip, leading to a large increase in [Ca2+]c. The evidence presented here suggests that although exposure of root hairs to toxic levels of A1 causes an alteration in cellular Ca2+ homeostasis, this is not the primary site of A1 toxicity. Similarly, although stresses can lead to increased [Ca2+]c this is not a generalized response of root hairs to all stresses.