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REVEILLE5 buffers the activity of CIRCADIAN CLOCK ASSOCIATED1 to modulate thermoresponsive hypocotyl growth in Arabidopsis [RNA-seq]

ABSTRACT: To understand how RVE5 regulates thermomorphogenic gene expression, we carried out an RNA-Seq analysis of WT and rve5-2 T-DNA mutant (GK_225C06) treated at 22°C and 29°C.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE180380 | GEO | 2022/12/01

REPOSITORIES: GEO

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REVEILLE5 buffers the activity of CIRCADIAN CLOCK ASSOCIATED1 to modulate thermoresponsive hypocotyl growth in Arabidopsis [ChIP-seq]

Project description:To further understand how RVE5 controls thermo-responses, we generated RVE5-MYC overexpression plants with the CaMV 35S promoter. Using these RVE5-MYC overexpression plants grown at 29°C, we performed Chromatin Immunoprecipitation-Sequencing (ChIP-Seq).

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REVEILLE5 buffers the activity of CIRCADIAN CLOCK ASSOCIATED1 to modulate thermoresponsive hypocotyl growth in Arabidopsis

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-12-01 | GSE180382 | GEO

REVEILLE5 buffers the activity of CIRCADIAN CLOCK ASSOCIATED1 to modulate thermoresponsive hypocotyl growth in Arabidopsis

Project description:REVEILLE5 buffers the activity of CIRCADIAN CLOCK ASSOCIATED1 to modulate thermoresponsive hypocotyl growth in Arabidopsis

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REVEILLE5 buffers the activity of CIRCADIAN CLOCK ASSOCIATED1 to modulate thermoresponsive hypocotyl growth in Arabidopsis [RNA-seq]

Project description:REVEILLE5 buffers the activity of CIRCADIAN CLOCK ASSOCIATED1 to modulate thermoresponsive hypocotyl growth in Arabidopsis [RNA-seq]

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REVEILLE5 buffers the activity of CIRCADIAN CLOCK ASSOCIATED1 to modulate thermoresponsive hypocotyl growth in Arabidopsis [ChIP-seq]

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The ELF4-ELF3-LUX complex links the circadian clock to diurnal control of hypocotyl growth.

Project description:The circadian clock is required for adaptive responses to daily and seasonal changes in environmental conditions. Light and the circadian clock interact to consolidate the phase of hypocotyl cell elongation to peak at dawn under diurnal cycles in Arabidopsis thaliana. Here we identify a protein complex (called the evening complex)--composed of the proteins encoded by EARLY FLOWERING 3 (ELF3), ELF4 and the transcription-factor-encoding gene LUX ARRHYTHMO (LUX; also known as PHYTOCLOCK 1)--that directly regulates plant growth. ELF3 is both necessary and sufficient to form a complex between ELF4 and LUX, and the complex is diurnally regulated, peaking at dusk. ELF3, ELF4 and LUX are required for the proper expression of the growth-promoting transcription factors encoded by PHYTOCHROME INTERACTING FACTOR 4 (PIF4) and PIF5 (also known as PHYTOCHROME INTERACTING FACTOR 3-LIKE 6) under diurnal conditions. LUX targets the complex to the promoters of PIF4 and PIF5 in vivo. Mutations in PIF4 and/or PIF5 are epistatic to the loss of the ELF4-ELF3-LUX complex, suggesting that regulation of PIF4 and PIF5 is a crucial function of the complex. Therefore, the evening complex underlies the molecular basis for circadian gating of hypocotyl growth in the early evening.

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Suprachiasmatic astrocytes modulate the circadian clock in response to TNF-?.

Project description:The immune and the circadian systems interact in a bidirectional fashion. The master circadian oscillator, located in the suprachiasmatic nuclei (SCN) of the hypothalamus, responds to peripheral and local immune stimuli, such as proinflammatory cytokines and bacterial endotoxin. Astrocytes exert several immune functions in the CNS, and there is growing evidence that points toward a role of these cells in the regulation of circadian rhythms. The aim of this work was to assess the response of SCN astrocytes to immune stimuli, particularly to the proinflammatory cytokine TNF-?. TNF-? applied to cultures of SCN astrocytes from Per2(luc) knockin mice altered both the phase and amplitude of PER2 expression rhythms, in a phase-dependent manner. Furthermore, conditioned media from SCN astrocyte cultures transiently challenged with TNF-? induced an increase in Per1 expression in NIH 3T3 cells, which was blocked by TNF-? antagonism. In addition, these conditioned media could induce phase shifts in SCN PER2 rhythms and, when administered intracerebroventricularly, induced phase delays in behavioral circadian rhythms and SCN activation in control mice, but not in TNFR-1 mutants. In summary, our results show that TNF-? modulates the molecular clock of SCN astrocytes in vitro, and also that, in response to this molecule, SCN astrocytes can modulate clock gene expression in other cells and tissues, and induce phase shifts in a circadian behavioral output in vivo. These findings suggest a role for astroglial cells in the alteration of circadian timing by immune activation.

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Circadian clock gene LATE ELONGATED HYPOCOTYL directly regulates the timing of floral scent emission in Petunia.

Project description:Flowers present a complex display of signals to attract pollinators, including the emission of floral volatiles. Volatile emission is highly regulated, and many species restrict emissions to specific times of the day. This rhythmic emission of scent is regulated by the circadian clock; however, the mechanisms have remained unknown. In Petunia hybrida, volatile emissions are dominated by products of the floral volatile benzenoid/phenylpropanoid (FVBP) metabolic pathway. Here we demonstrate that the circadian clock gene P. hybrida LATE ELONGATED HYPOCOTYL (LHY; PhLHY) regulates the daily expression patterns of the FVBP pathway genes and floral volatile production. PhLHY expression peaks in the morning, antiphasic to the expression of P. hybrida GIGANTEA (PhGI), the master scent regulator ODORANT1 (ODO1), and many other evening-expressed FVBP genes. Overexpression phenotypes of PhLHY in Arabidopsis caused an arrhythmic clock phenotype, which resembles those of LHY overexpressors. In Petunia, constitutive expression of PhLHY depressed the expression levels of PhGI, ODO1, evening-expressed FVBP pathway genes, and FVBP emission in flowers. Additionally, in the Petunia lines in which PhLHY expression was reduced, the timing of peak expression of PhGI, ODO1, and the FVBP pathway genes advanced to the morning. Moreover, PhLHY protein binds to cis-regulatory elements called evening elements that exist in promoters of ODO1 and other FVBP genes. Thus, our results imply that PhLHY directly sets the timing of floral volatile emission by restricting the expression of ODO1 and other FVBP genes to the evening in Petunia.

| S-EPMC4534231 | biostudies-literature

Oak extracts modulate circadian rhythms of clock gene expression in vitro and wheel-running activity in mice

Project description: Not available

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Trehalose-6-phosphate signaling regulates thermoresponsive hypocotyl growth in Arabidopsis thaliana

Project description:Growth plasticity is a key mechanism by which plants adapt to the ever-changing environmental conditions. Since growth is a high energy-demanding and irreversible process, it is expected to be regulated by the integration of endogenous energy status as well as environmental conditions. Here, we show that trehalose-6-phosphate (T6P) functions as a sugar signaling molecule that coordinates thermoresponsive hypocotyl growth with endogenous sugar availability. We found that the loss of T6P SYNTHASE 1 (TPS1) impaired high temperature-mediated hypocotyl growth. Consistently, the activity of PIF4, a positive transcription factor involved in hypocotyl growth, was compromised in the tps1 mutant. We further show that, in the tps1 mutant, a sugar signaling kinase KIN10 directly interacts with and phosphorylates PIF4, which destabilizes PIF4. T6P inhibits KIN10 activity in a GRIK-dependent manner, allowing PIF4 to promote hypocotyl growth at high temperatures. Together, our results demonstrate that T6P determines thermoresponsive growth through the KIN10-PIF4 signaling module. Such regulation of PIF4 by T6P integrates the temperature-signaling pathway with the endogenous sugar status, thus optimizing plant growth response to environmental stresses.

| S-SCDT-EMBOR-2019-47828-T | biostudies-other

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