Insertion in the 5' untranslated region, at position +58 from the predicted start of transcription.
spindle & oocyte
endos00003/endos215-4 oocytes show prolonged prophase I, failure to initiate or maintain metaphase I and highly dispersed or undetectable DNA at stage 14.
endos00003 oocytes arrest in prophase I, as occurs in wild type, but this arrest lasts longer than normal in the mutant oocytes, with 90% of mid stage 13 and 58% of late stage 13 oocytes still being in prophase I. By late stage 14, the mutant oocytes have exited prophase I, but only 3% are in metaphase I (virtually all wild-type oocytes are in metaphase I at this stage), and 93% of the mutant oocytes have dispersed or visually undetectable DNA. 87% of the mutant oocytes fail to form or maintain the meiotic spindle at stage 14 and 13% have abnormal spindle-like structures attached to the dispersed DNA.
The nuclear envelope persists for longer than normal in endos00003 oocytes.
Stage 14 mutant oocytes are not dehydrated (in contrast to wild-type oocytes at this stage) and have abnormal yolk morphology.
98% of 0- to 3-hour embryos derived from homozygous females have dispersed or undetectable DNA. Of these, approximately 25% have abnormal spindles associated with DNA masses. Approximately 2% of the embryos appear to initiate mitotic divisions, but have abnormal bipolar, tripolar or multipolar spindles.
Homozygous females show a 2-3 fold reduction in the rate of egg laying on a rich food source. The rate of follicle cell proliferation in homozygous females and control heterozygous females is very similar on a poor food source. However, on a rich food source, homozygous follicle cells proliferate at a reduced rate compared to controls. Stage 14 mutant egg chambers retain water and do not appear wrinkled (in contrast to wild-type egg chambers at this stage which appear wrinkled due to a normal process of dehydration). Once the mutant eggs are laid, they lose water and become collapsed within an hour. None of the eggs develop and the females are completely sterile. Mosaic egg chambers composed of mutant germline or mutant follicle cells, or both, develop at the same rate as and show similar morphology to that of neighbouring wild-type egg chambers. Mutant and wild-type follicle cells are observed in similar proportions in mosaic follicle cell layers, indicating that they divide at similar rates. Eggs derived from homozygous female germline clones are collapsed.
endos00003/endos215-4 has abnormal meiotic cell cycle | oogenesis phenotype, non-suppressible by tws[+]/twsj11C8
endos00003 has oocyte phenotype, suppressible by Hsap\ENSAUASp.cVSa/Scer\GAL4VP16.nanos.UTR
endos00003 has phenotype, non-suppressible by Scer\GAL4VP16.nanos.UTR/tweUASp.Tag:MYC
endos00003 has phenotype, non-suppressible by twehs.PVS
twsj11C8/+ does not rescue the meiotic maturation defect of endos00003/endos215-4 oocytes.
Expression of tweScer\UAS.P\T.T:Hsap\MYC under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 does not rescue the defects of endos00003 females.
Expression of twehs.PVS using heat shock does not rescue the defects of endos00003 females.
Expression of Hsap\ENSAScer\UAS.P\T.cVSa under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 significantly rescues the oocyte and fertility defects of endos00003 females.
endos00003 is rescued by Scer\GAL4VP16.nanos.UTR/endosUASp.cKa
endos00003 is rescued by endosS107A.UASp/Scer\GAL4VP16.nanos.UTR
endos00003 is rescued by endosUASp.cVSa/Scer\GAL4VP16.nanos.UTR
endos00003 is not rescued by Scer\GAL4VP16.nanos.UTR/endosS68A.UASp
endos00003 is not rescued by Scer\GAL4VP16.nanos.UTR/endosS68D.UASp
Expression of either endosS68D.Scer\UAS.P\T or endosS68A.Scer\UAS.P\T under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 fails to rescue meiotic maturation in endos00003 oocytes.
Expression of either endosScer\UAS.P\T.cKa or endosS107A.Scer\UAS.P\T under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 rescues meiotic maturation in endos00003 oocytes.
Precise excision of the P-element rescues the female sterile phenotype.