RecQ5 belongs to the family of RecQ DNA helicases. There are 5 RecQ homologs in mammals, and defects in 3 of them (BLM, WRN, and RECQL4) give rise to cancer predisposition syndromes in humans. Although no human disease has yet been genetically linked to a mutation in RecQ5, this enzyme is thought to have unique functions, based on its ubiquitous expression profile and specific C-terminal amino acid sequence, both of which are very different from those of other RecQ DNA helicase family members. The analysis of MEF and ES cells derived from RecQ5-deficient mice investigated by Hu et al. suggested an important role for RecQ5 in the DNA metabolism of the early embryo. However, it is unknown how RecQ5 deficiency destabilizes DNA. To address the DNA instabilities in RecQ5-deficient animals, we chose Drosophila melanogaster which has simple checkpoint systems in its syncytial embryos. By analyzing Drosophila syncytial embryos, we demonstrated that the loss of RecQ5 increased the frequency of spontaneous mitotic defects such as anaphase bridge formation. A pair of daughter nuclei that had been linked by such DNA bridges was simultaneously eliminated via a Chk2-dependent pathway. These findings suggest that the lack of RecQ5 causes spontaneous double-strand DNA breaks. RecQ5 may thus function in the resolution of anaphase DNA bridges during mitosis in syncytial embryo.