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====Maintenance of lysogeny==== [[File:Phage Lambda Integration Excision.jpg|thumb|right|upright=1.75|A simplified representation of the integration/excision paradigm and the major genes involved.]] * Lysogeny is maintained solely by cI. cI represses transcription from ''P<sub>L</sub>'' and ''P<sub>R</sub>'' while upregulating and controlling its own expression from ''P<sub>RM</sub>''. It is therefore the only protein expressed by lysogenic phage. [[File:Polymerase cl protien.svg|thumb|Lysogen repressors and polymerase bound to OR1 and recruits OR2, which will activate PRM and shutdown PR.]] * This is coordinated by the ''P<sub>L</sub>'' and ''P<sub>R</sub>'' operators. Both operators have three binding sites for cI: ''OL1'', ''OL2'', and ''OL3'' for ''P<sub>L</sub>'', and ''OR1'', ''OR2'' and ''OR3'' for ''P<sub>R</sub>''. * cI binds most favorably to ''OR1''; binding here inhibits transcription from ''P<sub>R</sub>''. As cI easily dimerises, the binding of cI to ''OR1'' greatly increases the affinity of the binding of cI to ''OR2'', and this happens almost immediately after ''OR1'' binding. This activates transcription in the other direction from ''P<sub>RM</sub>'', as the N terminal domain of cI on ''OR2'' tightens the binding of RNA polymerase to ''P<sub>RM</sub>'' and hence cI stimulates its own transcription. When it is present at a much higher concentration, it also binds to ''OR3'', inhibiting transcription from ''P<sub>RM</sub>'', thus regulating its own levels in a [[negative feedback]] loop. * cI binding to the ''P<sub>L</sub>'' operator is very similar, except that it has no direct effect on cI transcription. As an additional repression of its own expression, however, cI dimers bound to ''OR3'' and ''OL3'' bend the DNA between them to tetramerise. * The presence of cI causes immunity to superinfection by other lambda phages, as it will inhibit their ''P<sub>L</sub>'' and ''P<sub>R</sub>'' promoters.
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