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A triple-HLH/bHLH Cascade Controls Cell Elongation Downstream of Multiple Hormonal and Environmental Signaling Pathways

ABSTRACT: The environmental and endogenous signals, light, temperature, brassinosteroid (BR), and gibberellin (GA), regulate cell elongation largely by controlling the expression of the PRE family helix-Loop-helix (HLH) factors, which promote cell elongation by interacting antagonistically with another HLH factor, IBH1. But the molecular mechanism by which PREs and IBH1 regulate gene expression has remained unknown. Here we show that IBH1 interacts with and inhibits a DNA-binding bHLH protein HBI1. Overexpression of HBI1 increased hypocotyl and petiole elongation, whereas dominant inactivation of HBI1 and its homologs caused a dwarf phenotype, indicating that HBI1 is a positive regulator of cell elongation. In vitro and in vivo experiments showed that HBI1 directly bound to the promoters and activated two EXPANSIN genes encoding cell wall-loosening enzymes; HBI1’s DNA-binding and transcriptional activities were inhibited by IBH1, but the inhibitory effects of IBH1 were abolished by PRE1. The results indicate that PREs activate the DNA-binding bHLH factor HBI1 by sequestering its inhibitor IBH1. Altering each of the three factors affected plant sensitivities to BR, GA, temperature, and light. Our study demonstrates that PREs, IBH1 and HBI1 form a chain of antagonistic switches that controls cell elongation downstream of multiple external and endogenous signals.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE41766 | GEO | 2015/01/01

SECONDARY ACCESSION(S): PRJNA178143

REPOSITORIES: GEO

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A triple-HLH/bHLH Cascade Controls Cell Elongation Downstream of Multiple Hormonal and Environmental Signaling Pathways

Project description:The environmental and endogenous signals, light, temperature, brassinosteroid (BR), and gibberellin (GA), regulate cell elongation largely by controlling the expression of the PRE family helix-Loop-helix (HLH) factors, which promote cell elongation by interacting antagonistically with another HLH factor, IBH1. But the molecular mechanism by which PREs and IBH1 regulate gene expression has remained unknown. Here we show that IBH1 interacts with and inhibits a DNA-binding bHLH protein HBI1. Overexpression of HBI1 increased hypocotyl and petiole elongation, whereas dominant inactivation of HBI1 and its homologs caused a dwarf phenotype, indicating that HBI1 is a positive regulator of cell elongation. In vitro and in vivo experiments showed that HBI1 directly bound to the promoters and activated two EXPANSIN genes encoding cell wall-loosening enzymes; HBI1's DNA-binding and transcriptional activities were inhibited by IBH1, but the inhibitory effects of IBH1 were abolished by PRE1. The results indicate that PREs activate the DNA-binding bHLH factor HBI1 by sequestering its inhibitor IBH1. Altering each of the three factors affected plant sensitivities to BR, GA, temperature, and light. Our study demonstrates that PREs, IBH1 and HBI1 form a chain of antagonistic switches that controls cell elongation downstream of multiple external and endogenous signals. Compare the transcriptome of IBH1 and PRE1

2015-01-01 | E-GEOD-41766 | biostudies-arrayexpress

35S:AtIBH1-SRDX Arabidopsis vs. wild type

Project description:In plants, basic helix-loop-helix (bHLH) transcription factors play important roles in the control of cell elongation. Two bHLH proteins, PACLOBTRAZOL RESISTANCE1 (PRE1) and Arabidopsis ILI1 binding bHLH1 (IBH1), antagonistically regulate cell elongation in response to brassinosteroid and gibberellin signaling, but the detailed molecular mechanisms by which these factors regulate cell elongation remain unclear. Here, we identify the bHLH transcriptional activators for cell elongation (ACEs) and demonstrate that PRE1, IBH1, and the ACEs constitute a triantagonistic bHLH system that competitively regulates cell elongation. In this system, the ACE bHLH transcription factors directly activate the expression of enzyme genes for cell elongation by interacting with their promoter regions. IBH1 negatively regulates cell elongation by interacting with the ACEs and thus interfering with their DNA binding. PRE1 interacts with IBH1 and counteracts the ability of IBH1 to affect ACEs. Therefore, PRE1 restores the transcriptional activity of ACEs, resulting in induction of cell elongation. The balance of triantagonistic bHLH proteins, ACEs, IBH1, and PRE1, might be important for determination of the size of plant cells. The expression of IBH1 and PRE1 is regulated by brassinosteroid, gibberellins, and developmental phase dependent factors, indicating that two phytohormones and phase-dependent signals are integrated by this triantagonistic bHLH system.

2012-11-19 | GSE35098 | GEO

35S:AtIBH1-SRDX Arabidopsis vs. wild type

Project description:In plants, cell elongation is regulated by multi phytohormones and light signaling. Recently, atypical HLH proteins of PRE sub-family and their interacting proteins including AtIBH1 were shown as a positive or negative regulator of cell elongation under phytohormone signaling pathways. However, the regulatory mechanism of cell elongation by these factors has not been revealed. We show here that PRE1 and AtIBH1 are function in a tri-antagonistic bHLH system, which control cell elongation. We identified bHLH activators (THINs) which positively regulate cell elongation by direct activation of the expression of genes for cell elongation including EXPs. AtIBH1 suppress the cell elongation by inhibiting the activation activity of THINs through the heterodimerization, and the suppressive activity of AtIBH1 is interrupted by PRE1. The cell elongation in plants is antagonistically regulated by the interaction between PRE1 and AtIBH1, and AtIBH1 and THINs, and quantity balance of each bHLH proteins is important for regulation of elongation. Developmental-phase dependent factors related to the regulation of expression of AtIBH1, PRE1 and THINs suggested that the tri- antagonistic bHLH system play important role for regulation of cell elongation during the Arabidopsis development. Two-condition experiment, 35S:AtIBH1-SRDX Arabidopsis vs. wild type. Biological replicates: 3 for both.

2012-11-19 | E-GEOD-35098 | biostudies-arrayexpress

Brassinosteroid, gibberellin, and phytochrome impinge on a common transcription module in Arabidopsis

Project description:Brassinosteroid (BR) and gibberellin (GA) promote many similar developmental responses in plants; but their relationship remains unclear. Here we show that BR and GA act interdependently through a direct interaction between the BR-activated BZR1 and GAinactivated DELLA transcription regulators. GA promotion of cell elongation required BR signaling, whereas BR or active BZR1 can suppresssed the GA-deficient dwarf phenotype. DELLAs directly interacted with BZR1 and inhibited BZR1-DNA binding both in vitro and in vivo. Genome-wide analysis defined a BZR1-dependent GA-regulated transcriptome, which is enriched with light-regulated genes and genes involved in cell wall synthesis and photosynthesis/chloroplast. GA promotion of hypocotyl elongation requires both BZR1 and the phytochrome interacting factors (PIFs), as well as their common downstream targets PREs. The results demonstrate that GA releases DELLA-mediated inhibition of BZR1, and that the DELLA-BZR1-PIF4 interaction defines a core transcription module that mediates coordinated growth regulation by GA, BR and light signals.

2012-06-25 | GSE35408 | GEO

HBI1 integrates hormonal and environmental signals to regulate the trade-off between growth and immunity (ChIP-seq)

Project description:The trade-off between growth and immunity is crucial for survival in plants. An antagonistic interaction has been observed between the growth-promoting hormone brassinosteroid and pathogen associated molecular pattern (PAMP) signals, which induce immunity but inhibit growth, however the underlying molecular mechanism has remained unclear. The PRE-IBH1-HBI1 triple helix-loop-helix/basic helix-loop-helix (HLH/bHLH) cascade has been shown to mediate growth responses to several hormonal and environmental signals, but its downstream targets and role in immunity remain unknown. Here, we performed genome-wide analyses of HBI1 target genes in Arabidopsis. The results show that HBI1 regulates a set of genes that largely overlaps with targets of PIFs, but displays both similar and unique transcriptional activities compared to PIFs, supporting a role in fine-tuning the network through cooperation and antagonism with other DNA-binding factors of the network. Furthermore, HBI1 also negatively regulates a subset of defense response genes. Two PAMPs, flagellin and elongation factor, repressed HBI1 expression, whereas overexpression of HBI1 reduced the PAMP-induced growth inhibition, defense gene expression, reactive oxygen species (ROS) production, and flg22-induced resistance to Pseudomonas syringae pathovar tomato DC3000. These data indicate that HBI1 is a node for crosstalk between hormone and immune pathways. This study demonstrates that the PRE-IBH1-HBI1 module integrates hormone and pathogen signals, and thus plays a central role in the balance between growth and immunity in plants. Genome wide analysis the HBI1 binding target

2014-05-30 | E-GEOD-53099 | biostudies-arrayexpress

HBI1 integrates hormonal and environmental signals to regulate the trade-off between growth and immunity (RNA-seq)

2014-05-30 | E-GEOD-53078 | biostudies-arrayexpress

A basic helix-loop-helix transcription factors network mediates the brassinosteroid signal [RNA-seq]

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2014-03-05 | GSE51119 | GEO

Comparison of gene expression between wild type (N2) and hlh-30(tm1978) mutant worms

Project description:The hlh-30 gene encodes a C. elegans basic-helix-loop-helix (bHLH) transcription factor; We compared RNA from wild type worms and worms mutant for the hlh-30 gene to identify putative target genes of the HLH-30 transcription factor.

2009-07-24 | GSE15762 | GEO

HBI1 integrates hormonal and environmental signals to regulate the trade-off between growth and immunity (ChIP-seq)

2014-05-30 | GSE53099 | GEO

HBI1 integrates hormonal and environmental signals to regulate the trade-off between growth and immunity (RNA-seq)

2014-05-30 | GSE53078 | GEO