ABSTRACT
Brassinosteroids (BRs) play important roles in plant growth, development and responses to environmental cues. BRs signal through plasma membrane-localized receptors to control BES1/BZR1 family transcription factors, which mediate the expression of thousands of genes. BRs activate and repress approximately equal numbers of genes. BES1/BZR1 interact with other transcription factors, histone-modifying enzymes, and transcription elongation factors to activate BR-induced genes. However, the mechanisms by which BES1/BZR1 mediate the BR-repressed gene expression are not well understood. Recent studies revealed that 2 BR-repressed transcription factors, MYBL2 and HAT1, cooperate with BES1 to downregulate BR-repressed genes expression. Moreover, BIN2 kinase, a well-established negative regulator in the BR signaling pathway, phosphorylates MYBL2 and HAT1. While BIN2 phosphorylates and destabilizes BES1/BZR1, BIN2 phosphorylated MYBL2 and HAT1 appear to be stabilized. These results not only extended our understanding of BR-repressed gene expression, but also revealed multiple inputs of BR signaling into BR transcriptional networks.
Subject(s)
Arabidopsis Proteins/metabolism , Arabidopsis/metabolism , Brassinosteroids/metabolism , Gene Expression Regulation, Plant , Nuclear Proteins/metabolism , Protein Kinases/metabolism , DNA-Binding Proteins/metabolism , Histone Acetyltransferases , Phosphorylation , Transcription Factors/metabolismABSTRACT
Plant steroid hormones, brassinosteroids (BRs), play essential roles in modulating cell elongation, vascular differentiation, senescence and stress responses. BRs signal through plasma membrane-localized receptor and other components to modulate the BES1/BZR1 (BRI1-EMS SUPPRESSOR 1/BRASSINAZOLE RESISTANT 1) family of transcription factors that modulate thousands of target genes. Arabodopsis thaliana homeodomain-leucine zipper protein 1 (HAT1), which encodes a homeodomain-leucine zipper (HD-Zip) class II transcription factor, was identified through chromatin immunoprecipitation (ChIP) experiments as a direct target gene of BES1. Loss-of-function and gain-of-function mutants of HAT1 display altered BR responses. HAT1 and its close homolog HAT3 act redundantly, as the double mutant hat1 hat3 displayed a reduced BR response that is stronger than the single mutants alone. Moreover, hat1 hat3 enhanced the phenotype of a weak allele of the BR receptor mutant bri1 and suppressed the phenotype of constitutive BR response mutant bes1-D. These results suggest that HAT1 and HAT3 function to activate BR-mediated growth. Expression levels of several BR-repressed genes are increased in hat1 hat3 and reduced in HAT1OX, suggesting that HAT1 functions to repress the expression of a subset of BR target genes. HAT1 and BES1 bind to a conserved homeodomain binding (HB) site and BR response element (BRRE) respectively, in the promoters of some BR-repressed genes. BES1 and HAT1 interact with each other and cooperate to inhibit BR-repressed gene expression. Furthermore, HAT1 can be phosphorylated and stabilized by GSK3 (GLYCOGEN SYNTHASE KINASE 3)-like kinase BIN2 (BRASSINOSTEROID-INSENSITIVE 2), a well established negative regulator of the BR pathway. Our results thus revealed a previously unknown mechanism by which BR signaling modulates BR-repressed gene expression and coordinates plant growth.
