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Eukaryotic Cell, October 2006, p. 1688-1704, Vol. 5, No. 10
1535-9778/06/$08.00+0     doi:10.1128/EC.00167-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Transcriptome Analysis of Aspergillus nidulans Exposed to Camptothecin-Induced DNA Damage

Faculdade de Ciências Farmacêuticas de Ribeirão Preto,¹ Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto,⁵ Departmento de Microbiologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil,³ Universidade de Ribeirão Preto, São Paulo, Brazil,² Plant Science Initiative, University of Nebraska, Lincoln, Nebraska⁴

Received 6 June 2006/ Accepted 25 July 2006

We have used an Aspergillus nidulans macroarray carrying sequences of 2,787 genes from this fungus to monitor gene expression of both wild-type and uvsB^ATR (the homologue of the ATR gene) deletion mutant strains in a time course exposure to camptothecin (CPT). The results revealed a total of 1,512 and 1,700 genes in the wild-type and uvsB^ATR deletion mutant strains that displayed a statistically significant difference at at least one experimental time point. We characterized six genes that have increased mRNA expression in the presence of CPT in the wild-type strain relative to the uvsB^ATR mutant strain: fhdA (encoding a forkhead-associated domain protein), tprA (encoding a hypothetical protein that contains a tetratrico peptide repeat), mshA (encoding a MutS homologue involved in mismatch repair), phbA (encoding a prohibitin homologue), uvsC^RAD51 (the homologue of the RAD51 gene), and cshA (encoding a homologue of the excision repair protein ERCC-6 [Cockayne's syndrome protein]). The induced transcript levels of these genes in the presence of CPT require uvsB^ATR. These genes were deleted, and surprisingly, only the uvsC mutant strain was sensitive to CPT; however, the others displayed sensitivity to a range of DNA-damaging and oxidative stress agents. These results indicate that the selected genes when inactivated display very complex and heterogeneous sensitivity behavior during growth in the presence of agents that directly or indirectly cause DNA damage. Moreover, with the exception of UvsC, deletion of each of these genes partially suppressed the sensitivity of the uvsB strain to menadione and paraquat. Our results provide the first insight into the overall complexity of the response to DNA damage in filamentous fungi and suggest that multiple pathways may act in parallel to mediate DNA repair.

Supplemental material for this article may be found at http://ec.asm.org/.