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 (19)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Cosentino, L.
Right arrow Articles by Heddle, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cosentino, L.
Right arrow Articles by Heddle, J. A.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Mutagenesis, Vol. 14, No. 1, 113-119, January 1999
© 1999 UK Environmental Mutagen Society/Oxford University Press

A comparison of the effects of diverse mutagens at the lacZ transgene and Dlb-1 locus in vivo

Lidia Cosentino and John A. Heddle1

Department of Biology, York University, Toronto, Canada M3J 1P3

Transgenic assays permit the detection of mutations in any tissue, whereas endogenous mutations can be measured in very few. For this reason comparisons between these loci when both can be measured in the same cells are of considerable interest. Previous comparisons have been inconsistent: usually these loci have responded alike, however, in some cases the endogenous locus has been more sensitive and at other times the transgenic locus has been more sensitive. Here we report a comparison of the lacZ transgene of the MutaTMMouse and the endogenous Dlb-1 gene in the epithelium of the small intestine after acute exposure to seven mutagens. Benzo[a]pyrene, 5-bromo-2'-deoxyuridine, methyl methane sulphonate, ethyl methane sulphonate, N-ethyl-N-nitrosourea, mitomycin C and N-methyl-N-nitrosourea were all given by gavage to F1 (MutaMousexSWR) mice. Mutations were quantified 2 weeks after the end of treatment. The data shows that all of the agents induced similar mutant frequencies at the Dlb-1 locus and at the lacZ transgene. The acute treatments generally produced only modest increases in mutant frequency at both loci. The higher background frequency observed at the lacZ transgene reduces the ability of the transgenic assay to detect the same absolute increase in mutant frequency.

1 To whom correspondence should be addressed. Tel: +1 416 736 2100, ext. 33053; Fax: +1 416 736 5698; Email: lidiac{at}yorku.ca and jheddle@yorku.ca


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
MutagenesisHome page
E. Bilsland and J. A. Downs
Tails of histones in DNA double-strand break repair
Mutagenesis, May 1, 2005; 20(3): 153 - 163.
[Abstract] [Full Text] [PDF]


Home page
MutagenesisHome page
H.-L. Song, G. J.S. Jenkins, J. Ashby, H. Tinwell, and J. M. Parry
The application of the restriction site mutation assay to compare 1-ethyl-1-nitrosourea-induced mutations between the endogenous p53 gene and the transgenic LacZ gene in MutaMouse testes
Mutagenesis, January 1, 2001; 16(1): 59 - 64.
[Abstract] [Full Text] [PDF]


Home page
CarcinogenesisHome page
A. R. Clarke
Manipulating the germline: its impact on the study of carcinogenesis
Carcinogenesis, March 1, 2000; 21(3): 435 - 441.
[Abstract] [Full Text] [PDF]


Home page
MutagenesisHome page
J. A. Heddle
On clonal expansion and its effects on mutant frequencies, mutation spectra and statistics for somatic mutations in vivo
Mutagenesis, May 1, 1999; 14(3): 257 - 260.
[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.