title: Loss of RecQ5 leads to spontaneous mitotic defects and chromosomal aberrations in Drosophila melanogaster.
abstract: RecQ5 belongs to the RecQ DNA helicase family that includes genes causative of Bloom, Werner, and Rothmund-Thomson syndromes. Although no human disease has been genetically linked to a mutation in RecQ5, Drosophila melanogaster RecQ5 is highly expressed in early embryos, suggesting an important role for it in the DNA metabolism of the early embryo. In this present study, we generated RecQ5 mutants in D. melanogaster. Embryos lacking maternally derived RecQ5 contained irregular nuclei in early embryogenesis. These irregular nuclei emerged in nuclear cycle 11-13, lost cell-cycle markers, and were located below the surface monolayer of nuclei. By time-lapse microscopy, these irregular nuclei were observed not to divide, whereas all neighboring nuclei proceeded through normal mitotic division with synchrony. These data suggest that the irregular nuclei exited from the nuclear division cycle. This phenotype is reminiscent of the effect of X-ray irradiation on wild-type embryos and was rescued by expression of RecQ5. Thus, the maternal supply of RecQ5 is important for the nuclear cycles in syncytical embryos. Furthermore, the frequencies of spontaneous and induced chromosomal aberrations were increased in RecQ5 mutant neuroblasts. These data imply that DNA damage accumulates spontaneously in RecQ5 mutants. Therefore, endogenous genomic damage may be produced in Drosophila development, and RecQ5 would be involved in the maintenance of genomic stability by suppressing the accumulation of DNA damage.
authors.affiliation: Department of Biochemistry, Faculty of Pharmaceutical Sciences, Setsunan University, 45-1 Nagaotoge, Hirakata, Osaka 573-0101, Japan.
authors.forename: Minoru
authors.initials: M
authors.lastname: Nakayama
authors.forename: Shin-Ichiroh
authors.initials: S
authors.lastname: Yamaguchi
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Sagisu
authors.forename: Haruna
authors.initials: H
authors.lastname: Sakurai
authors.forename: Fumiaki
authors.initials: F
authors.lastname: Ito
authors.forename: Katsumi
authors.initials: K
authors.lastname: Kawasaki
mesh_terms: D000818:Animals; D002467:Cell Nucleus / Q000201:enzymology; D002869:Chromosome Aberrations; D053960:DNA Breaks; D004265:DNA Helicases; D029721:Drosophila Proteins / Q000172:deficiency* / Q000378:metabolism; D004331:Drosophila melanogaster / Q000166:cytology* / Q000196:embryology / Q000201:enzymology*; D004625:Embryo, Nonmammalian / Q000166:cytology / Q000201:enzymology; D007814:Larva / Q000166:cytology / Q000201:enzymology; D018613:Microscopy, Confocal; D008938:Mitosis; D009154:Mutation / Q000235:genetics; D053484:RecQ Helicases / Q000172:deficiency* / Q000378:metabolism; D013997:Time Factors
chemical_list: D029721:Drosophila Proteins; D004265:DNA Helicases; D053484:RecQ Helicases; C407462:RecQ5 protein, Drosophila