Abstract
In crop plants, aluminum (AI) rhizotoxicity is a major problem worldwide; however, the cause of AI toxicity remains elusive. The effects of AI on the inositol 1,4,5-trisphosphate $({\rm Ins}[1,4,5]{\rm P}_{3})\text{-mediated}$ signal transduction pathway were investigated in wheat roots. Exogenously applied AI (50 μM) rapidly inhibited root growth (<2 hr) but did not affect general root metabolism. An Ins(1,4,5) P3 transient was generated in root tips, either before or after exposure to AI for 1 hr, by treating the roots with H2 O2 (10 mM). Background (unstimulated) levels of Ins(1,4,5) P3 were similar in both AI-treated and AI-untreated root apices. However, H2 O2-stimulated levels of Ins(1,4,5) P3 in root apices showed a significant (>50%) reduction after AI exposure in comparison with untreated controls, indicating that AI may be interfering with the phosphoinositide signaling pathway. When phospholipase C (PLC) was assayed directly in the presence of AI or other metal cations in microsomal membranes, AlCl3 and AI-citrate specifically inhibited PLC action in a dose-dependent manner and at physiologically relevant AI levels. AI exposure had no effect on inositol trisphosphate dephosphorylation or on a range of enzymes isolated from wheat roots, suggesting that AI exposure may specifically target PLC. Possible mechanisms of PLC inhibition by AI and the role of Ins(1,4,5) P3 in AI toxicity and growth are discussed. This study provides compelling evidence that the phytotoxic metal cation AI has an intracellular target site that may be integrally involved in root growth.
