The bacteriophage T4 anti-sigma factor AsiA is not necessary for the inhibition of early promoters in vivo.

Abstract

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.