We acquired high-resolution data on the light responses of the Arabidopsis clock genes under a range of photoperiods, and for light treatments with a range of fluences of red or blue light.
We understood these complex, quantitative, dynamic data by comparison to simulations of three existing circadian clock models, using a new data analysis method and a new mathematical measure. This was the first test of molecular data from such detailed environmental manipulations against any in vivo clock model. It also stretched the limits of the experimental methods, and the models. Edwards et al. MSB 2010.
We developed a new clock model that explained the major discrepancy between the original models and the new data. The new model predicted a molecular interaction that was independently verified in our group and by a group in Japan. It also explained why one clock function is performed by a gene family (the five PRRs), not a single gene. Pokhilko et al. MSB 2010.
Working with a biotechnology company, Mendel Biotechnology Inc., we undertook a systems biology project on two crucial plant proteins, transcription factors that are degraded by light. Company scientists did experiments, we created a mathematical model (Pokhilko et al. J. Theor. Biol. 2011).
We also discovered that a clock gene, ELF3, that was identified several years ago is a repressor, not an activator as first thought: Dixon et al. Curr. Biol. 2011. This insight in turn led to a further revision of the clock gene circuit and together with the light-regulated degradation model, to a new clock model: Pokhilko et al. MSB 2012.