egg chamber & actin cytoskeleton | germ-line clone
Btk29Ak00206; pcsgs/pcsgs females show a suppression of the grandchildless phenotype and the early embryonic patterning phenotype compared to pcsgs/pcsgs females. However, the muscle development phenotype of pcsgs embryos is not suppressed by Btk29Ak00206.
The Btk29Ak00206 salivary gland phenotype is enhanced in chic221, Btk29Ak00206 double mutants as more cells remain on the surface at stage 14 compared with Btk29Ak00206 single mutants. The amount of actin disorganization that precedes the salivary gland phenotype is also increased in these double mutants. Additionally, chic221, Btk29Ak00206 double mutants exhibit a higher level of uncoordinated endoreplication at early stage 12, prior to the invagination defects, than Btk29Ak00206 single mutants. The actin disorganization and salivary gland phenotypes of Btk29Ak00206 single mutants are rescued in Btk29Ak00206; tsrk05633 double mutants. However, there is no decrease in the endoreplication defect seen in Btk29Ak00206 single mutants in the double mutants. Expression of CycEScer\UAS.cRa, under the control of Scer\GAL4prd.RG1, rescues the long salivary gland phenotype either completely or partially in 69% of Btk29Ak00206 embryos. Btk29Ak00206; Src42AE1 embryos show an enhanced salivary gland invagination phenotype compared to Btk29Ak00206 single mutants. More salivary glands show premature endoreplication in the double mutants. The double mutants also show the disorganised actin phenotype although it is not clear whether this is enhanced compared to Btk29Ak00206 embryos. Btk29Ak00206; Src64BPI double mutant embryos suffer gross abnormalities, such as lack of head segments. Btk29Ak00206/+; Src64BPI/+ double heterozygotes have no salivary gland defects, while around one third of Btk29Ak00206/+; Src64BPI double mutants show invagination defects.
Reducing the Btk29A dose in Src64BΔ17 homozygotes enhances the defective ovariole phenotype at room temperature: 57% of ovarioles contain fused egg chambers in Btk29Ak00206/+; Src64BΔ17 mutants. 45% of Btk29Ak00206/+; Src64BΔ19 double mutant ovarioles contain fused egg chambers. Most of the fused egg chambers, and some of the unfused, display features of apoptosis.
Strong dominant enhancer of the Ras85Dix12a eggshell phenotype; 0-20% of dorsal appendages are wild type.
The tor12D maternal effect phenotype is partially suppressed by homozygosity for Btk29Ak00206; embryos show a significant increase in the number of ventral denticle belts. The tor12D phenotype is also partially suppressed by Btk29Ak00206/Df(2L)TE29Aa-11.
Btk29Ak00206 Src42Amyri/Btk29Ak05610 Src42Amyri double homozygotes show complete embryonic lethality and some embryos have a dorsal open phenotype. The leading edge cells are only partially elongated during dorsal closure. The dorsal open phenotype is partially rescued by JraAsp.hs.sev. Dominantly enhances the lethality of Src42AJp45.
Posterior spiracle defects (length of the spiracular lumen and area of the spiracular chamber) seen in Btk29Ak00206 embryos are rescued by expression of Btk29AScer\UAS.RC under the control of Scer\GAL4salm-459.2.