Model Name: Arabidopsis_clock_P2012
P2012 model with the original light function replaced by an Input Signal Step Function, as described in Adams et al. J. Biol. Rhythms 2012. Initial values were also updated to ZT0 on the 12L:12D limit cycle.
|Model Format||SBML L2 V4|
This model is termed P2012 and derives from the article: Modelling the widespread effects of TOC1 signalling on the plant circadian clock and its outputs. Alexandra Pokhilko, Paloma Mas & Andrew J Millar BMC Syst. Biol. 2013; 7: 23, submitted 10 Oct 2012 and published 19 March 2013. Link
The model describes the circuit depicted in Fig. 1 of the paper (GIF will be attached soon). It updates the P2011 model from Pokhilko et al. Mol. Syst. Biol. 2012 model, PLM_64, by including:
SBML curation notes (please see Comments for each version):
version 1 here is the version published as Supplementary Information and submitted to the Biomodels database.
Copasi and MATLAB versions are attached to version 1.
NB. Use only 'v1' Matlab files. Matlab files named 'v0' have older parameter values for parameters g4, g23, g25, m6, m23, m24, though these differ only slightly. The Copasi version is the same as the published SBML version, and the 'v1' matlab files.
This model has formed the basis for further work by external groups, as described in the following links:
Fogelmark et al. PLoS CB 2014 - http://dx.doi.org/10.1371/journal.pcbi.1003705
Zhou et al. Nature 2015 - http://dx.doi.org/10.1038/nature14449
Calluwe et al. Frontiers 2016 - http://dx.doi.org/10.3389/fpls.2016.00074
|Contact/Model Admin||Andrew Millar, University of Edinburgh, firstname.lastname@example.org|
|Submitted By||Andrew Millar, University of Edinburgh, email@example.com|
|Submission Date||2013-04-03 20:23:37.0|
|Supplementary Data Files||
|Model Files||original file, simplified file (use simplified if your software cannot read the file, e.g. Sloppy Cell)|
|Display the Content of the Model (compartments, species, reactions, etc.). NB: A mathml enabled browser is required in order to successfully view model equations.|
|Journal||BMC Systems Biology|
|Title||Modelling the widespread effects of TOC1 signalling on the plant circadian clock and its outputs.|
|Authors||Alexandra Pokhilko, Paloma Mas & Andrew J Millar|
|Abstract||Background 24-hour biological clocks are intimately connected to the cellular signalling network, which complicates the analysis of clock mechanisms. The transcriptional regulator TOC1 (TIMING OF CAB EXPRESSION 1) is a founding component of the gene circuit in the plant circadian clock. Recent results show that TOC1 suppresses transcription of multiple target genes within the clock circuit, far beyond its previously-described regulation of the morning transcription factors LHY (LATE ELONGATED HYPOCOTYL) and CCA1 (CIRCADIAN CLOCK ASSOCIATED 1). It is unclear how this pervasive effect of TOC1 affects the dynamics of the clock and its outputs. TOC1 also appears to function in a nested feedback loop that includes signalling by the plant hormone Abscisic Acid (ABA), which is upregulated by abiotic stresses, such as drought. ABA treatments both alter TOC1 levels and affect the clock’s timing behaviour. Conversely, the clock rhythmically modulates physiological processes induced by ABA, such as the closing of stomata in the leaf epidermis. In order to understand the dynamics of the clock and its outputs under changing environmental conditions, the reciprocal interactions between the clock and other signalling pathways must be integrated. Results We extended the mathematical model of the plant clock gene circuit by incorporating the repression of multiple clock genes by TOC1, observed experimentally. The revised model more accurately matches the data on the clock’s molecular profiles and timing behaviour, explaining the clock’s responses in TOC1 over-expression and toc1 mutant plants. A simplified representation of ABA signalling allowed us to investigate the interactions of ABA and circadian pathways. Increased ABA levels lengthen the free-running period of the clock, consistent with the experimental data. Adding stomatal closure to the model, as a key ABA- and clock-regulated downstream process allowed to describe TOC1 effects on the rhythmic gating of stomatal closure. Conclusions The integrated model of the circadian clock circuit and ABA-regulated environmental sensing allowed us to explain multiple experimental observations on the timing and stomatal responses to genetic and environmental perturbations. These results crystallise a new role of TOC1 as an environmental sensor, which both affects the pace of the central oscillator and modulates the kinetics of downstream processes.|