Molecular Biology of the Cell click for CBE Life Science Education Page

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


Originally published as MBC in Press, 10.1091/mbc.E04-05-0375 on June 23, 2004

Vol. 15, Issue 9, 4321-4336, September 2004

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
E04-05-0375v1
15/9/4321    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Keller-Seitz, M. U.
Right arrow Articles by Fasullo, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Keller-Seitz, M. U.
Right arrow Articles by Fasullo, M.

Transcriptional Response of Yeast to Aflatoxin B1: Recombinational Repair Involving RAD51 and RAD1

Monika U. Keller-Seitz *, Ulrich Certa {dagger}, Christian Sengstag *, Friedrich E. Würgler *, Mingzeng Sun {ddagger}, and Michael Fasullo {ddagger} §

* Institute of Toxicology, Swiss Federal Institute of Technology ETH, CH-8603 Schwerzenbach, Switzerland; {dagger} Pharma Division, F. Hoffmann-La Roche Ltd., CH-4070 Basel, Switzerland; and {ddagger} Ordway Research Institute, Albany, NY 12208-03479

Submitted May 7, 2004; Revised June 9, 2004; Accepted June 14, 2004
Monitoring Editor: Keith Yamamoto

The potent carcinogen aflatoxin B1 is a weak mutagen but a strong recombinagen in Saccharomyces cerevisiae. Aflatoxin B1 exposure greatly increases frequencies of both heteroallelic recombination and chromosomal translocations. We analyzed the gene expression pattern of diploid cells exposed to aflatoxin B1 using high-density oligonucleotide arrays comprising specific probes for all 6218 open reading frames. Among 183 responsive genes, 46 are involved in either DNA repair or in control of cell growth and division. Inducible growth control genes include those in the TOR signaling pathway and SPO12, whereas PKC1 is downregulated. Eleven of the 15 inducible DNA repair genes, including RAD51, participate in recombination. Survival and translocation frequencies are reduced in the rad51 diploid after aflatoxin B1 exposure. In mec1 checkpoint mutants, aflatoxin B1 exposure does not induce RAD51 expression or increase translocation frequencies; however, when RAD51 is constitutively overexpressed in the mec1 mutant, aflatoxin B1 exposure increased translocation frequencies. Thus the transcriptional profile after aflatoxin B1 exposure may elucidate the genotoxic properties of aflatoxin B1.


Article published online ahead of print. Mol. Biol. Cell 10.1091/mbc.E04–05–0375. Article and publication date are available at www.molbiolcell.org/cgi/doi/10.1091/mbc.E04–05–0375.

§ Corresponding author. E-mail address: mfasullo{at}ordwayresearch.org.




This article has been cited by other articles:


Home page
Mol. Cell. Biol.Home page
Y. Guo, L. L. Breeden, H. Zarbl, B. D. Preston, and D. L. Eaton
Expression of a Human Cytochrome P450 in Yeast Permits Analysis of Pathways for Response to and Repair of Aflatoxin-Induced DNA Damage
Mol. Cell. Biol., July 15, 2005; 25(14): 5823 - 5833.
[Abstract] [Full Text] [PDF]




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Copyright © 2004 by The American Society for Cell Biology. Terms of copyright protection, warranties, and disclaimers.