Insertion within the second exon.
Homozygous syncytial embryos show a nuclear fall out phenotype (indicating failure of the cell cycle within populations of nuclei) and cell cycle asynchrony compared to wild type. Anaphase bridges are seen in the nuclei. There is a significant increase in the proportion of cells in mitosis in the mutant embryos compared to wild type.
Only 66% of the expected number of heterozygous flies are recovered in crosses between heterozygotes.
The brains of heterozygous third instar larvae show a number of mitotic defects, with one or more defects being seen in approximately 80% of mitotic nuclei. Mis-condensed, elongated and broken chromosomes, prematurely separated sister chromatids and aneuploidy are seen. There is a significant increase in the proportion of cells in mitosis compared to controls. The fraction of nuclei in S phase is not significantly different from wild type. There is a shift compared to wild type of the fraction of cells replicating euchromatin (early to mid S phase) versus heterochromatin (late S phase) in the heterozygous cells, with the ratio of euchromatin/heterochromatin replicating cells being 28% higher in the heterozygotes.
Salivary gland nuclei show a 48.1% reduction in volume on average compared to wild type, whereas DNA content of the salivary glands and number of nuclei per salivary gland is normal. The DNA packaging ratio of the mutant nuclei is 189% higher relative to wild-type controls.
35% of ovarioles from heterozygous females show apoptosis at stage 7. Eggs laid by heterozygous females do not show defects in chorion deposition.
Homozygous Psf2SH0805 embryos show no gastrulation defects.
Psf2SH0805 is rescued by Psf2+tCa
Psf2+tCa rescues the lethality of Psf2SH0805 homozygotes.
Psf2+tCa rescues the mitotic defects seen in the brains of Psf2SH0805/+ third instar larvae.