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Modeling of the genetic switch of bacteriophage TP901-1: A heteromer of CI and MOR ensures robust bistability (908)
BibTeX
@MISC{A908modelingof,
author = {Hiizu Nakanishi A and Margit Pedersen B and Anne K. Alsing B},
title = {Modeling of the genetic switch of bacteriophage TP901-1: A heteromer of CI and MOR ensures robust bistability},
year = {908}
}
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Abstract
The lytic-lysogenic switch of the temperate lactococcal phage TP901-1 is fundamentally different from that of phage lambda. In phage TP901-1, the lytic promoter PL is repressed by CI whereas repression of the lysogenic promoter PR requires the presence of both of the antagonistic regulator proteins, MOR and CI. We model the central part of the switch and compare the two cases for PR repression: the one where the two regulators interact only on the DNA, and the other where the two regulators form a heteromer complex in the cytoplasm prior to DNA binding. The models are analyzed for bistability, and the predicted promoter repression folds are compared to experimental data. We conclude that the experimental data are best reproduced the latter case, where a heteromer complex forms in solution. We further find that CI sequestration by the formation of MOR:CI complexes in cytoplasm makes the genetic switch robust. Key words: temperate bacteriophage TP901-1, genetic switch, mixed feedback loop, sequestration, protein interaction
Keyphrases
genetic switch robust bistability bacteriophage tp901-1 latter case temperate bacteriophage tp901-1 dna binding central part heteromer complex form predicted promoter repression fold lytic promoter pl mixed feedback loop protein interaction genetic switch robust heteromer complex ci sequestration antagonistic regulator protein temperate lactococcal phage tp901-1 pr repression ci complex key word phage tp901-1 lytic-lysogenic switch ci whereas repression lysogenic promoter pr experimental data phage lambda
