Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA178143 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR605657.fastq.gz | Fastqsanger.gz | |||
| SRR605658.fastq.gz | Fastqsanger.gz | |||
| SRR605659.fastq.gz | Fastqsanger.gz | |||
| SRR605660.fastq.gz | Fastqsanger.gz | |||
| SRR605661.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
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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
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
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. Compare the transcriptome of HBI1-Ox and wild type.
2014-05-30 | E-GEOD-53078 | biostudies-arrayexpress
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.
2015-01-01 | GSE41766 | GEO
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.
2014-05-30 | GSE53099 | GEO
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.
2014-05-30 | GSE53078 | GEO
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
Project description:Plant growth is coordinately regulated by environmental and hormonal signals. Brassinosteroid (BR) plays essential roles in growth regulation by light and temperature, but the interactions between BR and these environmental signals remain poorly understood at the molecular level. Here, we show that direct interaction between the dark- and heat-activated transcription factor phytochrome-interacting factor4 (PIF4) and the BR-activated transcription factor BZR1 integrates the hormonal and environmental signals. BZR1 and PIF4 interact with each other in vitro and in vivo, bind to nearly two thousand common target genes, and synergistically regulate many of these target genes, including the PRE family HLH factors required for promoting cell elongation. Genetic analysis indicates that BZR1 and PIFs are interdependent in promoting cell elongation in response to BR, darkness, or heat. These results show that the BZR1-PIF4 interaction controls a core transcription network, allowing plant growth co-regulation by the steroid and environmental signals. Genome-wide identification of PIF4 binding sites in etiolated Arabidopsis seedlings.
2012-07-07 | E-GEOD-35315 | biostudies-arrayexpress
Project description:Plant growth is coordinately regulated by environmental and hormonal signals. Brassinosteroid (BR) plays essential roles in growth regulation by light and temperature, but the interactions between BR and these environmental signals remain poorly understood at the molecular level. Here, we show that direct interaction between the dark- and heat-activated transcription factor phytochrome-interacting factor4 (PIF4) and the BR-activated transcription factor BZR1 integrates the hormonal and environmental signals. BZR1 and PIF4 interact with each other in vitro and in vivo, bind to nearly two thousand common target genes, and synergistically regulate many of these target genes, including the PRE family HLH factors required for promoting cell elongation. Genetic analysis indicates that BZR1 and PIFs are interdependent in promoting cell elongation in response to BR, darkness, or heat. These results show that the BZR1-PIF4 interaction controls a core transcription network, allowing plant growth co-regulation by the steroid and environmental signals. RNA-Seq for Col-0, bzr1-1D, pifq and pifq;bzr1-1D seedlings grown on BRZ-containing medium in the dark.
2012-07-07 | E-GEOD-37159 | biostudies-arrayexpress
Project description:Auxin is a major plant hormone for both development and environmental adaptation. Auxin responses are context dependent and highly modulated by light, temperature, the circadian clock, brassinosteroid, and gibberellin, but the underlying mechanisms remain unclear. Here, we show that auxin signaling integrates with other signals through direct interactions of AUXIN RESPONSE FACTOR6 (ARF6) with PHYTOCHROME INTERACTING FACTOR4 (PIF4), the brassinosteroid-signaling transcription factor BZR1, and the gibberellin-signaling repressor RGA. ChIP-Seq and RNA-Seq experiments show that ARF6, PIF4, and BZR1 bind to largely overlapping targets in the genome and synergistically activate gene expression. In vitro and in vivo assays show that ARF6-promoter binding is enhanced by PIF4 and BZR1 but blocked by RGA. Furthermore, a tripartite HLH/bHLH module feedback regulates PIF activity and thus modulates auxin sensitivity according to additional developmental and environmental cues. Our results demonstrate a central growth-regulation transcriptional network that coordinates hormonal, environmental, and developmental control of cell elongation and plant growth. Genome-wide identification of ARF6 DNA-binding sites in etiolated Arabidopsis seedlings.
2014-06-03 | E-GEOD-51770 | biostudies-arrayexpress