Premium
The bacteriophage T4 anti‐sigma factor AsiA is not necessary for the inhibition of early promoters in vivo
Author(s) -
Pène Carole,
Uzan Marc
Publication year - 2000
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2000.01787.x
Subject(s) - promoter , biology , transcription (linguistics) , in vivo , transcription factor , dna , microbiology and biotechnology , bacteriophage , sigma factor , plasmid , gene , genetics , virology , gene expression , escherichia coli , linguistics , philosophy
Bacteriophage T4 early promoters are utilized immediately after infection and are abruptly turned off 2–3 min later (at 30°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‐σ 70 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.