In swa^VA11 mutants, approximately 70% of stage 10 egg chambers contain thick aggregation of subcortical microtubules with a relative paucity of anterior/lateral microtubules, or occasionally microtubules that accumulate more strongly at the lateral complex compared to the anterior cortex.

swa^VA11 mutants exhibit defects in anterior/lateral microtubules at stage 10, prior to the initiation of streaming, but concomitant with the appearance of subcortical microtubules.

Approximately 70% of mature swa^VA11 oocytes exhibit oocyte nucleus mis-positioning. The nucleus is no longer found in its normal location but in apparently random positions in the ooplasm.

In a small number of swa^VA11 stage 10 oocytes (<20%), the nucleus can be observed in a more lateral position, and the proportion of oocytes with mis-positioned nuclei increases with increasing oocyte maturity.

There is no evidence that swa^VA11 mutant stage 9 embryos undergo premature streaming.

Embryos derived from swa^VA11/Df(1)JF5 females mated to wild-type males often show cuticle defects, ranging from embryos without cuticle and lacking any sign of development (40%), through embryos with a reduction in the number of abdominal segments to embryos that have 8 abdominal segments, with normal or nearly normal abdominal morphology. The most commonly represented cuticular class is embryos that have 4-6 abdominal segments, with the arrangement of segments usually abberant, with segments often fused (40%).

Defects in actin organisation are first detectable at about stage 10 in mutant oocytes. Small irregularly-shaped actin aggregates and actin spheres are seen below the actin-rich cortical layer. Most of the actin spheres are "hollow", having an actin-rich surface and an actin-poor core. About 30% of stage 10 oocytes have a relatively mild mutant phenotype in which a few clumps and spheres are limited to the anterior subcortical layer of the oocyte. About 10% of stage 10 egg chambers have a larger number of aggregates and spheres which are distributed throughout the oocyte and fused actin spheres. About 60% of oocytes between stages 11 to 14 have detectable defects in actin organisation. In these abnormal oocytes, actin spheres about 3-5μm in diameter are uniformly distributed from the subcortical layer into deeper central cytoplasm. The spheres are more numerous in later stages of oogenesis and a larger fraction of them are hollow. Occasional "double" spheres consisting of two spheres fused at their surface are seen. Tiny actin granules are visible on the surface of the spheres. Incomplete or defective actin furrows are seen at metaphase and anaphase during the blastoderm syncytial cleavages of embryos derived from mutant females, which result in fused actin caps at interphase of the subsequent cell cycle.

Homozygous females are completely sterile, producing eggs that often develop as far as an incipient larval stage, but which rarely hatch. The small fraction that do hatch have grossly abnormal anterior structures, never grow in size and die soon after hatching.

swa^VA11 has female sterile | recessive phenotype, suppressible by Dpse\swa^swa.PH

swa^VA11 has viable phenotype, suppressible by Dpse\swa^swa.PH