Prophage P4 immunity is elicited by a short, 69-nucleotide RNA (CI RNA) coded for within the untranslated leader region of the same operon it controls. CI RNA causes termination of transcription that starts at the promoter P(LE) and prevents the expression of the distal part of the operon that codes for P4 replication functions (α operon). In this work, we identify two sequences in the untranslated leader region of the α operon, seqA and seqC, that are the targets of the P4 immunity factor. seqA and seqC exhibit complementarity to a sequence internal to the CI RNA (seqB). Mutations in either seqA or seqC that alter its complementarity to seqB abolished or reduced P4 lysogenization proficiency and delayed the shutoff of the long transcripts originating from P(LE) that cover the entire operon. Both seqA and seqC single mutants were still sensitive to P4 prophage immunity, whereas P4 seqA seqC double mutants showed a virulent phenotype. Thus, both functional sites are necessary to establish immunity upon infection, whereas a single site appears to be sufficient to prevent lytic gene expression when immunity is established. A mutation in seqB that restored complementarity to both seqA and seqC mutations also restored premature termination of P(LE) transcripts, thus suggesting an important role for RNA-RNA interactions between seqB and seqA or seqC in P4 immunity.

Control of transcription termination by an RNA factor in bacteriophage P4 immunity : Identification of the target sites / P. Sabbattini, F. Forti, D. Ghisotti, G. Dehò. - In: JOURNAL OF BACTERIOLOGY. - ISSN 0021-9193. - 177:6(1995), pp. 1425-1434.

Control of transcription termination by an RNA factor in bacteriophage P4 immunity : Identification of the target sites

F. Forti
Secondo
;
D. Ghisotti
Penultimo
;
G. Dehò
Ultimo
1995

Abstract

Prophage P4 immunity is elicited by a short, 69-nucleotide RNA (CI RNA) coded for within the untranslated leader region of the same operon it controls. CI RNA causes termination of transcription that starts at the promoter P(LE) and prevents the expression of the distal part of the operon that codes for P4 replication functions (α operon). In this work, we identify two sequences in the untranslated leader region of the α operon, seqA and seqC, that are the targets of the P4 immunity factor. seqA and seqC exhibit complementarity to a sequence internal to the CI RNA (seqB). Mutations in either seqA or seqC that alter its complementarity to seqB abolished or reduced P4 lysogenization proficiency and delayed the shutoff of the long transcripts originating from P(LE) that cover the entire operon. Both seqA and seqC single mutants were still sensitive to P4 prophage immunity, whereas P4 seqA seqC double mutants showed a virulent phenotype. Thus, both functional sites are necessary to establish immunity upon infection, whereas a single site appears to be sufficient to prevent lytic gene expression when immunity is established. A mutation in seqB that restored complementarity to both seqA and seqC mutations also restored premature termination of P(LE) transcripts, thus suggesting an important role for RNA-RNA interactions between seqB and seqA or seqC in P4 immunity.
GENETIC ELEMENT P4 ; SATELLITE BACTERIOPHAGE-P4 ; ESCHERICHIA-COLI ; ANTISENSE RNA ; DNA-SEQUENCE ; PHAGE-P4 ; REGION ; PROPAGATION ; MUTAGENESIS ; EXPRESSION
Settore BIO/18 - Genetica
1995
Article (author)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/239161
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