A mutation in the anticodon of a single tRNAala is sufficient to confer auxin resistance in Arabidopsis.

Auxin-resistant mutants have been useful for dissecting the mechanisms that underlie auxin-mediated biological processes. Here we report the isolation and molecular characterization of a novel auxin-resistant mutant in Arabidopsis (Arabidopsis thaliana). Like known mutated AUX/IAA transcription factors, the mutant described here displayed dominant resistance to exogenously supplied auxins (sirtinol, 2,4-dichlorophenoxyacetic acid, indole-3-acetic acid) and a host of pleiotropic phenotypes, including apical hook deformation, defects in lateral root development, reduced stature, and homozygous lethality. This mutant showed the same sensitivity to the ethylene precursor 1-aminocyclopropane carboxylic acid as wild-type plants, and retained the ability to induce IAA19 expression in response to exogenously supplied indole-3-acetic acid. To our surprise, these phenotypes were not caused by a mutation in an AUX/IAA gene, but rather a mutation in a tRNA(ala) gene in which the anticodon was found changed from CGC to CAC. Such a change results in a tRNA that is charged with alanine but recognizes the second most highly used valine codon in Arabidopsis. Therefore, the observed phenotypes are likely the composite of stochastic mutations of many proteins, including downstream effectors.