Site c27 in phage P22 and control of the pathway to lysogeny

Tokuno, Shin-Ichi; Gough, Michael

doi:10.1007/bf02428109

Cited by 10 publications

(5 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…By this model, PRE is not the site marked by c27 (as suggested by Gough and Tokuno,45,123), but is instead located further to the right at the beginning of the b transcript. The c27 mutation would then be a mutation which creates, enhances, or renders cl/c3-insensitive a secondary premature termination site.…”

Section: Antirepressormentioning

confidence: 80%

“…This mutation, c27, appears to be defective in c2-repressor synthesis during establishment, but not maintenance, of lysogeny. However, it complements all cl and c3 mutants (45,79,123). It is exactly analogous in phenotype and map position to the A cy mutants (94); both the A cy and P22 c27 mutations map beyond ORPR and presumably lie outside the repressor structural gene (16,79).…”

Section: Antirepressormentioning

confidence: 92%

“…It is exactly analogous in phenotype and map position to the A cy mutants (94); both the A cy and P22 c27 mutations map beyond ORPR and presumably lie outside the repressor structural gene (16,79). Like the A cy mutations, P22 c27 is a candidate for a mutati5n in the site of cl and/or c3 gene action and/or the PRE promoter (45,123). Arguments are presented below which suggest that c27 is not a mutation in PRE itself.…”

Section: Antirepressormentioning

confidence: 97%

“…Using such a genetic approach, the immunity/ repression system of phage P22 has been elucidated in some detail (12,15,16,20,42,45,78,81,82,116,123,142). P22 prophages maintain the lysogenic state by directing the synthesis of two repressors, both of which are continuously required for the maintenance of repression in the cell.…”

Section: Repression and Immunitymentioning

confidence: 99%

See 3 more Smart Citations

Molecular genetics of bacteriophage P22.

Susskind¹,

Botstein²

1978

Microbiological Reviews

252

View full text Add to dashboard Cite

Section: Antirepressormentioning

confidence: 80%

Section: Antirepressormentioning

confidence: 92%

Section: Antirepressormentioning

confidence: 97%

Section: Repression and Immunitymentioning

confidence: 99%

See 2 more Smart Citations

Molecular genetics of bacteriophage P22.

Susskind¹,

Botstein²

1978

Microbiological Reviews

252

View full text Add to dashboard Cite

“…The C1-C3-c27 interaction has both a negative result and a positive result. The negative one is seen as a decrease in the rate of DNA synthesis in wild-type infections at 8 min (10) and a retardation in expression of genes involved in lytic growth (15,16). The positive result is promotion ofrepressor synthesis (6).…”

Section: Vol 21 1977mentioning

confidence: 99%

Regulation of Bacteriophage P22 DNA synthesis and repressor levels in P22cly infections

Tokuno¹,

Gough²

1977

J Virol

View full text Add to dashboard Cite

A rifampin-resistant mutant of Salmonella typhimurium carries an altered RNA polymerase. Wild-type (c+) phage P22 displays clear plaques and a reduced lysogenization frequency on this mutant host. The cly mutants of P22 were isolated on the basis of their ability to lysogenize such mutant hosts. Two classes of regulatory events, both of which are dependent on P22 gene cl activity, are necessary for the establishment of lysogeny in P22. The positive events culminate in repressor synthesis; the negative events cause a retardation in phage DNA synthesis. Neither the positive nor the negative events are observed in P22c+ infections of the mutant host. Both effects are found in P22cly infections of the mutant host. Observable results of both the negative and the positive events are exaggerated in P22cly infections of wild-type hosts as compared to P22c+ infections. The cly mutation apparently increases the positive and negative regulatory events so that they are detectable in the mutant host and exaggerated in wild-type hosts. Possible mechanisms that result in the high frequency of lysogenization that characterizes the cly mutation and the nature of the cly mutation are discussed.

show abstract

Effect of mutant host RNA polymerase on the bifunctional activities of P22 gene c1

et al. 1977

View full text Add to dashboard Cite

The product of phage P22 gene c1 has two functions: (1) it promotes synthesis of repressor and (2) during the first minutes of infection it retards expression of some lytic genes. We call the second, negative function "c1 retardation". We investigated c1 retardation in a mutant host of Salmonella typhimurium that is resistant to rifampicin and carries an altered RNA polymerase. No c1 retardation of DNA synthesis was detectable in this host after infection with wild-type phages. This elimination of the normally detectable c1 function leads to the conclusion that the mutant RNA polymerase interferes with the expression of c1 gene activity. Wild-type genes form clear plaques on the mutant host. Mutants of P22 called cly were isolated by others. These mutants form turbid plaques on the altered RNA polymerase host. Infections with P22 cly in the mutant host resulted in detectable c1 retardation. The cly mutation therefore restores c1 activity in a host which wild-type c1 is not expressed. Two spontaneous mutants were isolated from the mutant host. These two strains allowed partial expression of c1 retardation, although they remained rifampicin resistant. We interpret our data to indicate that expression of the normal functions of the gene c1 product requires an interaction of that product with the host RNA polymerase.

show abstract

Site c27 in phage P22 and control of the pathway to lysogeny

Cited by 10 publications

References 19 publications

Molecular genetics of bacteriophage P22.

Molecular genetics of bacteriophage P22.

Regulation of Bacteriophage P22 DNA synthesis and repressor levels in P22cly infections

Effect of mutant host RNA polymerase on the bifunctional activities of P22 gene c1

Contact Info

Product

Resources

About