Imprecise excision of P{GT1}RecQ5BG01967 generates a deletion in RecQ5 that removes 1641bp of RecQ5 from the 2st exon to the 2nd intron, along with an insertion of 13bp.
centrosome | maternal effect (with RecQ5D2)
embryo | maternal effect (with RecQ5D2)
nucleus | maternal effect (with RecQ5D2)
testis | adult stage (with RecQ5D2)
RecQ5D1/RecQ5D2 mutant adult males do not show any obvious defects in the meiotic divisions and spermiogenesis, no gross morphological abnormalities are seen in spermatogonia, spermatocytes, spermatids or other cells in the mutant testes and active motile sperm are present. However, the apical region of the mutant testes is swelled compared to controls and the mutant testes display increased frequency of waste bags.
Embryos lacking maternally derived RecQ5 (i.e. from RecQ5D1/RecQ5D2 homozygous mothers), display asynchronous nuclei. Most comprised of pairs of nuclei, but sometimes more than three irregular nuclei are found to be clustered together. These pairs of abnormal nuclei are clonally generated from single parent nuclei. The parent nucleus and its daughter nuclei proceed synchronously with the surrounding nuclei in prophase, metaphase, anaphase, telophase and interphase.
The frequency of DNA bridging in embryos from RecQ5D1 mutant mothers is 4-fold higher than that in wild-type embryos at cycles 10-13. The lack of maternal RecQ5 causes defects in chromosome segregation such as un-wreathing of the knot-like structure that forms between sister chromatids.
Spindle microtubule dynamics in RecQ5D1/RecQ5D2 embryos are indistinguishable in terms of shape and size from that in wild-type embryos.
Homozygous RecQ5D1 mutants are viable and fertile with no apparent morphological abnormalities.
Embryos derived from RecQ5D1 homozygous mothers display normal syncytial nuclei division. However, every mutant embryo has at least 1 abnormal nucleus at cycle 13. In addition, the irregular nuclei are round in shape, even at anaphase, whereas the other nuclei show condensed chromosomes. The irregular nuclei exit from the synchronous cycles of normal syncytial mitosis.
Embryos derived from females heterozygous for wild-type and RecQ5D1 are similar to wild-type embryos.
RecQ5D1/Df(3L)fz-D21 mutant larval neuroblasts subjected to 2.2 Gy of X-ray irradiation show a 3-fold greater frequency of aberration than wild-type neuroblasts subjected to the same degree of irradiation. The majority of aberrations generated were chromatid or isochromatid breaks.
RecQ5D1 has abnormal mitotic cell cycle | maternal effect phenotype, suppressible by lokp6
RecQ5D1 has embryo | maternal effect phenotype, suppressible by lokp6
RecQ5D1 has nucleus | maternal effect phenotype, suppressible by lokp6
RecQ5D1 has centrosome | maternal effect phenotype, suppressible by lokp6
RecQ5D1 is rescued by RecQ5UAS.cNb/Scer\GAL4arm.PS