Arabidopsis MYB30 is a direct target of BES1 and cooperates with BES1 to regulate brassinosteroid-induced gene expression

Academic Article
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publication date

  • April 2009

abstract

  • A paradox of plant hormone biology is how a single small molecule can affect a diverse array of growth and developmental processes. For instance, brassinosteroids (BRs) regulate cell elongation, vascular differentiation, senescence and stress responses. BRs signal through the BES1/BZR1 (bri1-Ethylmethane Sulphonate suppressor 1/brassinazole-resistant 1) family of transcription factors, which regulate hundreds of target genes involved in this pathway, yet little is known of this transcriptional network. Through microarray and chromatin immunoprecipitation (ChIP) experiments, we identified a direct target gene of BES1, AtMYB30, which encodes an MYB family transcription factor. AtMYB30 null mutants display decreased BR responses and enhance the dwarf phenotype of a weak allele of the BR receptor mutant bri1. Many BR-regulated genes have reduced expression and/or hormone-induction in AtMYB30 mutants, indicating that AtMYB30 functions to promote expression of a subset of BR target genes. AtMYB30 and BES1 bind to a conserved MYB-binding site and E-box sequences, respectively, in the promoters of genes that are regulated by both BRs and AtMYB30. Finally, AtMYB30 and BES1 interact with each other both in vitro and in vivo. These results demonstrate that BES1 and AtMYB30 function cooperatively to promote BR target gene expression. Our results therefore establish a new mechanism by which AtMYB30, a direct target of BES1, functions to amplify BR signaling by helping BES1 activate downstream target genes.