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Originally published as Genetics Published Articles Ahead of Print on February 1, 2008.

Genetics, Vol. 178, 675-691, February 2008, Copyright © 2008
doi:10.1534/genetics.107.080879

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Genetic Interactions of the Aspergillus nidulans atmAATM Homolog With Different Components of the DNA Damage Response Pathway

Iran Malavazi*, Joel Fernandes Lima*, Patrícia Alves de Castro*, Marcela Savoldi*, Maria Helena de Souza Goldman{dagger} and Gustavo Henrique Goldman*,1

* Faculdade de Ciências Farmacêuticas de Ribeirão Preto and {dagger} Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, Universidade de São Paulo, São Paulo 14040-903, Brazil

1 Corresponding author: Departamento de Ciências Farmacêuticas Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Av. do Café S/N, Ribeirão Preto, São Paulo 14040-903, Brazil.
E-mail: ggoldman{at}usp.br

Ataxia telangiectasia mutated (ATM) is a phosphatidyl-3-kinase-related protein kinase that functions as a central regulator of the DNA damage response in eukaryotic cells. In humans, mutations in ATM cause the devastating neurodegenerative disease ataxia telangiectasia. Previously, we characterized the homolog of ATM (AtmA) in the filamentous fungus Aspergillus nidulans. In addition to its expected role in the DNA damage response, we found that AtmA is also required for polarized hyphal growth. Here, we extended these studies by investigating which components of the DNA damage response pathway are interacting with AtmA. The AtmAATM loss of function caused synthetic lethality when combined with mutation in UvsBATR. Our results suggest that AtmA and UvsB are interacting and they are probably partially redundant in terms of DNA damage sensing and/or repairing and polar growth. We identified and inactivated A. nidulans chkACHK1 and chkBCHK2 genes. These genes are also redundantly involved in A. nidulans DNA damage response. We constructed several combinations of double mutants for {Delta}atmA, {Delta}uvsB, {Delta}chkA, and {Delta}chkB. We observed a complex genetic relationship with these mutations during the DNA replication checkpoint and DNA damage response. Finally, we observed epistatic and synergistic interactions between AtmA, and bimEAPC1, ankAWEE1 and the cdc2-related kinase npkA, at S-phase checkpoint and in response to DNA-damaging agents.






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