Dissection of the bacteriophage T4 late promoter complex.

摘要: Abstract Activated transcription of the bacteriophage T4 late genes is generated by a mechanism that stands apart from common modalities transcriptional regulation: activator gp45, viral replisome's sliding clamp; two sliding-clamp-binding proteins, gp33 and gp55, replace host RNA polymerase (RNAP) σ subunit. We have mutagenized, reconfigured selectively disrupted individual interactions clamp with gp55 monitored effects on transcription. The C-terminal epitopes are perfectly interchangeable, but functions these RNAP–sliding connections differ: only gp33–gp45 linkage essential for activation, while loss gp55–gp45 impairs does not abolish activation. Formation transcription-ready promoter complexes sliding-clamp-activated wild-type RNAP resists competition high concentrations polyanion heparin. This avid formation requires both linkages to clamp. Preopening compensates linkage. interpret relationship findings our prior analysis model initiation in bacteria terms parallel pathways, holoenzymes DNA templates: (1) gp55–RNAP execute basal transcription; (2) gp55–gp33–RNAP its mobile enhancer, clamp, activated perform σ-like functions, recognition (as well as gp55) enhancer recognition. operates switch between pathways repressing