Originally published as Genetics Published Articles Ahead of Print on October 11, 2005.

Genetics, Vol. 172, 113-125, January 2006, Copyright © 2006
doi:10.1534/genetics.105.041756

Growth Defect and Mutator Phenotypes of RecQ-Deficient Neurospora crassa Mutants Separately Result From Homologous Recombination and Nonhomologous End Joining During Repair of DNA Double-Strand Breaks

Akihiro Kato and Hirokazu Inoue1

Laboratory of Genetics, Department of Regulation Biology, Faculty of Science, Saitama University, 338-8570 Saitama, Japan

1 Corresponding author: Laboratory of Genetics, Department of Regulation Biology, Faculty of Science, Saitama University, Sakura-ku, Shimo-okubo 255, 338-8570 Saitama, Japan.
E-mail: hinoue{at}post.saitama-u.ac.jp

RecQ helicases function in the maintenance of genome stability in many organisms. The filamentous fungus Neurospora crassa has two RecQ homologs, QDE3 and RECQ2. We found that the qde-3 recQ2 double mutant showed a severe growth defect. The growth defect was alleviated by mutation in mei-3, the homolog of yeast RAD51, which is required for homologous recombination (HR), suggesting that HR is responsible for this phenotype. We also found that the qde-3 recQ2 double mutant showed a mutator phenotype, yielding mostly deletions. This phenotype was completely suppressed by mutation of mus-52, a homolog of the human KU80 gene that is required for nonhomologous end joining (NHEJ), but was unaffected by mutation of mei-3. The high spontaneous mutation frequency in the double mutant is thus likely to be due to NHEJ acting on an elevated frequency of double-strand breaks (DSBs) and we therefore suggest that QDE3 and RECQ2 maintain chromosome stability by suppressing the formation of spontaneous DSBs.




This article has been cited by other articles:


Home page
 Nucleic Acids ResHome page
R. M. Brosh Jr and V. A. Bohr
Human premature aging, DNA repair and RecQ helicases
Nucleic Acids Res., December 3, 2007; 35(22): 7527 - 7544.
[Abstract] [Full Text] [PDF]