Abstract
In a screen for enhancers of tir1-1 auxin resistance, we identified two novel alleles of the putative mitochondrial pyruvate dehydrogenase E1alpha-subunit, IAA-Alanine Resistant4 (IAR4). In addition to enhancing the auxin response defects of tir1-1, iar4 single mutants exhibit numerous auxin-related phenotypes including auxin-resistant root growth and reduced lateral root development, as well as defects in primary root growth, root hair initiation, and root hair elongation. Remarkably, all of these iar4 mutant phenotypes were rescued when endogenous indole-3-acetic acid (IAA) levels were increased by growth at high temperature or overexpression of the YUCCA1 IAA biosynthetic enzyme, suggesting that iar4 mutations may alter IAA homeostasis rather than auxin response. Consistent with this possibility, iar4 mutants exhibit increased Aux/IAA stability compared to wild type under basal conditions, but not in response to an auxin treatment. Measurements of free IAA levels detected no significant difference between iar4-3 and wild-type controls. However, we consistently observed significantly higher levels of IAA-amino acid conjugates in the iar4-3 mutant. Furthermore, using stable isotope-labeled IAA precursors, we observed a significant increase in the relative utilization of the Trp-independent IAA biosynthetic pathway in iar4-3. We therefore suggest that the auxin phenotypes of iar4 mutants are the result of altered IAA homeostasis.
Highlights
In a screen for enhancers of tir1-1 auxin resistance, we identified two novel alleles of the putative mitochondrial pyruvate dehydrogenase E1a-subunit, indole-3-acetic acid (IAA)-Alanine Resistant4 (IAR4)
We find that while iar4 mutants exhibit several phenotypes consistent with reduced auxin response, these phenotypes can be suppressed by increasing endogenous IAA levels
In a genetic screen to identify additional factors involved in auxin signaling in Arabidopsis, we identified two novel alleles of IAA-Alanine Resistant4 (IAR4), which encodes a putative E1a-subunit of the mitochondrial pyruvate dehydrogenase complex (PDC)
Summary
In a screen for enhancers of tir auxin resistance, we identified two novel alleles of the putative mitochondrial pyruvate dehydrogenase E1a-subunit, IAA-Alanine Resistant (IAR4). In addition to enhancing the auxin response defects of tir, iar single mutants exhibit numerous auxin-related phenotypes including auxin-resistant root growth and reduced lateral root development, as well as defects in primary root growth, root hair initiation, and root hair elongation All of these iar mutant phenotypes were rescued when endogenous indole-3-acetic acid (IAA) levels were increased by growth at high temperature or overexpression of the YUCCA1 IAA biosynthetic enzyme, suggesting that iar mutations may alter IAA homeostasis rather than auxin response. A complex system of auxin influx and efflux carriers (Kramer and Bennett, 2006) transports the hormone to its target cells where it is perceived by the nuclear-localized TIR1/auxin F-box (AFB) family of receptors, triggering the SCFTIR1/AFBmediated ubiquitylation of Aux/IAA proteins (Gray et al, 2001; Dharmasiri et al, 2005) Subsequent degradation of these transcriptional repressors results in changes in auxin-regulated gene expression and corresponding changes in plant growth and development (Quint and Gray, 2006). LeClere et al (2004) and colleagues identified mutations in the Arabidopsis (Arabidopsis thaliana) IAAAlanine Resistant (IAR4) gene in a mutant screen for seedlings resistant to IAA-Ala and other IAA-amino
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