spir¹/Df(2L)Exel6046 females are sterile. Their eggs do not hatch. Their oocytes lack actin mash at any stage and they exhibit premature onset of fast cytoplasmic streaming.

Expression of Scer\GAL4^{nos.UTR.T:Hsim\VP16}>spir^{RD.Scer\UAS.P\T.T:Avic\GFP} in spir¹/Df(2L)Exel6046 females results in oocytes with an actin mesh and fast streaming is prevented. When fertility is measured, only 12% of the eggs laid by the mutant flies hatch.

spir¹/Df(2L)Exel6046 females expressing Scer\GAL4^{nos.UTR.T:Hsim\VP16}>spir^{Scer\UAS.P\T.RB.T:Avic\GFP} are mostly fertile: 59% of the eggs hatch.

spir¹/Df(2L)Exel6046 females expressing Scer\GAL4^{nos.UTR.T:Hsim\VP16}>spir^{Scer\UAS.P\T.RB} are mostly fertile: 48% of the eggs hatch.

spir¹/Df(2L)Exel6046 females expressing Scer\GAL4^{nos.UTR.T:Hsim\VP16}>spir^{Y232K.Scer\UAS.P\T.RB.T:Avic\GFP} are sterile. The mutant oocytes have no detectable actin mesh during mid-oogenesis and consistently exhibit premature streaming. At later stages of oogenesis, no mesh is visible and fast streaming is observed at stage 11.

Mutant oocytes show premature cytoplasmic streaming at stage 9. In addition, the microtubules are aligned in arrays along the oocyte cortex, instead of the wild-type anterior-to-posterior gradient.

Mutant stage 9 oocytes do not contain the actin mesh (a uniform network of actin filaments present throughout the cytoplasm) that is seen in wild-type oocytes at this stage. Any remaining cytoplasmic F-actin in the mutant oocytes forms small dots.

25-30% of oocytes in spir¹ mutants show severe defects in karyosome morphology and abnormal G-actin accumulation.

The oocyte nucleus fails to localise properly to its normal anterodorsal position in the egg chambers of homozygous females.

Dorsalised egg chambers.

Prevents the posterior accumulation of G-iα65A protein.

hts RNA localization unaltered in embryos derived from spir mutant mothers.

spir¹;6xP{osk⁺108} embryos exhibit a class of embryos with abdominal deletions typical of posterior group mutations.

Strong abdominal defects.

Does not interact with RpII140^wimp maternal effect.

Variable expansion (dorsalization) of dorsal appendages, at expense f main body shell. Absence of polar granules, pole cells and abdominal segments in embryos.

Localization of vas protein to pole cells and polar granules abolished.

Homozygous spir¹ embryos derived from homozygous females have no polar granules, fail to form pole cells, have deletions of abdominal structures and defects associated with dorsal/ventral pattern formation. Posterior localization of vas and CycB transcripts is completely abolished.

Homozygous mothers produce dorsalized egg shells and embryos. The first sign of dorsalization in embryos can be seen during gastrulation, when the ventral furrow is reduced or absent. Dorsalization in the egg chamber is evident in the shape of the follicle cells. While the number of follicle cells around the main body of the egg shell is reduced, dorsal appendages are expanded, often fused dorsally and/or extended ventrally. The embryos lack polar granules and pole cells, and show cellularization defects. Embryos show abdominal segmentation defects similar to those produced by mutations in the grandchildless-knirps or posterior class of maternal effect loci.

maternal-effect lethal homozygous females lay eggs which sometimes (5-10%) have a "peak" (spire) of dorsal appendage material sitting over the anterior end of the egg, instead of two distinct dorsal appendages. Such eggs are similar to eggs formed by the female-sterile mutation fs(1)K10, but the extent of dorsal appendage material on spir eggs is much more variable than that of fs(1)K10 eggs. Mutant females produce embryos lacking polar granules, pole cells and normal abdominal segmentation. In combination with BicD, however, abdominal segmentation does develop in the anterior half of the embryo; improper localization of abdominal determinants also indicated by the lack of posterior localization of vasa protein. Cellularization of the blastoderm irregularly defective with nuclei of different sizes and densities. Resemble embryos formed by other grandchildless-knirps-like mutations, such as vasa or tudor, but in addition, some of the embryos from spire females appear also to be dorsalized.

spir[+]/spir¹ is an enhancer of abnormal neuroanatomy | adult stage phenotype of ccb^ks127

spir[+]/spir¹ is an enhancer of abnormal neuroanatomy | adult stage phenotype of ccb^ks145

ccb^ks127, spir[+]/spir¹ has increased mortality during development phenotype

ccb^ks145, spir[+]/spir¹ has increased mortality during development phenotype

spir¹ has oocyte | oogenesis stage S9 phenotype, suppressible by Scer\GAL4^{VP16.nanos.UTR}/capu^ΔN.UASp.GFP

spir¹ has filamentous actin | oogenesis stage S9 phenotype, suppressible by Scer\GAL4^{VP16.nanos.UTR}/capu^ΔN.UASp.GFP

spir¹ has egg chamber phenotype, suppressible by Cf2^s.hs

spir[+]/spir¹ is an enhancer of ellipsoid body phenotype of ccb^ks127

spir[+]/spir¹ is an enhancer of ellipsoid body phenotype of ccb^ks145

spir[+]/spir¹ is a non-enhancer of phenotype of ct^L188

spir[+]/spir¹ is a non-enhancer of phenotype of ct^C145

spir¹ is a non-enhancer of phenotype of ct^C145

capu^EY12344, spir¹ has oocyte phenotype

capu^EY12344, spir¹ has meiotic spindle phenotype

capu^EY12344, spir¹ has filamentous actin | oogenesis phenotype

capu^EY12344, spir¹ has spindle microtubule | oogenesis phenotype