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

ABSTRACT: 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.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE53099 | GEO | 2014/05/30

SECONDARY ACCESSION(S): PRJNA230831

REPOSITORIES: GEO

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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)

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2014-05-30 | GSE53078 | GEO

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

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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.

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