Pokhilko2013 - TOC1 signalling in Arabidopsis circadian clock

Pokhilko2013 - TOC1 signalling in Arabidopsis
circadian clock

In this model, Pokhilko
et al. has incorporated the negative transcriptional
regulations of the core clock genes by TOC1 and the up-regulation
of TOC1 expression by ABA signalling, to their previous model
BIOMD0000000412

This model is described in the article:

Modelling the widespread
effects of TOC1 signalling on the plant circadian clock and its
outputs.

Pokhilko A, Mas P, Millar AJ.
BMC Syst Biol 2013; 7: 23
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.

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