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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE180382 | 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 [RNA-seq]

Project description: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.

2022-12-01 | GSE180380 | 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]

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

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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.

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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) in Arabidopsis thaliana impaired high-temperature-mediated hypocotyl growth. Consistently, the activity of PIF4, a transcription factor that positively regulates hypocotyl growth, was compromised in the tps1 mutant. We further show that, in the tps1 mutant, a sugar signaling kinase KIN10 directly phosphorylates and 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.

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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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TOC1-PIF4 interaction mediates the circadian gating of thermoresponsive growth in Arabidopsis.

Project description:Arabidopsis adapts to elevated temperature by promoting stem elongation and hyponastic growth through a temperature-responsive transcription factor PIF4. Here we show that the evening-expressed clock component TOC1 interacts with and inactivates PIF4, thereby suppressing thermoresponsive growth in the evening. We find that the expression of PIF4 target genes show circadian rhythms of thermosensitivity, with minimum responsiveness in the evening when TOC1 level is high. Loss of function of TOC1 and its close homologue PRR5 restores thermosensitivity in the evening, whereas TOC1 overexpression causes thermo insensitivity, demonstrating that TOC1 mediates the evening-specific inhibition of thermoresponses. We further show that PIF4 is required for thermoadaptation mediated by moderately elevated temperature. Our results demonstrate that the interaction between TOC1 and PIF4 mediates the circadian gating of thermoresponsive growth, which may serve to increase fitness by matching thermoresponsiveness with the day-night cycles of fluctuating temperature and light conditions.

| S-EPMC5171658 | biostudies-literature

B-box family proteins BBX18 and BBX23 control thermoresponsive hypocotyl growth in Arabidopsis

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

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