Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (7)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Breña-Valle, M.
Right arrow Articles by Serment-Guerrero, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Breña-Valle, M.
Right arrow Articles by Serment-Guerrero, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Mutagenesis vol. 13 no. 6 pp. 637-641, 1998
© 1998 UK Environmental Mutagen Society/Oxford University Press

research-article

SOS induction by {gamma}-radiation in Escherichia coli strains defective in repair and/or recombination mechanisms

Matilde Breña-Valle1 and Jorge Serment-Guerrero

Departamento de Biología, Instituto Nacional de Investigadores Nucleares PO Box 18-1027, CP 11801, México DF, México

Ionizing radiation causes several types of DNA lesions, mainly single- or double-strand breaks and base damage. By means of the chromotest, an assay that allows the level of the SOS response to be monitored via ß-galactosidase enzymatic activity, the roles of several repair (uvrA, recN and oxyR) and recombination (recB, recJ and recO) genes in the response of Escherichiacoli to {gamma}-radiation were studied. The results indicate that all the repair- and recombination- deficient strains were more sensitive to the lethal effects of ionizing radiation. However, the SOS activation pattern was somewhat different. The minimal inducing dose in uvrA and recN mutants was lower than in the wild-type, whereas their SOS response was higher at all doses. Conversely, in the strains lacking an active recB, recJ or recO gene, the doubling dose was almost the same as in the wild-type but the level of induction remained stable over a wide dose range. These findings suggest that neither single- nor double-strand breaks are in themselves direct SOS inducers and that while uvrA, recN and oxyR take part in different repair or protective pathways, apparently recB, recj and recO participate in damage processing leading to SOS induction, as well as in recombination repair.

1To whom correspondence should be addressed. Tel: +52 5 329 72 30. Fax: 52 5 521 9893; Email: mbv{at}nuclear.inin.mx


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Bacteriol.Home page
J. R. Pohlhaus, D. T. Long, E. O'Reilly, and K. N. Kreuzer
The {varepsilon} Subunit of DNA Polymerase III Is Involved in the Nalidixic Acid-Induced SOS Response in Escherichia coli
J. Bacteriol., August 1, 2008; 190(15): 5239 - 5247.
[Abstract] [Full Text] [PDF]

Home page
 MutagenesisHome page
J. Serment-Guerrero, M. Brena-Valle, and J. J. Espinosa-Aguirre
In vivo role of Escherichia coli single-strand exonucleases in SOS induction by gamma radiation
Mutagenesis, July 1, 2008; 23(4): 317 - 323.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.