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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)

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

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

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

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

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.

2015-01-01 | GSE41766 | GEO

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

Coordinated regulation of Arabidopsis microRNA biogenesis and red light signaling through Dicer-like 1 and phytochrome-interacting factor 4

Project description:Light and microRNAs (miRNAs) are key external and internal signals for plant development respectively. However the relationship between light signaling and miRNA biogenesis pathways remains unknown. Here we found that miRNA processer DCL1/HYL1 interacts with a basic helix–loop–helix (bHLH) transcription factor, phytochrome-interacting factor 4 (PIF4), which mediates the destabilization of DCL1 during dark-red light transition. PIF4 acts as a transcription factor for some miRNA genes and is necessary for the proper accumulation of miRNAs. DCL1/HYL1 and mature miRNAs play roles in the regulation of plant hypocotyl growth. These results uncovered a previously unknown crosstalk between miRNA biogenesis and red light signaling through the PIF4-dependent regulation of miRNA transcription and processing to affect red light-directed plant photomorhogenesis.

2018-02-27 | GSE109038 | GEO

Spatiotemporal analysis of shade-induced transcriptional reprogramming in Arabidopsis reveals patterns underlying organ-specific growth

Project description:In response to neighbor proximity plants increase growth of specific organs (e.g. hypocotyl) to enhance access to sunlight. Shade enhances the activity of Phytochrome Interacting Factors (PIFs) by releasing those bHLH transcription factors from phytochrome B-mediated inhibition. PIFs promote elongation by inducing auxin production in cotyledons. In order to elucidate spatiotemporal aspects of the neighbor proximity response, we analyzed changes in transcript abundance at different time points during a shade treatment in dissected cotyledons and hypocotyls. We concentrated our analysis on these two organs because the former is considered as the primary shade-sensing organ while elongation is rapidly triggered in the hypocotyl. We conclude that PIFs initiate transcriptional reprogramming in both organs within 15 minutes comprising regulated expression of several early auxin response genes. This suggests that hypocotyl growth is elicited by both local and distal auxin signals. With time the transcriptional response diverges increasingly between organs. We identify genes whose differential expression may underlie organ-specific elongation. Finally, we uncover a growth promotion gene expression signature shared between responses to different environments and organs.

2017-01-17 | GSE81202 | GEO

Role of MPK4 in pathogen-associated molecular pattern-triggered alternative splicing in Arabidopsis

Project description:Alternative splicing (AS) of pre-mRNAs in plants is an important mechanism of gene regulation in environmental stress tolerance but plant signals involved are essentially unknown. Pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) is mediated by mitogen-activated protein kinases and the majority of PTI defense genes are regulated by MPK3, MPK4 and MPK6. These responses have been mainly analyzed at the transcriptional level, however many splicing factors are direct targets of MAPKs. Here, we studied alternative splicing induced by the PAMP flagellin in Arabidopsis.

2020-03-03 | GSE146189 | GEO

JA-INDUCIBLE MYC2-LIKE1 acts as a repressor and negatively regulates jasmonate signaling in Arabidopsis

Project description:Jasmonate (JA) is a plant hormone that controls trade-offs between plant growth and responses to biotic and abiotic stresses. Although recent studies uncover core mechanism for JA-induced responses in Arabidopsis thaliana, it remains elusive how plants attenuate those responses. We report here that a basic-helix-loop-helix type transcription factor named JA-INDUCIBLE MYC2-LIKE1 (JAM1) acts as a transcriptional repressor and negatively regulates JA signaling. Arabidopsis plants expressing the chimeric repressor for JAM1 exhibited a substantial reduction of JA responses, including JA-induced inhibition of root growth, accumulation of anthocyanin, and male fertility. These plants were also compromised in resistance to attack by Spodoptera exigua. Conversely, jam1-4 loss-of-function mutants showed enhanced JA responsiveness, including increased resistance to the insect attack. Competitive binding of JAM1 and MYC2 to the target sequence of MYC2 suggested negative regulation of JA signaling by JAM1 and suppression of MYC2 function. These results indicate that JAM1 plays a pivotal role in fine-tuning of JA-mediated stress responses and plant growth by negatively regulating JA signaling. Transcriptomes of ProJAM1:JAM1-SRDX, ProMYC2:MYC2-SRDX and wild-type Arabidopsis seedlings with or without jasmonic acid were compared.

2013-07-03 | E-GEOD-42552 | biostudies-arrayexpress

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