Missense mutation.
Homozygous egg chambers contain binucleate cells. Fragments of ring canals are seen.
Greater than 75% of embryos laid by homozygous females are ventralised. Abnormal microtubule distribution in stage 8 and 9 egg chambers (distribution resembles that of stage 10 egg chambers), long and thick tubulin fibres are seen wrapping around the cortex of mutant oocytes. Egg chambers undergo premature microtubule based cytoplasmic streaming.
Disrupt posterior and dorsoventral patterning in embryos. Disrupt organisation of developing microtubules during stages 8 to 10. Developmental onset of microtubule-dependent ooplasmic streaming is affected causing premature ooplasmic streaming in the mutant ovaries. The progress and termination of streaming is unaffected.
capu2;6xP{osk+108} embryos exhibit a class of embryos with abdominal deletions typical of posterior group mutations.
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.
capu2 is an enhancer of lethal | embryonic stage | maternal effect | dominant phenotype of Rho1rev220
Df(2L)ed1/capu2 has oocyte | oogenesis stage S9 phenotype, non-suppressible by Scer\GAL4VP16.nanos.UTR/spirRD.UASp.GFP
Df(2L)ed1/capu2 has filamentous actin | oogenesis stage S9 phenotype, non-suppressible by Scer\GAL4VP16.nanos.UTR/spirRD.UASp.GFP
capu[+]/capu2 is a non-suppressor of embryonic head phenotype of miraαTub67C.mGFP6
capu2, ctC145 has egg chamber phenotype
capu2, ctC145 has nurse cell ring canal phenotype
The bicaudal phenotype of embryos derived from miraαTub67C.T:Avic\GFP-m6/+ females is not suppressed if the females are also heterozygous for capu2.
Expression of spirRD.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 does not rescue the premature cytoplasmic streaming and abnormal microtubule distribution seen in stage 9 capu2/Df(2L)ed1 oocytes.
The loss of the actin mesh in the cytoplasm of stage 9 capu2/Df(2L)ed1 oocytes is not rescued by expression of spirRD.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL4nos.UTR.T:Hsim\VP16.
ctC145/+ ; capu2/+ double heterozygotes produce egg chambers with binucleate cells. The majority of egg chambers contain a single binucleate cell, although occasionally more than one binucleate cell per egg chamber is seen. The binucleate cells can occur anywhere among the nurse cells and contain remnants of ring canals. The binucleate cells are not seen prior to stage 5.
Egg chambers transheterozygous for Rho1rev220 and capu mutants show disruptions of the ovarian cytoskeleton and ring canals similar to that seen in females heterozygous for Rho1rev220 and RpII140wimp.
Injection of nosN5 RNA into hemizygous embryos completely rescues the abdominal phenotype.
Df(2L)ed1/capu2 is rescued by capuUASp.cDa.GFP/Scer\GAL4VP16.nanos.UTR
Df(2L)ed1/capu2 is rescued by Scer\GAL4VP16.nanos.UTR/capuΔN.UASp.GFP
Expression of either capuScer\UAS.P\T.cDa.T:Avic\GFP or capuΔN.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 suppresses the premature cytoplasmic streaming seen in capu2/Df(2L)ed1 oocytes and restores normal microtubule organisation.
The loss of the actin mesh in the cytoplasm of capu2/Df(2L)ed1 oocytes is rescued up to stage 10B by expression of capuΔN.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL4nos.UTR.T:Hsim\VP16. Ectopic actin mesh-like structures are also induced in the nurse cells in these animals.
The loss of the actin mesh in the cytoplasm of stage 9 capu2/Df(2L)ed1 oocytes is rescued by expression of capuScer\UAS.P\T.cDa or capuScer\UAS.P\T.cDa.T:Avic\GFP under the control of Scer\GAL4nos.UTR.T:Hsim\VP16.
Does not interact with RpII140wimp maternal effect.
Although tud protein is present in mutant embryo extracts, its localization in the embryo is altered.
Transcripts from oskolc1 behave as those of the endogenous osk gene.
Mutation does not affect posterior follicle cell determination.
Moderate to strong capu allele.