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MBC in Press, published online ahead of print June 23, 2004
Mol. Biol. Cell 10.1091/mbc.E04-05-0375

A more recent version of this article appeared on September 1, 2004
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Submitted on May 7, 2004
Revised on June 9, 2004
Accepted on June 14, 2004

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}{sect}

*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, {ddagger}Ordway Research Institute, Albany, NY 12208-03479

Monitoring Editor: Keith Yamamoto

The potent carcinogen aflatoxin B1 is a weak mutagen but a strong recombinagen in S. 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 ORFs. 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, while PKC1 is down-regulated. 11 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.

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






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