Skip Navigation

This Article
Right arrow Full Text Freely available
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 ISI Web of Science
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 (1)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Felczak, M.
Right arrow Articles by Pietrzykowska, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Felczak, M.
Right arrow Articles by Pietrzykowska, I.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Mutagenesis, Vol. 14, No. 3, 295-300, May 1999
© 1999 UK Environmental Mutagen Society/Oxford University Press

The isfA mutation specifically inhibits the SOS-dependent mutagenic pathway and does not selectively affect any particular base substitution

Magdalena Felczak1, Anna Bebenek and Irena Pietrzykowska

Institute of Biochemistry and Biophysics, Polish Academy of Sciences, 5A Pawinskiego Str., 02-106 Warszawa, Poland

We have previously described a new mutation in Escherichia coli, isfA, which causes inhibition of SOS mutagenesis (UV-induced in rec+ and spontaneous in recA730 strains) and several SOS-dependent phenomena. Antimutagenic activity of the isfA mutation in the recA730 strain was shown to be related to inhibition of processing of UmuD to UmuD' by RecA* coprotease. In the present study we have analysed the specificity of the antimutagenic activity of the isfA mutation by employing F' plasmids carrying a set of mutant lacZ genes that can individually detect two types of transitions and four types of transversions. Analysis revealed that isfA inhibits UV-induced G:C->A:T and A:T->G:C transitions, but does not affect the same G:C->A:T transitions induced by EMS, an SOS-independent mutagen. Analysis of the antimutagenic activity of the isfA mutation in two mutator strains, recA730 and mutL, showed that isfA inhibits SOS-dependent transversions in recA730, but not transitions generated as replication errors in the mutL strain. In the double mutant recA730 mutL, both transitions and transversions were enhanced and isfA inhibits most transversions and only those transitions generated by the recA730 mutation. The results indicate that the antimutagenic activity of the isfA mutation is specific for the SOS, UmuD'C-dependent mutagenic pathway but does not selectively affect any particular base substitution. Moreover, studies on the effect of the isfA mutation on transitions and transversions in different genetic backgrounds enable us to recognize different mutagenic pathways active in recA730 cells.

1 To whom correspondence should be addressed. Tel: +48 658 47 19; Fax: +48 39 12 16 23; Email: magfel{at}ibb.waw.pl


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
 Genes Dev.Home page
O. N. Voloshin, B. E. Ramirez, A. Bax, and R. D. Camerini-Otero
A model for the abrogation of the SOS response by an SOS protein: a negatively charged helix in DinI mimics DNA in its interaction with RecA
Genes & Dev., February 15, 2001; 15(4): 415 - 427.
[Abstract] [Full Text]


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.