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Background  DNA double-strand breaks (DSBs) are induced by exogenous insults such as ionizing radiation and chemical exposure, and they can also arise as a consequence of stalled or collapsed DNA replication forks. Failure to repair DSBs can lead to genomic instability or cell death and cancer in higher eukaryotes. The  Schizosaccharomyces pombe fbh1  gene encodes an F-box DNA helicase previously described to play a role in the Rhp51 (an orthologue of  S. cerevisiae RAD51 )-dependent recombinational repair of DSBs. Fbh1 fused to GFP localizes to discrete nuclear foci following DNA damage.    Results  To determine the functional roles of the highly conserved F-box and helicase domains, we have characterized  fbh1  mutants carrying specific mutations in these domains. We show that the F-box mutation  fbh1-fb  disturbs the nuclear localization of Fbh1, conferring an  fbh1  null-like phenotype. Moreover, nuclear foci do not form in  fbh1-fb  cells with DNA damage even if Fbh1-fb is targeted to the nucleus by fusion to a nuclear localization signal sequence. In contrast, the helicase mutation  fbh1-hl  causes the accumulation of Fbh1 foci irrespective of the presence of DNA damage and confers damage sensitivity greater than that conferred by the null allele. Additional mutation of the F-box alleviates the hypermorphic phenotype of the  fbh1-hl  mutant.    Conclusion  These results suggest that the F-box and DNA helicase domains play indispensable but distinct roles in Fbh1 function. Assembly of the SCF Fbh1  complex is required for both the nuclear localization and DNA damage-induced focus formation of Fbh1 and is therefore prerequisite for the Fbh1 recombination function.

Essential and distinct roles of the F-box and helicase domains of Fbh1 in DNA damage repair