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PMID: 8113195 Published · ppublish English Comparative Study Journal Article Research Support, U.S. Gov't, P.H.S.

Escherichia coli RNA polymerase mutants that enhance or diminish the SOS response constitutively expressed in the absence of RNase HI activity.

Journal of bacteriology ·Vol. 176 ·No. 5 ·1994-03-00 ·Pages 1521-3

Kogoma T

Abstract

Escherichia coli rnhA mutants lacking RNase HI chronically express the SOS response (T. Kogoma, X. Hong, G. W. Cadwell, K. G. Barnard, and T. Asai, Biochimie 75:89-99, 1993). Seventeen rpoB (Rifr) mutant alleles, which encode altered beta subunits of RNA polymerase, giving rise to resistance to rifampin, were screened for the ability to enhance or diminish constitutive expression of the SOS response in rnhA mutants. Two mutations, rpoB3595 and rpoB2, were found to enhance the SOS response 5- and 2.5-fold, respectively, only when RNase HI is absent. These mutations rendered rnhA mutant cells very sensitive to broth; i.e., the plating efficiency of the double mutants was drastically reduced when tested on broth plates. Two mutations, rpoB8 and rpoB3406, were found to diminish constitutive SOS expression in rnhA mutants by 43 and 30%, respectively. It was suggested that RNA polymerase may have a property that influences the size of DNA-RNA hybrids, the frequency of their formation, or both and that the property resides at least in part in the beta subunit of the polymerase.

MeSH Terms
Alleles DNA-Directed RNA Polymerases/genetics,metabolism Drug Resistance, Microbial/physiology Escherichia coli/enzymology,genetics,growth & development Gene Expression Regulation, Bacterial Genes, Bacterial Genotype Macromolecular Substances Recombinant Fusion Proteins/metabolism Ribonuclease H/genetics,metabolism Rifampin/toxicity SOS Response, Genetics Sequence Deletion beta-Galactosidase/metabolism
Chemicals
Macromolecular Substances Recombinant Fusion Proteins DNA-Directed RNA Polymerases Ribonuclease H ribonuclease HI beta-Galactosidase Rifampin
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Kogoma T
Department of Cell Biology, University of New Mexico School of Medicine, Albuquerque 87131.
References (18)
18 references, click to expand
  1. Termination efficiency at rho-dependent terminators depends on kinetic coupling between RNA polymerase and rho.
    Proc Natl Acad Sci U S A. 1992 Feb 15;89(4):1453-7 PMID: 1741399
  2. A combination of RNase H (rnh) and recBCD or sbcB mutations in Escherichia coli K12 adversely affects growth.
    Mol Gen Genet. 1991 Jul;227(3):424-32 PMID: 1650908
  3. Requirement of homologous recombination functions for viability of the Escherichia coli cell that lacks RNase HI and exonuclease V activities.
    Biochimie. 1993;75(1-2):89-99 PMID: 8389213
  4. MECHANISM OF RNA POLYMERASE ACTION: FORMATION OF DNA-RNA HYBRIDS WITH SINGLE-STRANDED TEMPLATES.
    J Mol Biol. 1964 Feb;8:297-313 PMID: 14126298
  5. The origin of replication, oriC, and the dnaA protein are dispensable in stable DNA replication (sdrA) mutants of Escherichia coli K-12.
    EMBO J. 1983;2(3):463-8 PMID: 11894964
  6. Attachment of nascent RNA molecules to superhelical DNA.
    J Mol Biol. 1975 Nov 5;98(3):565-79 PMID: 811809
  7. An inducible DNA replication-cell division coupling mechanism in E. coli.
    Nature. 1981 Apr 30;290(5809):797-9 PMID: 7012641
  8. DNA sequence of the gene coding for Escherichia coli ribonuclease H.
    J Biol Chem. 1983 Jan 25;258(2):1276-81 PMID: 6296074
  9. Mutations of the beta subunit of RNA polymerase alter both transcription pausing and transcription termination in the trp operon leader region in vitro.
    J Biol Chem. 1983 Jul 10;258(13):8146-50 PMID: 6345540
  10. RNase H-defective mutants of Escherichia coli.
    J Bacteriol. 1986 May;166(2):361-3 PMID: 3009391
  11. Mode of initiation of constitutive stable DNA replication in RNase H-defective mutants of Escherichia coli K-12.
    J Bacteriol. 1987 Jun;169(6):2650-8 PMID: 3034862
  12. Mapping and sequencing of mutations in the Escherichia coli rpoB gene that lead to rifampicin resistance.
    J Mol Biol. 1988 Jul 5;202(1):45-58 PMID: 3050121
  13. Characterization of the termination phenotypes of rifampicin-resistant mutants.
    J Mol Biol. 1988 Jul 20;202(2):245-53 PMID: 3050123
  14. Effects of rifampicin resistant rpoB mutations on antitermination and interaction with nusA in Escherichia coli.
    J Mol Biol. 1988 Nov 20;204(2):247-61 PMID: 2464690
  15. Characterization of the pleiotropic phenotypes of rifampin-resistant rpoB mutants of Escherichia coli.
    J Bacteriol. 1989 Sep;171(9):5229-31 PMID: 2670912
  16. Nature of the SOS-inducing signal in Escherichia coli. The involvement of DNA replication.
    J Mol Biol. 1990 Mar 5;212(1):79-96 PMID: 2108251
  17. Footprinting analysis of mammalian RNA polymerase II along its transcript: an alternative view of transcription elongation.
    Proc Natl Acad Sci U S A. 1991 May 15;88(10):4245-9 PMID: 1709738
  18. The elongation-termination decision in transcription.
    Science. 1992 Feb 14;255(5046):809-12 PMID: 1536005
Article Info
Journal
Journal of bacteriology
Abbr.
J Bacteriol
ISSN
0021-9193
Published
1994-03-00
Pages
1521-3
Language
English
Region
United States
NLM ID
2985120R
PMCID
PMC205222
Subset
IM
Grants
NIGMS NIH HHS · GM22092 · United States
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