Identification of Arabidopsis thaliana PRR9 regulated clock components and circadian outputs through genome-wide binding sites analysis
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE71397 | GEO | 2015/12/03
SECONDARY ACCESSION(S): PRJNA291090
REPOSITORIES: GEO
Similar Datasets
Project description:We identified genome-wide PRR9 targets by conducting chromatin immunoprecipitation followed by high-throughput sequencing. Plants were grown in cycling 12 h light/12 h dark for two weeks before harvesting at ZT4. The four samples include the immunoprecipitated and input control for prr9-1 PRR9::HA-PRR9 CCR2::LUC #109 (HA9) and the prr9-1 (s9c) parental control. PRR5 PRR7 and TOC1 raw data available from the following Series: PRR5: GSE36361 TOC1: GSE35952 PRR7: GSE49282 (GSM1196649 and GSM1196650)
2015-12-03 | E-GEOD-71397 | biostudies-arrayexpress
Project description:We identified genome-wide PRR7 targets by conducting chromatin immunoprecipitation combined with high-throughput sequencing.
2013-07-27 | GSE49282 | GEO
Project description:We identified genome-wide PRR7 targets by conducting chromatin immunoprecipitation combined with high-throughput sequencing. Lines include prr7-3 and prr7-3 PRR7::HA-PRR7 #151, and we conducted immunoprecipitations using an anti-HA antibody.
2013-07-27 | E-GEOD-49282 | biostudies-arrayexpress
Project description:The circadian clock controls many physiological processes in higher plants and causes a large fraction of the genome to be expressed with a 24h rhythm. The transcripts encoding the RNA-binding proteins AtGRP7 (Arabidopsis thaliana Glycine Rich Protein 7) and AtGRP8 oscillate with evening peaks. The circadian clock components CCA1 and LHY negatively affect AtGRP7 expression at the level of transcription. AtGRP7 and AtGRP8, in turn, negatively auto-regulate and reciprocally cross-regulate post-transcriptionally: high protein levels promote the generation of an alternative splice form that is rapidly degraded. This clock-regulated feedback loop has been proposed to act as a molecular slave oscillator in clock output. While mathematical models describing the circadian core oscillator in Arabidopsis thaliana were introduced recently, we propose here the first model of a circadian slave oscillator. We define the slave oscillator in terms of ordinary differential equations and identify the model's parameters by an optimization procedure based on experimental results. The model successfully reproduces the pertinent experimental findings such as waveforms, phases, and half-lives of the time-dependent concentrations. Furthermore, we obtain insights into possible mechanisms underlying the observed experimental dynamics: the negative auto-regulation and reciprocal cross-regulation via alternative splicing could be responsible for the sharply peaking waveforms of the AtGRP7 and AtGRP8 mRNA. Moreover, our results suggest that the AtGRP8 transcript oscillations are subordinated to those of AtGRP7 due to a higher impact of AtGRP7 protein on alternative splicing of its own and of the AtGRP8 pre-mRNA compared to the impact of AtGRP8 protein. Importantly, a bifurcation analysis provides theoretical evidence that the slave oscillator could be a toggle switch, arising from the reciprocal cross-regulation at the post-transcriptional level. In view of this, transcriptional repression of AtGRP7 and AtGRP8 by LHY and CCA1 induces oscillations of the toggle switch, leading to the observed high-amplitude oscillations of AtGRP7 mRNA.
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Project description:Circadian pace is modulated by light intensity, known as the Aschoff’s rule, with largely unrevealed mechanisms. Here we report that photoreceptor CRY2 mediates blue light input to circadian clock by directly interacting with clock core component PRR9 in blue light dependent manner. This physical interaction dually blocks the accessibility of PRR9 protein to its co-repressor TPL/TPRs and the resulting kinase PPKs. Notably, phosphorylation of PRR9 by PPKs is critical for its DNA binding and repressive activity, hence to ensure proper circadian speed. Given the labile nature of CRY2 in strong blue light, our findings provide a mechanistic explanation for Aschoff’s rule in plants, i.e., blue light triggers CRY2 turnover in proportional to its intensity, which accordingly releasing PRR9 to fine tune circadian speed. Our findings not only reveal a novel network mediating light input into circadian clock, but also unmask a mechanism by which Arabidopsis circadian clock sensing light intensity.
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Project description:Circadian clocks provide a competitive advantage in an environment that is heavily influenced by the rotation of the Earth, by driving daily rhythms in behaviour, physiology and metabolism in bacteria, fungi, plants and animals. Circadian clocks comprise transcription-translation feedback loops, which are entrained by environmental signals such as light and temperature to adjust the phase of rhythms to match the local environment. The production of sugars by photosynthesis is a key metabolic output of the circadian clock in plants. Here we show that these rhythmic, endogenous sugar signals can entrain circadian rhythms in Arabidopsis thaliana by regulating the gene expression of circadian clock components early in the photoperiod, thus defining a 'metabolic dawn'. By inhibiting photosynthesis, we demonstrate that endogenous oscillations in sugar levels provide metabolic feedback to the circadian oscillator through the morning-expressed gene PSEUDO-RESPONSE REGULATOR 7 (PRR7), and we identify that prr7 mutants are insensitive to the effects of sucrose on the circadian period. Thus, photosynthesis has a marked effect on the entrainment and maintenance of robust circadian rhythms in A. thaliana, demonstrating that metabolism has a crucial role in regulation of the circadian clock.
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