This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Yamamoto, N. Articles by Takebe, H. Search for Related Content PubMed PubMed Citation Articles by Yamamoto, N. Articles by Takebe, H.

Effect of a Potent Carcinogen, 4-Nitroquinoline 1-Oxide, and Its Reduced Form, 4-Hydroxylaminoquinoline 1-Oxide, on Bacterial and Bacteriophage Genomes¹

Fels Research Institute and Department of Microbiology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140 [N. Y., S. F.], and Division of Biology, Southwest Center for Advanced Sciences, Dallas, Texas 75230 [H. T.]

4-Nitroquinoline 1-oxide (4NQO)-sensitive mutants of Salmonella typhimurium were found to be sensitive to ultraviolet light (UV) and ß-propiolactone. These mutants were subdivided into two groups: host cell reactivation minus (hc) mutants lacking repair activity for the UV-damaged superinfecting phage and recombination-deficient (rec^-) mutants. The hc mutant is known to lack an enzyme to excise pyrimidine dimers formed in UV-irradiated DNA.

4NQO, ß-propiolactone, and UV induced prophages from hc and wild-type strains but not from re strains. Prophage induction from hc strains was far more efficient than that from wild-type strain.

A metabolic intermediate of 4NQO, 4-hydroxylamino-quinoline 1-oxide (4HAQO), which is highly carcinogenic, inactivated Salmonella phage P22 in vitro whereas 4NQO did not. When 4HAQO-treated P22 was assayed simultaneously on hc, re, and wild-type strains lysogenic for P221b, no difference in inactivation rates on these indicator hosts was found. This indicates that the 4HAQO-damaged phage genome is not repairable by the hosts. Moreover, although a greatly increased frequency of recombination was found between the 4HAQO-treated P22 and the prophage P221b in wild-type and hc hosts, no significant increase of recombination was found in re strains. Thus, it was concluded that the bacterial recombination mechanism plays an important role in recombination between the damaged P22 and the prophage P221b.

¹ Supported in part by NIH Grants AI-06429 and CA-10439, USPHS, and National Science Foundation Grant NSF-GB-8503. The work carried out in Dallas (by H. T.) was supported by USPHS Grant NIH-AI-06971 (awarded to Dr. J. Jagger).

² Present address: Department of Fundamental Radiology, Faculty of Medicine, Osaka University Kita-ku, Osaka 530, Japan.

Received 2/11/70. Accepted 6/22/70.