No mutations are detected in the protein coding region.
actin filament & egg chamber
Eggs produced by females carrying homozygous germline clones have exactly the same range of phenotypes as those derived from homozygous females; the eggs are smaller than normal and have single or double, short and broad dorsal appendages.
Chromatin fails to decondense in the nuclei of stage 10 nurse cells of egg chambers containing homozygous germ-line clones; some nuclei have a "five blob" organisation (a pattern characteristic of younger egg chambers) and some show inhomogeneous distribution of chromatin.
Mutant females produce eggs with a "dumpless" phenotype.
Border cells in stage 9 egg chambers of homozygous females migrate ahead of border cells in wild-type egg chambers, relative to main-body follicle cell (MBFC) migration and reach the anterior margin (the border between the oocyte and nurse cells) sooner than the MBFCs do.
Border cell migration is normal in egg chambers of females containing homozygous germ-line clones, but these egg chambers show aberrant centripetal follicle cell migration.
Eggs laid by homozygous females containing follicle cell clones are indistinguishable from those laid by their wild-type siblings. Border cell migration is normal in some egg chambers containing follicle cell clones, and is accelerated in others, independent of the size or position of the follicle cell clone. Border cell clusters that are completely mutant do form and are able to complete their migration to the anterior margin (the border between the oocyte and nurse cells). Mosaic border cell clusters containing both mutant and wild-type cells sometimes migrate normally and sometimes show accelerated migration. Precociously migrating border cell clusters show a loss of alignment of the polar cells (they are normally aligned in parallel to the direction of migration of the border cell cluster).
Approximately 35-40% of stage 10B-12 egg chambers of heterozygous or homozygous females show excessive actin bundling along the central region of the nurse cell cluster, most prominently at the posterior of the nurse cell cluster.
eggs laid by homozygous females have dorsal-ventral polarity defects and have a range of dorsal appendage phenotypes. 20% have normal dorsal appendages, 32% have fused dorsal appendages with extra material at the tip, 4% have residual or no dorsal appendages, 37% have short, broad, paddle-like dorsal appendages, 5% have one broad dorsal appendage on the midline, and less than 3% have a net-like chorion with no apparent dorsal-ventral polarity.
More than 50% of stage 11 or older egg chambers have a "dumpless" phenotype, where the nurse cells fail to transfer their entire content into the oocyte, in homozygous females. This results in eggshells with an open anterior end. The ring canals appear to have normal morphology in homozygous egg chambers.
The shape of centripetal follicle cells at the edge of migration is abnormal in homozygous stage 10 egg chambers.
Only 4.5% of egg chambers older than stage 6 have nurse cell nuclei with normal appearance in homozygous females. 4.5% display a characteristic "five-blob" appearance (which is normally seen at earlier stages in wild-type egg chambers), 60% have a loose "five-blob" appearance and 31% have an inhomogeneous distribution of chromatin.
spoon1/spoon[+] is a suppressor | partially of dorsal appendage phenotype of cup1
spoon1/spoon[+] is a suppressor of dorsal appendage phenotype of chic01320
spoon1/spoon[+] is a suppressor of dorsal appendage phenotype of qua1
Only 39.2% of eggs laid by qua1/+ spoon1/+ double heterozygous females have short and broad double or single dorsal appendages.
Only 13.4% of eggs laid by chic01320/+ spoon1/+ double heterozygous females have a mutant phenotype.
Only 15.1% of eggs laid by cup1/+ spoon1/+ double heterozygous females have a mutant dorsal appendage phenotype.
The reduced actin bundling seen in the nurse cells of stage 10B-12 egg chambers of qua1/+ females is suppressed by spoon1/+, with less than 20% of the double mutant egg chambers showing an actin polymerisation defect.
Separable from: an unrelated P-element insertion.