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Mathematical Medicine and Biology Advance Access originally published online on January 29, 2009
Mathematical Medicine and Biology 2009 26(2):117-132; doi:10.1093/imammb/dqn026
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© The author 2009. Published by Oxford University Press on behalf of the Institute of Mathematics and its Applications. All rights reserved.

A bistable genetic switch which does not require high co-operativity at the promoter: a two-timescale model for the PU.1–GATA-1 interaction

Pavol Bokes{dagger} and John R. King

Centre for Mathematical Medicine and Biology, School of Mathematical Sciences, University of Nottingham, Nottingham NG7 2RD, UK

Matthew Loose

Institute of Genetics, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, UK

{dagger} Email: pmxpb{at}nottingham.ac.uk

Received on June 27, 2008. Revised on October 30, 2008. Accepted on December 9, 2008.

The transcription factors PU.1 and GATA-1 antagonize each other in common myeloid progenitors and their relative abundance is thought to decide whether the cell follows the erythrocyte/megakaryocyte lineage or the granulocyte/macrophage lineage. We propose a kinetic model for the PU.1–GATA-1 interaction, analyse its phase space and interpret the results of our analysis. The conclusions have broader implications for the modelling of cell-fate selection.

Keywords: systems biology; hematopoiesis; transcription factor


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