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Aluminum-Resistant Arabidopsis Mutants That Exhibit Altered Patterns of Aluminum Accumulation and Organic Acid Release from Roots1

Paul B. Larsen, Jörg Degenhardt, Chin-Yin Tai2, Laura M. Stenzler, Stephen H. Howell, and Leon V. Kochian*

United States Plant, Soil, and Nutrition Laboratory, United States Department of Agriculture-Agriculture Research Station, Tower Road, Cornell University, Ithaca, New York 14853 (P.B.L., J.D., L.V.K.); and Boyce Thompson Institute, Tower Road, Cornell University, Ithaca, New York 14853 (C.-Y.T., L.M.S., S.H.H.)

Al-resistant (alr) mutants of Arabidopsis thaliana were isolated and characterized to gain a better understanding of the genetic and physiological mechanisms of Al resistance. alr mutants were identified on the basis of enhanced root growth in the presence of levels of Al that strongly inhibited root growth in wild-type seedlings. Genetic analysis of the alr mutants showed that Al resistance was semidominant, and chromosome mapping of the mutants with microsatellite and random amplified polymorphic DNA markers indicated that the mutants mapped to two sites in the Arabidopsis genome: one locus on chromosome 1 (alr-108, alr-128, alr-131, and alr-139) and another on chromosome 4 (alr-104). Al accumulation in roots of mutant seedlings was studied by staining with the fluorescent Al-indicator dye morin and quantified via inductively coupled argon plasma mass spectrometry. It was found that the alr mutants accumulated lower levels of Al in the root tips compared with wild type. The possibility that the mutants released Al-chelating organic acids was examined. The mutants that mapped together on chromosome 1 released greater amounts of citrate or malate (as well as pyruvate) compared with wild type, suggesting that Al exclusion from roots of these alr mutants results from enhanced organic acid exudation. Roots of alr-104, on the other hand, did not exhibit increased release of malate or citrate, but did alkalinize the rhizosphere to a greater extent than wild-type roots. A detailed examination of Al resistance in this mutant is described in an accompanying paper (J. Degenhardt, P.B. Larsen, S.H. Howell, L.V. Kochian [1998] Plant Physiol 117: 19-27).

1   This work was initiated through the support of the Cornell Biotechnology program and was supported in part by the U.S. Environmental Protection Agency, Office of Research and Development (project no. R82-0001-010).
2   Present address: Department of Pediatric Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115.
*   Corresponding author; e-mail lvk1{at}cornell.edu; fax 1-607-255-2459.

Plant Physiol. (1998) 117: 9-17
Copyright Clearance Center:   0032-0889/98/117/0009/09
© 1998 American Society of Plant Physiologists




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