Our lab is interested in the systems biology and evolution of epigenetic switches (bistability) and clocks (oscillators) in gene regulatory networks. We use experiment and theory, biology and physics, systems and synthetic biology to study the cell cycle, metabolic rhythms, and circadian clocks. How do oscillators with different frequencies co-exist in the same cell? Are there mechanisms and regulatory principles that ensure functional harmony between oscillators?
This paper combined experiment and theory to demonstrate that newly discovered circadian redox rhythms regulate the plant circadian clock through NPR1, a master immune regulator. Sargis Karapetyan developed a mathematical model of the plant circadian clock to uncover new regulatory links (red arrows). We learned that NPR1 activates the expression of key circadian clock genes (TOC1, PRR7, LHY) in a “balanced” fashion, such that the amplitude is boosted with no change in period or phase during acute redox perturbation. This was a fun and productive collaboration with the Dong lab. Read more about it here on the Duke Today website.
Zhou M, Wang W, Karapetyan S, Mwimba M, Marques J, Buchler NE, Dong X. Redox rhythm reinforces circadian clock to gate immune response. Nature 523: 472 (2015)
Heungwon Park used microfluidics to trap bacteria and measure cell size and gene expression via long-term fluorescence timelapse. Experiments & modelling show that noisy regulation of cell size homeostasis can explain the apparent oscillations we observed in both size and gene expression in bacteria. This was an amusing collaboration with the laboratory of Lingchong You. Pratt News summary and movie can also be found here.
Tanouchi Y, Pai A, Park H, Huang S, Stamatov R, Buchler NE, You L. “A noisy linear map underlies oscillations in cell size and gene expression in bacteria” Nature 523: 357 (2015).
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