The bacteriophage T4 anti-sigma factor AsiA is not necessary for the inhibition of early promoters in vivo.
Bacteriophage T4 early promoters are utilized immediately after infection and are abruptly turned off 2-3 min later (at 30 degrees C) when the middle promoters are activated. The viral early protein AsiA has been suspected to bring about this transcriptional switch: not only does it activate transcription at middle promoters in vivo and in vitro but it also shows potent anti-sigma70 activity in vitro, suggesting that it is responsible for the shut-off of early transcription. We show here that after infection with a phage deleted for the asiA gene the inhibition of early transcription occurs to the same extent and with the same kinetics as in a wild-type infection. Thus, another AsiA-independent circuit efficiently turns off early transcription. The association of a mutation in asiA with a mutation in mod, rpbA, motA or motB has no effect on the inhibition of early promoters, showing that none of these phage-encoded transcriptional regulators is necessary for AsiA-independent shut-off. It is not known whether AsiA is able to inhibit early promoters in vivo, but host transcription is strongly inhibited in vivo upon induction of AsiA from a multicopy plasmid.
Pène
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Institut Jacques Monod, UMR7592 of CNRS-Universités Paris 6 and Paris 7, 2 Place Jussieu, 75251 Paris cedex 05, France.
Uzan
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D001426:Bacterial Proteins / Q000096:biosynthesis; D017122:Bacteriophage T4 / Q000235:genetics* / Q000378:metabolism; D004926:Escherichia coli / Q000235:genetics; D017353:Gene Deletion; D009154:Mutation; D010957:Plasmids; D011401:Promoter Regions, Genetic / Q000235:genetics*; D014158:Transcription, Genetic; D014764:Viral Proteins / Q000235:genetics / Q000502:physiology*
C078876:AsiA protein, Enterobacteria phage T4; D001426:Bacterial Proteins; D014764:Viral Proteins