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ARS Home » Northeast Area » Ithaca, New York » Robert W. Holley Center for Agriculture & Health » Research » Publications at this Location » Publication #63450
Title: ALUMINUM INHIBITION OF THE INS(1,4,5,)P3 SIGNAL TRANSDUCTION PATHWAY IN WHEAT ROOTS: A ROLE IN ALUMINUM TOXICITY?

Author
item JONES, DAVID - CORNELL UNIVERSITY
item Kochian, Leon

Submitted to: The Plant Cell
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/30/1995
Publication Date: N/A
Citation: N/A

Interpretive Summary: A large proportion of the world s lands (c.a. 40%) contain acid soils, and in these soils, aluminum (Al) toxicity is the major factor limiting crop growth. In order to begin to design and develop more Al resistant crop varieties, we need to gain an understanding of the physiological processes disrupted in plants that result in Al toxicity. In this study, we investigated the possibility that Al interacts with a signal sensing syste that is found in the outer membrane of all cells, that helps cells sense different environmental cues and produce the appropriate cellular response. We found that Al inhibits this signal transduction pathway in cells of the wheat root apex, under conditions where the same Al exposure inhibited root growth (the primary symptom of Al toxicity). These results are significant, for they represent the first evidence in the literature for a specific target in plant cells that is disrupted by Al during the onset of Al toxicity.

Technical Abstract: In crop plants, Al rhizotoxicity is a major world problem, however, the cause of Al toxicity remains elusive. The effects of phytotoxic levels of Al on the inositol 1,4,5-triphosphate (Ins(1,4,5)P3) mediated signal trans- duction pathway were investigated in the wheat. It was found that exogenous application of Al (50 uM) rapidly inhibited root growth (<2h). An Ins(1,4,5)P3 transient was generated in vivo (+/- Al, 50 uM, 1 h) by treat ing the roots with H2O2 (10 mM). Background (unstimulated) levels of Ins(1,4,5)P3 were similar in both Al-treated and Al-untreated root apics. However, H2O2-stimulated levels of Ins(1,4,5)P3 in root apices showed a significant (> 50%) reduction after Al exposure in comparison with un- treated controls, indicating that Al may be interfering with the phospho- inositide signalling pathway. To directly assess the specific action of Al on phospholipase C (PLC), which mediates the cleavage of phosphatidyl 4,5- bisphosphate (PtdInsP2) to Ins(1,4,5)P3, microsomal membranes were isolate from wheat roots and PLC was assayed in vitro in the presence of either AlCl3, Al-citrate and other metal cations. AlCl3 or Al-citrate at physio- logically relevant levels of 20 uM and 100 uM respectively. Al exposure had no effect on Ins(1,4,5)P3 dephosphorylation or on a range of enzymes isolated from wheat roots, suggesting that Al exposure must specifically target phospholipase C. Possible mechanisms of PLC inhibition by Al and the role of Ins(1,4,5)P3 in Al toxicity and growth are discussed. The current study is significant for it provides the first evidence that the phytotoxic metal cation, Al, has a specific intracellular target site which may be integrally involved in root growth.