"In response to daily light and temperature cycles, organisms have evolved a 24 h circadian clock, which in plants controls gene expression, stomatal opening and the timing component of photoperiodism.
The genetic structure of the circadian network in Arabidopsis can be separated into three components: a central genetic oscillator and entrainment and outputs pathways. However, the reality is less clear, as circadian-outputs may modulate inputs to the clock and there is also a loop of cytosolic signalling molecules that forms part of the plant circadian clock. In this context, it has been proposed that one of the intermediates in the cold signalling pathway, cyclic adenosine diphosphate ribose (cADPR) is required to drive circadian oscillations of cytosolic-free Ca2+ ([Ca2+]cyt) and also modulate the nuclear transcriptional feedback loop of the Arabidopsis circadian oscillator. However, we have a poor understanding of the mechanisms by which Ca2+ regulates circadian clock gene expression.
Previous results obtained in Dr Webb’s lab have identified genes encoding the calcium-binding proteins CALMODULIN-LIKE 23 (CML23) and CML24 as Ca2+-signalling components that regulate the circadian network. This project will use a multidisciplinary approach including a mathematical model, molecular biology and biochemistry to determine key molecular targets of CML23/24, identify CML23/24 interacting proteins and determinate their effects on oscillator function and identify genetic interactions between CML23/24 and clock/light signalling genes. It will allow us to establish that CML23 and CML24 are components of the circadian network in Arabidopsis forming a cytosolic feedback loop together with cADPR and Ca2+. This will establish the relationship between daily [Ca2+]cyt dynamics and the control of the circadian network."
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