Embryos from swa¹/swa³ females have a reduced embryonic head.

Embryos derived from swa¹/Df(1)JF5 females mated to wild-type males often show cuticle defects, ranging from embryos without cuticle and lacking any sign of development (64%), 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 in embryos that develop is embryos that have 8 abdominal segments, with normal or nearly normal abdominal morphology (38%).

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.

In embryos from mutant females the ople plasm is no longer tightly apposed to the posterior pole and seems to have fallen off into the egg cytoplasm.

Embryos from swa mutant mothers show abnormal delocalization of hts RNA, commencing at stage 8 of oogenesis, 12 hours before delocalization of bcd RNA begins. During delocalization hts RNA first spreads posteriorly along the dorsal side of the embryo, only later becoming uniformly distributed.

Pregastrula and gastrula embryos exhibit nuclear defects, an excess of irregularly shaped internal chromatin masses, blastoderm nuclei are non-uniform in size and chromatin condensation and asynchronous in the cell cycle. Embryos have uneven blastoderm nuclear sizes, and fewer than normal nuclei at the beginning of gastrulation. There is an excess of irregularly shaped internal chromatin masses, and chromatin condensation is asynchronous. During preblastoderm and early blastoderm cleavages lagging chromosomes during anaphase are common.

Does not interact with RpII140^wimp maternal effect.

Embryos laid by swa¹ homozygous mothers have a variable bcd RNA distribution: no localization or a weak anterior-to-posterior gradient. A gradient becomes more pronounced as development proceeds due to posterior degradation of the RNA.

The thoracic and segmented head anlagen is enlarged while the posterior pattern is compressed. Low levels of bcd protein are distributed in a shallow gradient throughout the embryo.

Strong allele.

At 29^oC (permissive temperature), embryos derived from swa¹/Df(1)JF5 females have a similar phenotype to embryos derived from homozygous exu¹ females. At 18^oC, all embryos derived from swa¹/Df(1)JF5 females show abdominal segmentation defects, the majority retaining less than six denticle belts. The temperature-critical period is during oogenesis. Embryos derived from bcd⁶/bcd⁷ females show some development of at least thoracic and frequently head structures when injected at the anterior tip with cytoplasm taken from the anterior tip of wild-type embryos. Cytoplasm taken from the anterior tip of embryos derived from swa¹/swa² females shows reduced rescuing activity compared to wild-type cytoplasm when injected into the anterior tip of embryos derived from bcd⁶/bcd⁷ females. The phenotype of embryos derived from swa¹/swa² females is more or less unmodified if cytoplasm is removed from the anterior tip of the embryo.

maternal-effect lethal strong allele female-sterile.

swa³/swa¹ is a suppressor of visible | homeotic phenotype of mira^{Δ103.αTub67C.mGFP6}

swa[+]/swa¹ is a suppressor of female sterile | semidominant phenotype of αTub67C³

swa³/swa¹ is a suppressor of embryonic abdomen | ectopic phenotype of mira^{Δ103.αTub67C.mGFP6}

swa³/swa¹ is a suppressor of embryonic thorax phenotype of mira^{Δ103.αTub67C.mGFP6}

swa[+]/swa¹ is a suppressor of embryonic/first instar larval cuticle | maternal effect phenotype of αTub67C³