Open AccessMultiple regulatory mechanisms controlling phage‐plasmid P4 propagation
Author(s) -
Ghisotti Daniela,
Briani Federica,
Forti Francesca,
Piazza Flavia,
Polo Simona,
Sabbattini Pierangela,
Sturniolo Tiziana,
Terzano Susanna,
Zangrossi Sandro,
Zappone Massimo,
Sironi Gianpiero,
Dehò Gianni
Publication year - 1995
Publication title -
fems microbiology reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.91
H-Index - 212
eISSN - 1574-6976
pISSN - 0168-6445
DOI - 10.1111/j.1574-6976.1995.tb00194.x
Subject(s) - lytic cycle , biology , plasmid , operon , transcription (linguistics) , promoter , lysogenic cycle , gene , bacteriophage , dna replication , genetics , microbiology and biotechnology , escherichia coli , gene expression , virus , linguistics , philosophy
Bacteriophage P4 autonomous replication may result in the lytic cycle or in plasmid maintenance, depending, respectively, on the presence or absence of the helper phage P2 genome in the Escherichia coli host cell. Alternatively, P4 may lysogenize the bacterial host and be maintained in an immune‐integrated condition. A key step in the choice between the lytic / plasmid vs. the lysogenic condition is the regulation of P4 α operon. This operon may be transcribed from two promoters, P LE and P LL , and encodes both immunity (promoter proximal) and replication (promoter distal) functions. P LE is a constitutive promoter and transcription of the downstream replication genes is regulated by transcription termination. The trans ‐acting immunity factor that controls premature transcription termination is a short RNA encoded in the P LE proximal part of the operon. Expression of the replication functions in the lytic/plasmid condition is achieved by activation of the P LL promoter. Transcription from P LL is insensitive to the termination mechanism that acts on transcription starting from P LE . P LL is also negatively regulated by P4 orf88 , the first gene downstream of P LL . An additional control on P4 DNA replication is exerted by the P4 cnr gene product.