Transcription antitermination: the λ paradigm updated

Friedman, David I.; Court, Donald L.

doi:10.1111/j.1365-2958.1995.mmi_18020191.x

Cited by 128 publications

(99 citation statements)

References 54 publications

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“…The boxA sequences are found in cis-acting RNAs, such as the bacteriophage Nut site, and have been shown to capture proteins (Nus factors) that alter the behaviour of RNA polymerase (Barik et al, 1987). At least one ribosomal protein, S10, is known to be involved in the antitermination process in vivo, but its role is unclear (reviewed in Friedman and Court, 1995;Mogridge et al, 1995). In this regard, prgS-encoded RNA has been found in translation complexes associated with prgB mRNA (Bensing and Dunny, 1997), although it has not been determined if this region interacts directly with ribosomes, and if it is also required for translation of prgB.…”

Section: Discussionmentioning

confidence: 99%

Pheromone cCF10 and plasmid pCF10‐encoded regulatory molecules act post‐transcriptionally to activate expression of downstream conjugation functions

Bensing

Manias

Dunny

1997

Molecular Microbiology

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SummaryExpression of aggregation protein Asc10 from the prgB gene of conjugative plasmid pCF10 in Enterococcus faecalis is induced by the peptide pheromone cCF10. Genes required for Asc10 production, prgQ and prgS, lie 3-5 kb upstream, but can function at much greater distances. The prgQ transcripts encode a pheromone inhibitor peptide (iCF10) at the extreme 5Ј end. Neither production of this peptide nor translation of the 5Ј end of prgQ transcripts was found to be necessary for prgB expression. Pheromone cCF10 is required to activate prgB expression, even in the absence of iCF10 production, and does not affect initiation of transcription. The prgS gene encodes a 10.5 kDa protein that appears to be required for translation of prgB, and a non-coding RNA at the 3Ј end of prgS may be required for readthrough of transcription to prgB from the prgQ promoter. Although the entire positive control region is transcribed constitutively from the prgQ promoter, translation of PrgS and transcriptional readthrough to prgB occur only after induction with pheromone. The combined data are consistent with a model in which the positive regulatory molecules and pheromone cCF10 activate prgB expression post-transcriptionally.

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Section: Discussionmentioning

confidence: 99%

Pheromone cCF10 and plasmid pCF10‐encoded regulatory molecules act post‐transcriptionally to activate expression of downstream conjugation functions

Bensing

Manias

Dunny

1997

Molecular Microbiology

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“…As we have found that the rpoA341 mutation has a negative effect on this process this would not have been picked up in their assay. In addition, Schauer et al (1996) propose the existence of an inhibitor of N-mediated antitermination which may interact with the ␣CTD (see also Friedman and Court, 1995). According to their model this inhibitor may interact less efficiently with the D305→E ␣ subunit.…”

Section: Figmentioning

confidence: 99%

An RNA polymerase α subunit mutant impairs N‐dependent transcriptional antiterminationin Escherichia coli

Obuchowski

Węgrzyn

Szalewska-Pałasz

et al. 1997

Molecular Microbiology

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SummaryWe show that the rpoA341 mutation in the gene encoding the ␣ subunit of Escherichia coli RNA polymerase results in a decreased level of transcripts originating from the lytic promoters p L and p R of infecting phage. However, using lacZ fusions we demonstrate that initiation of transcription from both p L and p R is not impaired in the rpoA341 host. Rather, it is the level of the longer, antiterminated p L -and p R -derived transcripts which is altered: the activity of ␤-galactosidase in bacteria harbouring a source of N and a p L -nutL-t L1 -t I -lacZ or p R -nutR-t R1 -lacZ fusion is considerably lower in the rpoA341 mutant relative to the rpoA + strain. In the absence of the antiterminator protein N no difference is observed in the level of longer p R -derived transcripts between wild-type (rpoA + ) and mutant (rpoA341) hosts. Although synthesis of N appears to be similar in both phageinfected rpoA + and rpoA341 cells, overexpression of the N gene leads to restoration of wild-type levels of the longer p L -and p R -derived transcripts in the mutant host. While this mutation does not appear to affect vegetative phage growth in nus + backgrounds, in combination with certain nus mutations it retards lytic development. Therefore, we conclude that the rpoA341 mutation specifically interferes with the function of the N-antitermination complex, suggesting that the C-terminal domain of the RNA polymerase ␣ subunit may play an important role in N-dependent transcriptional antitermination.

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“…The existence of the transcriptional antiterminator Q and the related cis-acting DNA elements such as the late promoter pR', qut, terminators tR1' and tR2', suggest that the late gene transcription is activated by the antitermination function of Q, which has been well studied in the lambda system (Friedman and Court, 1995; Therefore, the expression of the stx2 genes is likely to be positively regulated by Q, like the expression of the downstream genes. This region is almost identical to that of 933W (Plunkett et al, 1999).…”

Section: Identification Of the Attachment Site Of Vt2-sakaimentioning

confidence: 99%

“…Transcription antitermination in lambda requires the phage nut sites (Friedman and Gottesman, 1983). N protein attaches to RNA polymerase at the nut sites to form a termination-resistant complex (Friedman and Court, 1995;Das, 1992). The nut sites can be divided into a promoter-proximal sequence, boxA, conserved among several lambdoid phages, and boxB, a non-conserved region of hyphenated dyad symmetry (Friedman and Gottesman, 1983;Friedman et al, 1990).…”

Section: Identification Of the Attachment Site Of Vt2-sakaimentioning

confidence: 99%

Complete nucleotide sequence of the prophage VT2-Sakai carrying the verotoxin 2 genes of the enterohemorrhagic Escherichia coli O157:H7 derived from the Sakai outbreak.

et al. 1999

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The enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain RIMD 0509952, derived from an outbreak in Sakai city, Japan, in 1996, produces two kinds of verotoxins, VT1 and VT2, encoded by the stx1 and stx2 genes. In the EHEC strains, as well as in other VT-producing E. coli strains, the toxins are encoded by lysogenic bacteriophages. The EHEC O157:H7 strain RIMD 0509952 did not produce plaque-forming phage particles upon inducing treatments. We have determined the complete nucleotide sequence of a prophage, VT2-Sakai, carrying the stx2A and stx2B genes on the chromosome, and presumed the putative functions of the encoded proteins and the cis-acting DNA elements based on sequence homology data. To our surprise, the sequences in the regions of VT2-Sakai corresponding to the early gene regulators and replication proteins, and the DNA sequences recognized by the regulators share very limited homology to those of the VT2-encoding 933W phage carried by the EHEC O157:H7 strain EDL933 reported by Plunkett et al. (J. Bacteriol., p1767-1778, 181, 1999, although the sequences corresponding to the structural components are almost identical. These data suggest that these two phages were derived from a common ancestral phage and that either or both of them underwent multiple genetic rearrangements. An IS629 insertion was found downstream of the stx2B gene and upstream of the lysis gene S, and this might be responsible for the absence of plaque-forming activity in the lysate obtained after inducing treatments.

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Transcription antitermination: the λ paradigm updated

Cited by 128 publications

References 54 publications

Pheromone cCF10 and plasmid pCF10‐encoded regulatory molecules act post‐transcriptionally to activate expression of downstream conjugation functions

Pheromone cCF10 and plasmid pCF10‐encoded regulatory molecules act post‐transcriptionally to activate expression of downstream conjugation functions

An RNA polymerase α subunit mutant impairs N‐dependent transcriptional antiterminationin Escherichia coli

Complete nucleotide sequence of the prophage VT2-Sakai carrying the verotoxin 2 genes of the enterohemorrhagic Escherichia coli O157:H7 derived from the Sakai outbreak.

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