Summary We examined whether auxin/indole‐3‐acetic acid (Aux/IAA) proteins, which are key players in auxin‐signal transduction, are involved in brassinosteroid (BR) responses. iaa7/axr2‐1 and iaa17/axr3‐3 mutants showed aberrant BR sensitivity and aberrant BR‐induced gene expression in an organ‐dependent manner. Two auxin inhibitors were tested in terms of BR responses. Yokonolide B inhibited BR responses, whereas p ‐chlorophenoxyisobutyric acid did not inhibit BR responses. DNA microarray analysis revealed that 108 genes were up‐regulated, while only eight genes were down‐regulated in iaa7 . Among the genes that were up‐ or down‐regulated in axr2 , 22% were brassinolide ‐inducible genes, 20% were auxin‐inducible genes, and the majority were sensitive neither to BR nor to auxin. An inhibitor of BR biosynthesis, brassinazole, inhibited auxin induction of the DR5‐GUS gene, which consists of a synthetic auxin‐response element, a minimum promoter, and a β ‐glucuronidase. These results suggest that Aux/IAA proteins function in auxin‐ and BR‐signaling pathways, and that IAA proteins function as the signaling components modulating BR sensitivity in a manner dependent on organ type.
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Nakamura et al. (2005) studied this question.
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