Imprecise excision of P{EPgy2}nesEY22898 generates a 1.9kb deletion that removes most of the open reading frame.
Approximate endpoints of the 1.86 kb deletion resulting from the imprecise excision of P{EPgy2}nesEY22898. Position of deletion on reference sequence inferred by FlyBase curator.
nesΔ52 mutant flies survive to adulthood with no apparent morphological defects.
nesΔ52, oysΔ67 has male sterile phenotype
nesΔ52, oysΔ67 has female semi-sterile phenotype
nesΔ52, oysΔ67 has spermatozoon phenotype
nesΔ52, oysΔ67 has individualization stage spermatid phenotype
oysΔ67;nesΔ52 double mutant males are sterile. Female fertility is also reduced; 70% of embryos resulting from a cross to heterozygous males fail to hatch and 24% display extensive degeneration of cell membranes. Removal of zygotic oys and nes further reduces adult viability to 10% of the number of flies carrying wild-type paternal copies of both genes.
oysΔ67;nesΔ52 mutant testes appear relatively normal by light and phase-contrast microscopy and contain elongated spermatids. The early stages of spermatogenesis proceed normally in oysΔ67;nesΔ52 mutants. oysΔ67;nesΔ52 onion-stage spermatids contain individual Nebenkerne of normal size, indicating normal cytokinesis. Axonemes exhibit no defects in elongation and major and minor mitochondrial derivatives in pre-individualized spermatids display normal morphology. As no mature motile sperm are found in mutant seminal vesicles, oys and nes must act in the final stages of spermatid differentiation and maturation.
Individualization complexes (ICs) are visible in oysΔ67;nesΔ52 double mutants in the basal region of the testis, in association with the cyst nuclei. However, very few progressing ICs are detectable and no ICs collect in the apical testis. Actin cones assemble normally around the spermatid nuclei, but dissociate away from each other as they move away from the nuclei, disassembling the IC. Intact ICs are almost never found apical to the nuclei, and individual stray actin cones are frequently observed.
Embryos laid by oysΔ67;nesΔ52 mutant mothers contain a significant number of germ cells that fail to reach the gonads. These germ cells appear to migrate through the midgut epithelium normally, but they remain associated with the basal surface of the gut rather than attaching to the somatic gonadal precursors or scattering throughout the embryo. This phenotype is not observed in single mutants or controls.
