Host-virus interactions in the control of T4 prereplicative transcription

Caruso, Maurizia; Coppo, Anna; Manzi, Andrea; Pulitzer, John F.

doi:10.1016/0022-2836(79)90522-9

Cited by 26 publications

(26 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…T4 is reported to regulate the expression of its genome by a mechanism of terminationantitermination that utilizes sequences homologous to the X nut sites (5,17,19,38). Our results are consistent with the idea that the host components of the T4 antitermination system are similar or identical to those of A.…”

Section: Discussionsupporting

confidence: 89%

Effect of Escherichia coli nusG function on lambda N-mediated transcription antitermination

1992

View full text Add to dashboard Cite

The Escherichia coli Nus factors act in conjunction with the bacteriophage K N protein to suppress transcription termination on the A chromosome. NusA binds both N and RNA polymerase and may also interact with other Nus factors. To search for additional components of the N antitermination system, we isolated host revertants that restored N activity in nusAl mutants. One revertant, nusG4, was mapped to the rifregion of the E. coli chromosome and shown to represent a point mutation near the 3' end of the nusG gene.The nusG4 mutation also suppressed nusE71 but not nusAs,1, nusB5, nusC60 (rpoB60), or nusDO26 (rhoO26).However, nusG+ expressed from a multicopy plasmid suppressed nusD026 and related rho mutants for both k and phage T4 growth. These results suggest that NusG may act as a component of the N antitermination complex. In addition, the data imply a role for NusG in Rho-dependent termination.Modulation of transcription termination is a mechanism of gene regulation in both prokaryotes and eukaryotes (26, 37). The efficiency of termination is determined by nucleic acid sequences and by protein factors that interact with these sequences, with RNA polymerase, or with each other.The bacteriophage X N antitermination system is the best-characterized example of such regulation (11). Transcription complexes initiating at the A PR and PL early promoters are modified by N protein at cis-acting nut sequences (30, 31). The modified complexes pass through distal Rho-dependent and Rho-independent terminators.A set of host factors required for N activity have been defined by mutations (nus [N utilization substance]) that inhibit A growth (10). These include NusA, NusB, and NusE (the small ribosomal subunit S10) (11). Certain mutations in Rho (nusD) block N antitermination at Rho-dependent sites (8,29). The NusA, NusB, and NusE proteins are thought to be components, along with N protein, of the N-modified transcription complex (4, 18).The activities of the Rho (28) and NusA (6) factors have been extensively studied. NusA is a 69-kDa protein that either stimulates or suppresses termination, depending on the template sequence and the availability of protein cofactors (15,16,20,25,35,42). NusA binds to the RNA polymerase core (13) and may generally be associated with elongating polymerase (13,18). Binding of NusA to N (14), and possibly to Rho (34), has also been demonstrated in vitro.Mutations in nusB suggest a role for this factor in Rhodependent termination (42) and in the processive transcription of the rRNA operons (36). The role of S10 in termination or antitermination is unclear.We have isolated host mutations that permitted X growth on nusAl mutants (41). Several suppressors were mapped to nusB. With the hope of detecting additional factors that participate in transcription termination and antitermination, * Corresponding author.

show abstract

Section: Discussionsupporting

confidence: 89%

Effect of Escherichia coli nusG function on lambda N-mediated transcription antitermination

1992

View full text Add to dashboard Cite

show abstract

“…These compensatory mutations, called comC or goF, were mapped mainly in two places on the chromosome: upstream of gene 39, in a nonessential region of the T4 genome, and between genes 55 and e (5,7,17,36,38,42 involved in replication and in head assembly, respectively. Infection of a super-rho strain (hdf/rhoO26) with wild-type phage leads to an increased proportion of RNA ending at a specific site within gene 40 and to a decrease in the uvsX-40-41 polycistronic RNA (12).…”

mentioning

confidence: 99%

“…They were called tabC (5,40,41) or hdf (38). It has been suggested that the altered p proteins made in these mutants are insensitive to T4-induced antitermination factors (31,38).…”

mentioning

confidence: 99%

mentioning

confidence: 99%

“…T4comCa8O3, T4comCaS5.6, and T4goFl contain mutations that allow the phage to grow on tabC803, tabC5521, and hdf hosts, respectively (5,7,38,40). hdf mutations, like tabC, are mutations in rho that strongly restrict growth of T4 wild-type (38).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Sequence and characterization of the bacteriophage T4 comC alpha gene product, a possible transcription antitermination factor

Sanson

Uzan

1992

J Bacteriol

View full text Add to dashboard Cite

We have sequenced a 1,340-bp region of the bacteriophage T4 DNA spanning the comCa gene, a gene which has been implicated in transcription antitermination. We show that comCav, identified unambiguously by sequencing several missense and nonsense mutations within the gene, codes for an acidic polypeptide of 141 residues, with a predicted molecular weight of 16,680. We have identified its product on one-and two-dimensional gel systems and found that it migrates abnormally as a protein with a molecular weight of 22,000. One of the missense mutations (comCa803) is a glycine-to-arginine change, and the resulting protein exhibits a substantially faster electrophoretic mobility. The ComCa protein appears immediately after infection. Its rate of synthesis is maximum around 2 to 3 min postinfection (at 37°C) and then starts to decrease slowly. Some residual biosynthesis is still detectable during the late period of phage development.The notion that termination and antitermination mechanisms may be operating in bacteriophage T4 development initially came from the observation of a strong polarity on early transcription when infection is carried out in the absence of translation. In vivo experiments that used inhibitors of protein synthesis, as well as in vitro studies, have shown that this polarity is due to the action of the host transcription terminator p (2). The question of whether translation of phage RNA is required just to mask potential rho-dependent termination sites and/or to allow the synthesis of viral antitermination proteins could not be answered on the basis of experiments that used inhibitors of protein synthesis. Furthermore, analysis of this problem is complicated by the fact that many genes, transcribed by elongation of transcripts initiated at distal early promoters, are also transcribed from proximal promoters (the middle promoters) activated soon after infection (2,10,13,24,30,45,46).Another set of experiments showing the involvement of p in T4 development derives from the isolation of rho mutants unable to support growth of T4 wild-type phage. They were called tabC (5, 40, 41) or hdf (38). It has been suggested that the altered p proteins made in these mutants are insensitive to T4-induced antitermination factors (31, 38). Thus, these mutations can be considered as producing a "super-rho" phenotype. Further support for this view is provided by the observation that one of these rho mutations (rhoO26; also called nusDO26) (37,38) was shown to impede the antitermination activity of XN, specifically at rho-dependent terminators (8).Phage mutants able to grow on tabC/hdf rho host mutants were isolated. These compensatory mutations, called comC or goF, were mapped mainly in two places on the chromosome: upstream of gene 39, in a nonessential region of the T4 genome, and between genes 55 and e (5,7,17,36,38,42 involved in replication and in head assembly, respectively. Infection of a super-rho strain (hdf/rhoO26) with wild-type phage leads to an increased proportion of RNA ending at a specific site within g...

show abstract

In VitroCharacterization of Transcription Termination Factor Rho fromEscherichia coli rho(nusD)Mutants

Washburn

Stitt

1996

Journal of Molecular Biology

View full text Add to dashboard Cite

Host-virus interactions in the control of T4 prereplicative transcription

Cited by 26 publications

References 36 publications

Effect of Escherichia coli nusG function on lambda N-mediated transcription antitermination

Effect of Escherichia coli nusG function on lambda N-mediated transcription antitermination

Sequence and characterization of the bacteriophage T4 comC alpha gene product, a possible transcription antitermination factor

In VitroCharacterization of Transcription Termination Factor Rho fromEscherichia coli rho(nusD)Mutants

Contact Info

Product

Resources

About