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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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