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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #165918

Title: ILR2, A NOVEL GENE REGULATING IAA CONJUGATE SENSITIVITY AND METAL TRANSPORT IN ARABIDOPSIS THALIANA

Author
item MAGIDIN, MONICA - RICE UNIVERSITY
item PITTMAN, JON - BAYLOR COLL MEDICINE
item Hirschi, Kendal
item BARTEL, BONNIE - RICE UNIVERSITY

Submitted to: Plant Journal
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/30/2003
Publication Date: 8/31/2003
Citation: Magidin, M., Pittman, J.K., Hirschi, K., Bartel, B. 2003. ILR2, a novel gene regulating IAA conjugate sensitivity and metal transport in Arabidopsis thaliana. Plant Journal. 35(4):523-534.

Interpretive Summary: The ability to manipulate plants to increase yield and nutrient content depends on our ability to manipulate plant growth. Here we describe a novel gene involved in plant metal transport. Eventually, we can manipulate this gene to alter the nutritional content of important crops.

Technical Abstract: Plants can regulate levels of the auxin indole-3-acetic acid (IAA) by conjugation to amino acids or sugars, and subsequent hydrolysis of these conjugates to release active IAA. These less active auxin conjugates constitute the majority of IAA in plants. We isolated the Arabidopsis ilr2-1 mutant as a recessive IAA-leucine resistant mutant that retains wild-type sensitivity to free IAA. ilr2-1 is also defective in lateral root formation and primary root elongation. In addition, ilr2-1 is resistant to manganese- and cobalt-mediated inhibition of root elongation, and microsomal preparations from the ilr2-1 mutant exhibit enhanced ATP-dependent manganese transport. We used a map-based positional approach to clone the ILR2 gene, which encodes a novel protein with no predicted membrane-spanning domains that is polymorphic among Arabidopsis accessions. Our results demonstrate that ILR2 modulates a metal transporter, providing a novel link between auxin conjugate metabolism and metal homeostasis.