The epidermis coordinates thermoresponsive growth through the phyB-PIF4-auxin pathway
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ABSTRACT:
PROVIDER: PRJNA551939 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9622061_1.fastq.gz | Fastqsanger.gz | |||
| SRR9622061_2.fastq.gz | Fastqsanger.gz | |||
| SRR9622062_1.fastq.gz | Fastqsanger.gz | |||
| SRR9622062_2.fastq.gz | Fastqsanger.gz | |||
| SRR9622063_1.fastq.gz | Fastqsanger.gz |
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Project description:In plants, an elevation in ambient temperature induces morphological changes including elongation hypocotyls, considered to be adaptive responses to alleviate the heat-induced damages. The high temperature-induced morphological changes are called thermomorphogenesis, which is predominantly regulated by a bHLH transcription factor PIF4. Although PIF4 is expressed in all aerial tissues including the epidermis, mesophyll, and vascular bundle, its tissue-specific functions in thermomorphogenesis are not known. Here, we found that epidermis-specific expression of PIF4 induced constitutive long hypocotyls, while vasculature-specific expression of PIF4 had no effect on hypocotyl growth. Consistently, RNA-Seq and qRT-PCR analyses revealed that auxin responsive genes and growth-related genes were highly activated by epidermal, but not by vascular, PIF4. The epidermal, but not vascular, inactivation of PIF4 by a PIF4 artificial microRNA or a dominant negative form of PIF4 suppressed thermoresponsive gene expression and hypocotyl growth. Additionally, both the block of epidermal auxin signaling and the epidermal overexpression of a thermosensor phytochrome B (phyB) inhibited thermoresponsive growth, indicating that epidermal PIF4-auxin pathway are essential for the temperature responses. We further show that epidermal PIF4 is increased by high temperatures mainly through the transcriptional activation of PIF4. Taken together, our study demonstrates that the epidermis regulates thermoresponsive growth through the phyB-PIF4-auxin pathway.
2020-01-26 | GSE133564 | GEO
Project description:In plants, an elevation in ambient temperature induces adaptive morphological changes including elongated hypocotyls, which is predominantly regulated by a bHLH transcription factor, PIF4. Although PIF4 is expressed in all aerial tissues including the epidermis, mesophyll, and vascular bundle, its tissue-specific functions in thermomorphogenesis are not known. Here, we show that epidermis-specific expression of PIF4 induces constitutive long hypocotyls, while vasculature-specific expression of PIF4 has no effect on hypocotyl growth. RNA-Seq and qRT-PCR analyses reveal that auxin-responsive genes and growth-related genes are highly activated by epidermal, but not by vascular, PIF4. Additionally, inactivation of epidermal PIF4 or auxin signaling, and overexpression of epidermal phyB suppresses thermoresponsive growth, indicating that epidermal PIF4-auxin pathways are essential for the temperature responses. Further, we show that high temperatures increase both epidermal PIF4 transcription and the epidermal PIF4 DNA-binding ability. Taken together, our study demonstrates that the epidermis regulates thermoresponsive growth through the phyB-PIF4-auxin pathway.
| S-EPMC7044213 | biostudies-literature
Project description:The increasing ambient temperature significantly impacts plant growth, development, and reproduction. Uncovering the temperature-regulating mechanisms in plants is of high importance, not only for boosting our plant biology knowledge but also for assisting plant breeders in improving plant resilience to these stress conditions. Numerous studies on the molecular mechanisms by which plants regulate temperature responses revealed that plants employ distinct transcription factors to regulate thermomorphogenesis specific to each tissue type. A significant discovery in this field was the identification of PHYTOCHROME-INTERACTING FACTORs (PIFs) as key regulators of thermomorphogenesis during vegetative growth. PIF4, a regulator of auxin-mediated signaling pathways, is crucial in controlling high-temperature responses. In this study, we screened the temperature responses of the wild type and several PhyB-PIF4 pathway Arabidopsis mutant lines in combined and integrative phenotyping platforms for root in soil, shoot, inflorescence, and seed. We demonstrated that high ambient temperature differentially impacts vegetative and reproductive organs through this pathway. Suppression of the PhyB-PIF4 components mimics the response to a high ambient temperature in wild-type plants. We also identified correlative responses to high ambient temperature between shoot and root tissues. This integrative and automated phenotyping was complemented by monitoring the changes in transcript levels in reproductive organs. Transcriptomic profiling of the pistils from plants grown under high ambient temperature identified key elements that may provide clues to the molecular mechanisms behind temperature-induced reduced fertilization rate, such as a downregulation of auxin metabolism, upregulation of genes involved auxin signalling, miRNA156 and miRN160 pathways, pollen tube attractants.
2024-07-03 | GSE263964 | GEO
Project description:Warm ambient temperatures do not trigger stress responses in plants but stimulate the growth of specific organs. The basic helix-loop-helix transcription factor PHYTOCHROME-INTERACTING FACTOR 4 (PIF4) plays a central role in regulating thermomorphogenetic hypocotyl elongation in various plant species, including the model dicotyledonous plant Arabidopsis thaliana. Although it is well known that PIF4 promotes plant thermosensory growth by activating key genes involved in the biosynthesis and signaling of the phytohormone auxin, the detailed molecular mechanism of such transcriptional activation is still not clear. Our previous studies demonstrated that HEMERA (HMR), a transcription co-activator of PIF4, promotes the thermo-induced expression of PIF4 target genes through the nine-amino-acid transactivation domain (9aaTAD) in its carboxy-terminus. In this report, we investigate the role of the Mediator complex in the PIF4/HMR-mediated thermoresponsive gene expression. Through the characterization of various mutants of the Mediator complex, a tail subunit named MED14 is identified as an essential factor for thermomorphogenetic hypocotyl growth. MED14 is required for the thermal induction of key PIF4 target genes but has a marginal effect on the levels of PIF4 and HMR. Further transcriptomic analyses confirm that the expression of numerous PIF4/HMR-dependent, auxin-related genes requires MED14 at a warm temperature. Moreover, PIF4 and HMR physically interact with MED14 and both are indispensable for the association of MED14 with the promoters of these thermoresponsive genes. Together, these results unveil an important thermomorphogenetic mechanism, in which PIF4 and its coactivator HMR recruit the Mediator complex to activate auxin-related growth-promoting genes when plants sense moderate increases in ambient temperature.
2022-09-26 | GSE196969 | GEO
Project description:Plants coordinate their growth and developmental programs with various endogenous signals and environmental challenges such as seasonal and diurnal temperature fluctuations. The bHLH transcription factor PIF4 plays critical roles in thermoresponsive hypocotyl growth in Arabidopsis, and the evening complex component ELF3 negatively regulates PIF4's activity for downstream gene expression and hypocotyl elongation at elevated temperature. However, how warm temperature signal is transmitted to ELF3 is not known. Here, we report the identification of two B-Box protein BBX18/BBX23 as new regulators of thermomorphogenesis in Arabidopsis. Mutations of BBX18/BBX23 confer reduced thermoresponsive hypocotyl elongation. Overexpression of BBX18 enhances the sensitivity of hypocotyl growth to elevated temperature, which is dependent on the function of PIF4 and RING E3 ligase COP1, respectively. Both BBX18 and BBX23 interact with ELF3 or COP1, relegating the protein abundance of ELF3 at warm temperature. Further, the expression of multiple thermoresponsive genes is impaired in both the PIF4 single mutant and BBX18/BBX23 double mutant. In addition, both the transcription and protein levels of BBX18/BBX23 are up-regulated by elevated ambient temperature. Thus, our findings reveal the important roles of B-Box proteins in plant thermomorphogenesis, and build a new connection from warm temperature information to ELF3 and its downstream signaling components.
2018-12-21 | GSE108162 | GEO
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
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. Seedlings (Col-0 and iaa3) were grown on medium containing 2 µM propiconazole (PPZ) in the dark for 5 days and treated with mock or 100 nM BL for 4 hr before harvesting for total RNA extraction.
2014-06-03 | E-GEOD-51772 | 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.
2014-06-03 | GSE51772 | GEO
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.
2014-06-03 | GSE51770 | GEO
Project description:Seedling hypocotyls display negative gravitropism in the dark but agravitropism in the light. The Arabidopsis thaliana pif quadruple mutant (pifQ), which lacks four PHYTOCHROME-INTERACTING FACTORS (PIFs), is agravitropic in the dark. Endodermis-specific expression of PIF1 rescues gravitropism in pifQ mutant seedlings. Since phytochromes induce light responses by inhibiting PIFs and the COP1-SPA ubiquitin E3 ligase complex in the nucleus, we asked whether phyB can cell autonomously inhibit hypocotyl negative gravitropism in the endodermis. We found that while epidermis-specific expression of PHYB rescues hypocotyl negative gravitropism and all other phyB mutant phenotypes, endodermis-specific expression of PHYB does not. Epidermal phyB induces the phosphorylation and degradation of endodermal PIFs in response to red light. This induces a global gene expression pattern similar to that induced by red light treatment of seedlings expressing PHYB under the control of its own endogenous promoter. Our results imply that epidermal phyB generates an unidentified mobile signal that travels to the endodermis where it promotes PIF degradation and inhibits hypocotyl negative gravitropism.
2017-02-08 | GSE87591 | GEO