Skip to main content
PMC home page
Genetics logoLink to Genetics
. 1978 Sep;90(1):1–18. doi: 10.1093/genetics/90.1.1

Genetic Studies of Acridine-Induced Mutants in STREPTOCOCCUS PNEUMONIAE

A M Gasc 1, A M Sicard 1
PMCID: PMC1213869  PMID: 29824

Abstract

The mutagenic properties of acridines on pneumococcus are described. All seven acridines tested were mutagenic at the amiA locus conferring a resistance to 10-5 m aminopterin. The effects of quinacrine were more specifically investigated. It was observed that: mutants can be obtained only by treatment of exponentially growing cells; a sharp maximum mutagenic effect occurs at a concentration slightly lower than the bacteriostatic value; and the amount of quinacrine required to yield the maximum mutagenic effect decreases with the pH of the medium. Moreover, the number of mutants detected after quinacrine treatment varies from locus to locus. The majority of quinacrine-induced mutants are readily reverted by quinacrine, but not by nitrosoguanidine treatment. This suggests that in pneumococcus quinacrine induces mainly frameshift mutations. A further study of the revertants obtained by quinacrine treatment of quinacrine-induced mutants strengthens this interpretation: most of the revertants result from a mutation at the same site; some partial revertants exhibiting an intermediate resistance to aminopterin were found to contain two very closely linked mutated sites, each mutation conferring the maximum level of resistance to aminopterin. Thus, the majority of quinacrine-induced mutants at the amiA locus of pneumococcus consists of frameshift mutations. Nearly all of the isolated mutants induced by quinacrine as well as other acridines belong to the low efficiency class of transformation. It was concluded that the mismatch resulting from the pairing between the wild type and the frameshift-containing sequence is recognized by the excision-repair system involved in the discrimination function in a way similar to that in which it recognizes mismatched base pairs between a transition mutation and the wild-type sequence.

Full Text

The Full Text of this article is available as a PDF (1.1 MB).

Selected References

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

  1. Ames B. N., Whitfield H. J., Jr Frameshift mutagenesis in Salmonella. Cold Spring Harb Symp Quant Biol. 1966;31:221–225. doi: 10.1101/sqb.1966.031.01.030. [DOI] [PubMed] [Google Scholar]
  2. Berger H., Brammar W. J., Yanofsky C. Spontaneous and ICR191-A-induced frameshift mutations in the A gene of Escherichia coli tryptophan synthetase. J Bacteriol. 1968 Nov;96(5):1672–1679. doi: 10.1128/jb.96.5.1672-1679.1968. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Bernheimer H. P., Wermundsen I. E. Homology in capsular transformation reactions in Pneumococcus. Mol Gen Genet. 1972;116(1):68–83. doi: 10.1007/BF00334261. [DOI] [PubMed] [Google Scholar]
  4. Chan L. M., Van Winkle Q. Interaction of acriflavine with DNA and RNA. J Mol Biol. 1969 Mar 28;40(3):491–495. doi: 10.1016/0022-2836(69)90167-3. [DOI] [PubMed] [Google Scholar]
  5. EPHRUSSI-TAYLOR H., LATARJET R. Inactivation, par les rayons x, d'un facteur transformant du pneumocoque. Biochim Biophys Acta. 1955 Feb;16(2):183–197. doi: 10.1016/0006-3002(55)90203-1. [DOI] [PubMed] [Google Scholar]
  6. Fink G. R., Klopotowski T., Ames B. N. Histidine regulatory mutants in Salmonella typhimurium. IV. A positive selection for polar histidine-requiring mutants from histidine operator constitutive mutants. J Mol Biol. 1967 Nov 28;30(1):81–95. doi: 10.1016/0022-2836(67)90245-8. [DOI] [PubMed] [Google Scholar]
  7. Gasc A. M., Sicard A. M. Mutagenèse induite par l'hydroxylamine sur l'ADN du pneumocoque. C R Acad Sci Hebd Seances Acad Sci D. 1972 Jul 10;275(2):285–287. [PubMed] [Google Scholar]
  8. Hotchkiss R. D., Marmur J. DOUBLE MARKER TRANSFORMATIONS AS EVIDENCE OF LINKED FACTORS IN DESOXYRIBONUCLEATE TRANSFORMING AGENTS. Proc Natl Acad Sci U S A. 1954 Feb;40(2):55–60. doi: 10.1073/pnas.40.2.55. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Kohno T., Roth J. R. Proflavin mutagenesis of bacteria. J Mol Biol. 1974 Oct 15;89(1):17–32. doi: 10.1016/0022-2836(74)90160-0. [DOI] [PubMed] [Google Scholar]
  10. Lacks S. Integration efficiency and genetic recombination in pneumococcal transformation. Genetics. 1966 Jan;53(1):207–235. doi: 10.1093/genetics/53.1.207. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Roger M. Mismatch excision and possible polarity effects result in preferred deoxyribonucleic acid strand of integration in pneumococcal transformation. J Bacteriol. 1977 Jan;129(1):298–304. doi: 10.1128/jb.129.1.298-304.1977. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. SICARD A. M. A NEW SYNTHETIC MEDIUM FOR DIPLOCOCCUS PNEUMONIAE, AND ITS USE FOR THE STUDY OF RECIPROCAL TRANSFORMATIONS AT THE AMIA LOCUS. Genetics. 1964 Jul;50:31–44. doi: 10.1093/genetics/50.1.31. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Sicard A. M., Ephrussi-Taylor H. Genetic recombination in DNA-induced transformation of Pneumococcus. II. Mapping the amiA region. Genetics. 1965 Dec;52(6):1207–1227. doi: 10.1093/genetics/52.6.1207. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Streisinger G., Okada Y., Emrich J., Newton J., Tsugita A., Terzaghi E., Inouye M. Frameshift mutations and the genetic code. This paper is dedicated to Professor Theodosius Dobzhansky on the occasion of his 66th birthday. Cold Spring Harb Symp Quant Biol. 1966;31:77–84. doi: 10.1101/sqb.1966.031.01.014. [DOI] [PubMed] [Google Scholar]
  15. Stuart J. J., Ravin A. W. Levels of resistance in ribosomes from genetically linked, streptomycin-resistant mutants of pneumococcus. J Gen Microbiol. 1968 May;51(3):411–424. doi: 10.1099/00221287-51-3-411. [DOI] [PubMed] [Google Scholar]
  16. Tiraby J. G., Fox M. S. Marker discrimination in transformation and mutation of pneumococcus. Proc Natl Acad Sci U S A. 1973 Dec;70(12):3541–3545. doi: 10.1073/pnas.70.12.3541. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from Genetics are provided here courtesy of Oxford University Press

RESOURCES