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. 1994 Mar;176(5):1521–1523. doi: 10.1128/jb.176.5.1521-1523.1994

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

T Kogoma 1
PMCID: PMC205222  PMID: 8113195

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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. CHAMBERLIN M., BERG P. MECHANISM OF RNA POLYMERASE ACTION: FORMATION OF DNA-RNA HYBRIDS WITH SINGLE-STRANDED TEMPLATES. J Mol Biol. 1964 Feb;8:297–313. doi: 10.1016/s0022-2836(64)80139-x. [DOI] [PubMed] [Google Scholar]
  2. Fisher R. F., Yanofsky C. 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):8146–8150. [PubMed] [Google Scholar]
  3. Huisman O., D'Ari R. An inducible DNA replication-cell division coupling mechanism in E. coli. Nature. 1981 Apr 30;290(5809):797–799. doi: 10.1038/290797a0. [DOI] [PubMed] [Google Scholar]
  4. Itaya M., Crouch R. J. 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):424–432. doi: 10.1007/BF00273933. [DOI] [PubMed] [Google Scholar]
  5. Jin D. J., Burgess R. R., Richardson J. P., Gross C. A. 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):1453–1457. doi: 10.1073/pnas.89.4.1453. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Jin D. J., Cashel M., Friedman D. I., Nakamura Y., Walter W. A., Gross C. A. Effects of rifampicin resistant rpoB mutations on antitermination and interaction with nusA in Escherichia coli. J Mol Biol. 1988 Nov 20;204(2):247–261. doi: 10.1016/0022-2836(88)90573-6. [DOI] [PubMed] [Google Scholar]
  7. Jin D. J., Gross C. A. Characterization of the pleiotropic phenotypes of rifampin-resistant rpoB mutants of Escherichia coli. J Bacteriol. 1989 Sep;171(9):5229–5231. doi: 10.1128/jb.171.9.5229-5231.1989. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Jin D. J., Gross C. A. 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. doi: 10.1016/0022-2836(88)90517-7. [DOI] [PubMed] [Google Scholar]
  9. Jin D. J., Walter W. A., Gross C. A. Characterization of the termination phenotypes of rifampicin-resistant mutants. J Mol Biol. 1988 Jul 20;202(2):245–253. doi: 10.1016/0022-2836(88)90455-x. [DOI] [PubMed] [Google Scholar]
  10. Kanaya S., Crouch R. J. DNA sequence of the gene coding for Escherichia coli ribonuclease H. J Biol Chem. 1983 Jan 25;258(2):1276–1281. [PubMed] [Google Scholar]
  11. Kogoma T., Hong X., Cadwell G. W., Barnard K. G., Asai T. 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. doi: 10.1016/0300-9084(93)90029-r. [DOI] [PubMed] [Google Scholar]
  12. Kogoma T. RNase H-defective mutants of Escherichia coli. J Bacteriol. 1986 May;166(2):361–363. doi: 10.1128/jb.166.2.361-363.1986. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Kogoma T., von Meyenburg K. 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):463–468. doi: 10.1002/j.1460-2075.1983.tb01445.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Rice G. A., Kane C. M., Chamberlin M. J. 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):4245–4249. doi: 10.1073/pnas.88.10.4245. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Richardson J. P. Attachment of nascent RNA molecules to superhelical DNA. J Mol Biol. 1975 Nov 5;98(3):565–579. doi: 10.1016/s0022-2836(75)80087-8. [DOI] [PubMed] [Google Scholar]
  16. Sassanfar M., Roberts J. W. Nature of the SOS-inducing signal in Escherichia coli. The involvement of DNA replication. J Mol Biol. 1990 Mar 5;212(1):79–96. doi: 10.1016/0022-2836(90)90306-7. [DOI] [PubMed] [Google Scholar]
  17. von Hippel P. H., Yager T. D. The elongation-termination decision in transcription. Science. 1992 Feb 14;255(5046):809–812. doi: 10.1126/science.1536005. [DOI] [PubMed] [Google Scholar]
  18. von Meyenburg K., Boye E., Skarstad K., Koppes L., Kogoma T. Mode of initiation of constitutive stable DNA replication in RNase H-defective mutants of Escherichia coli K-12. J Bacteriol. 1987 Jun;169(6):2650–2658. doi: 10.1128/jb.169.6.2650-2658.1987. [DOI] [PMC free article] [PubMed] [Google Scholar]

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