swa is required for overall actin organisation and for the maintenance of a distinct subset of microtubules in the oocyte.

swa protein transiently but tightly co-localizes with bcd RNA in mid-oogenesis, at stage 10. swa protein also localizes to the anterior pole of the oocyte in the absence of bcd RNA. This localization does not require exu protein but does require microtubules. ctp is a swa-binding protein. swa protein may act as an adaptor for the dynein complex enabling dynein to transport bcd RNA along microtubules to their minus ends at the anterior pole of the oocyte.

In a sample of 79 genes with multiple introns, 33 showed significant heterogeneity in G+C content among introns of the same gene and significant positive correspondence between the intron and the third codon position G+C content within genes. These results are consistent with selection adding against preferred codons at the start of genes.

Compared to the swa sequence swaΨ exhibits eight deletions in the coding region ranging from 3 to 138bp. No insertions are found. Data suggests that the preponderance of relatively large mutations is likely to be a general property of mutation.

swa function is required to maintain the position of several localised mRNAs and localised ribonucleoprotein (RNP) complexes in the cortex of the oocyte (including bcd and hts mRNA).

There is not a simple relationship between the position of the swa protein and the site of its action in bcd RNA localisation. Studies of the distribution of swa protein during early embryogenesis reveals a cycle whereby the swa gene product enters each nucleus at the beginning of mitosis, occupies a position complementary to that of condensed chromatin, and leaves each nucleus at the end of mitosis.

Some blastoderms irregularly populated, with some areas on surface devoid of nuclei, others display asynchronous nuclear divisions and nuclei of non uniform size. Gastrulation occurs before full complement of nuclei achieved; mitosis continues into gastrulation. Developmental arrest at time of first muscular activity. Morphology of developing embryos shows variable temperature-sensitive failure of head-segment development and abdominal segmentation defects. Anterior defects more severe at 29^oC and posterior ones cold-sensitive, strongly enhanced at 18^oC. ftz expression pattern abnormal; number of stripes varies from three (PS 2, 4, & 6) at 18^oC to seven at 29^oC.

The swa genomic region contains two copies of a swa-like sequence. Only one copy is thought to be the functional swa gene, the other copy (swaΨ) is thought to be non-functional.

Mutations in maternal anterior class gene swa do not interact with RpII140^wimp.

The effects of taxol treatment on swa mutants suggest general roles for the swa gene product in the multi-step bcd mRNA localization process.

swa mutants exhibit weak anterior deletions and segmentation defects in the abdomen.

Mature follicles are immunologically stained for asymmetric distribution of ecdysteroid-related antigen. During late oogenesis localisation of the antigen changes dramatically suggesting the antigen plays a role in early embryogenesis and, perhaps, in pattern formation.

swa mutations disrupt the third stage of bcd RNA localization during oogenesis, localization to the cortex at the anterior end of the oocyte.

Unlike wild-type cytoplasm, anterior cytoplasm from embryos of swa mothers ineffective in rescuing bcd phenotype; also embryos from swa females resistant to the bcd-phenocopying effects of removing anterior cytoplasm.

Embryos carrying mutations at swa display clypeolabrum defects.

Mutations in swa affect cephalogenesis.