Abstract
The plant hormone auxin can be regulated by formation and hydrolysis of amide-linked indole-3-acetic acid (IAA) conjugates. Here, we report the characterization of the dominant Arabidopsis iaa-leucine resistant3 (ilr3-1) mutant, which has reduced sensitivity to IAA-Leu and IAA-Phe, while retaining wild-type responses to free LAA. The gene defective in ilr3-1 encodes a basic helix-loop-helix leucine zipper protein, bHLH105, and the ilr3-1 lesion results in a truncated product. Overexpressing ilr3-1 in wild-type plants recapitulates certain ilr3-1 mutant phenotypes. In contrast, the loss-of-function ilr3-2 allele has increased IAA-Leu sensitivity compared to wild type, indicating that the ilr3-1 allele confers a gain of function. Microarray and quantitative real-time PCR analyses revealed five downregulated genes in ilr3-1, including three encoding putative membrane proteins similar to the yeast iron and manganese transporter Ccc1p. Transcript changes are accompanied by reciprocally misregulated metal accumulation in ilr3-1 and ilr3-2 mutants. Further, ilr3-1 seedlings are less sensitive than wild type to manganese, and auxin conjugate response phenotypes are dependent on exogenous metal concentration in ilr3 mutants. These data suggest a model in which the ILR3/bHLH105 transcription factor regulates expression of metal transporter genes, perhaps indirectly modulating IAA-conjugate hydrolysis by controlling the availability of metals previously shown to influence IAA-amino acid hydrolase protein activity.
Original language | English |
---|---|
Pages (from-to) | 1841-1857 |
Number of pages | 17 |
Journal | Genetics |
Volume | 174 |
Issue number | 4 |
Early online date | 8 Oct 2006 |
DOIs | |
Publication status | Published - Dec 2006 |
Keywords
- transcriptional activation domains
- iron-deficiency
- indoleacetic-acid
- factor family
- gene family
- genome-wide
- thaliana
- transporter
- sensitivity
- mutants