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Originally published as Genetics Published Articles Ahead of Print on August 3, 2005.
Genetics, Vol. 171, 1003-1015, November 2005, Copyright © 2005
doi:10.1534/genetics.105.041376
The csnD/csnE Signalosome Genes Are Involved in the Aspergillus nidulans DNA Damage Response
Joel Fernandes Lima*,
Iran Malavazi*,
Marcia Regina von Zeska Kress Fagundes*,
Marcela Savoldi*,
Maria Helena S. Goldman
,
Elke Schwier
,
Gerhard H. Braus and
Gustavo Henrique Goldman*,1
* Faculdade de Ciências Farmacêuticas de Ribeirão Preto and Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, Universidade de São Paulo, São Paulo, 1404-903 Brazil and Department of Molecular Microbiology and Genetics, Institute for Microbiology and Genetics, Georg-August-University Göttingen, 37077 Germany
1 Corresponding author: Departamento de Ciências Farmacêuticas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Av. do Café S/N, CEP 14040-903, Ribeirão Preto, São Paulo, 1404-903 Brazil.
E-mail: ggoldman{at}usp.br
The signalosome (CSN) is a conserved multiprotein complex involved in regulation of eukaryotic development and is also required to activate ribonucleotide reductase for DNA synthesis. In Aspergillus nidulans, csnD/csnE are key regulators of sexual development. Here, we investigated whether the csnD/csnE genes are involved in the DNA damage response in this fungus. The growth of the csnD/csnE deletion mutants was reduced by subinhibitory concentrations of hydroxyurea, camptothecin, 4-nitroquinoline oxide, and methyl methanesulfonate. A. nidulans increases csnD/csnE mRNA levels when it is challenged by different DNA-damaging agents. There is no significant transcriptional induction of the csnE promoter fused with lacZ gene in the presence of DNA-damaging agents, suggesting that increased mRNA accumulation is due to increased mRNA stability. Septation was not inhibited in the csnD/csnE deletion mutants while 
uvsB csnE presented an increase in septation upon DNA damage caused by methyl methanesulfonate, suggesting that uvsBATR and csnE genetically interact during checkpoint-dependent inhibition of septum formation. The double csnD/csnE npkA mutants were more sensitive to DNA-damaging agents than were the respective single mutants. Our results suggest that csnD/csnE genes are involved in the DNA damage response and that NpkA and UvsBATR genetically interact with the signalosome.
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