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The lytic-lysogenic switch of the temperate lactococcal phage TP901-1 isfundamentally different from that of phage lambda. In phage TP901-1, the lyticpromoter PL is repressed by CI whereas repression of the lysogenic promoter PRrequires the presence of both of the antagonistic regulator proteins, MOR andCI. We model the central part of the switch and compare the two cases for PRrepression: the one where the two regulators interact only on the DNA, and theother where the two regulators form a heteromer complex in the cytoplasm priorto DNA binding. The models are analyzed for bistability, and the predictedpromoter repression folds are compared to experimental data. We conclude thatthe experimental data are best reproduced the latter case, where a heteromercomplex forms in solution. We further find that CI sequestration by theformation of MOR:CI complexes in cytoplasm makes the genetic switch robust.

Modeling of the genetic switch of bacteriophage TP901-1: A heteromer of CI and MOR ensures robust bistability