Local transposition of P{lwB.D}BGT-T063-w.mut; the original P{lwB.D}BGT-T063-w.mut insertion remains, and a second insertion (P{lwB.D}Src64BPI) is present in the second intron, approximately 2.5kb downstream of the original insertion.
alpha-lobe & axon
beta-lobe & axon
Mutant embryos have salivary glands that curve ventrally at the tip, instead of lying parallel to the midline as in wild-type embryos.
Src64BPI embryos show no salivary gland abnormalities.
After several generations, the fertility of Src64BPI homozygous lines increases and the number and severity of egg chamber defects decreases. In the ovarioles of Src64BPI mutants, 25% contain fused egg chambers at 18oC; this value drops to 15% at 25oC. Germline clones for Src64BPI have similar morphology (18oC - 30%).
Ovaries of Src64BPI mutants show nurse cell fusions.
Src64BPI is homozygous viable and shows a clear mushroom body phenotype. The beta lobes fuse, the alpha axons are reduced in number and both sets of axons show defasciculation. When analyzed in clones in the mushroom body, the axons of the beta-lobe cross the interhemispheric boundary. This phenotype is more penetrant when Src64BPI is hemizygous than when it is homozygous.
The diameters of the inner and outer rims of the ring canals are smaller than normal in homozygous females.
Homozygous females have reduced fertility; eggs laid by these females hatch at a reduced frequency (5.5%) compared to wild-type. Egg chambers of homozygous females show a defect in cytoplasmic transfer; in contrast to wild-type, 55% of late stage homozygous egg chambers have nurse cell cytoplasm remaining at the anterior end of the oocyte. Eggs from these females range in length from 50-100% wild-type egg length. Ring canals are smaller than wild-type, and show defects in growth during both early and late stages of their morphogenesis. Approximately 70% of stage 9-10 egg chambers show fusions between nurse cells. 45% of stage 10A egg chambers contain fewer than 15 ring canals.
Src64BPI has abnormal neuroanatomy phenotype, enhanceable by Df(2R)lio2
Src64B[+]/Src64BPI is an enhancer of embryonic/larval segmentation phenotype phenotype of Src42A26-1/Src42A[+], Stat92E06346
Src42AE1, Src42A[+], Src64B[+], Src64BPI is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of FakK24/FakN30
Src64BPI is a suppressor of visible phenotype of RetMEN2B.GMR
Src64BPI is a suppressor of visible phenotype of RetMEN2A.GMR
Src64BPI is a suppressor of lethal | pupal stage phenotype of Cskj1D8/CskS030003
Src64B[+]/Src64BPI is a suppressor of abnormal neuroanatomy phenotype of RhoGAPp190RNAi.GAP.UAS, Scer\GAL4ey-OK107
Src42AE1/Src42A[+], Src64BPI has abnormal neuroanatomy | third instar larval stage phenotype
FakN30/FakKG00304, Src64B[+]/Src64BPI has abnormal neuroanatomy | third instar larval stage phenotype
Src64BPI has egg chamber phenotype, enhanceable by Btk29A[+]/Btkk05610
Src64BPI has beta-lobe & axon phenotype, enhanceable by Df(2R)lio2
Src64BPI has mushroom body phenotype, enhanceable by Df(2R)lio2
Src64BPI has nurse cell phenotype, non-enhanceable by Src42A26-1
Src64BPI has outer nurse cell ring canal rim phenotype, suppressible by Akap200k07118a/Akap200[+]
Src64BPI has inner nurse cell ring canal rim phenotype, suppressible by Akap200k07118a/Akap200[+]
Src64B[+]/Src64BPI is an enhancer of embryonic/larval spiracle phenotype of Src42A26-1/Src42A[+], Stat92E06346
Src64B[+]/Src64BPI is an enhancer of embryonic head phenotype of Src42A26-1/Src42A[+], Stat92E06346
Src64BPI is an enhancer of embryonic/larval dorsal tracheal branch | embryonic stage phenotype of Src42Amyri
Src42AE1, Src42A[+], Src64B[+], Src64BPI is an enhancer of neuromuscular junction | third instar larval stage phenotype of FakK24/FakN30
Src64BPI is an enhancer of presumptive embryonic salivary gland phenotype of Btkk00206
Src64B[+]/Src64BPI is an enhancer of embryo | dorsal closure stage phenotype of Src42A26-1
Src64BPI is a suppressor of eye phenotype of RetMEN2B.GMR
Src64BPI is a suppressor of eye phenotype of RetMEN2A.GMR
Src64B[+]/Src64BPI is a suppressor of mushroom body vertical lobe phenotype of RhoGAPp190RNAi.GAP.UAS, Scer\GAL4ey-OK107
Src42AE1/Src42A[+], Src64BPI has neuromuscular junction | third instar larval stage phenotype
FakN30/FakKG00304, Src64B[+]/Src64BPI has neuromuscular junction | third instar larval stage phenotype
FakN30/FakKG00304, Src64B[+]/Src64BPI has NMJ bouton | increased number | third instar larval stage phenotype
Btkk00206, Src64BPI has embryonic head segment phenotype
Src42A26-1, Src64B[+]/Src64BPI has embryonic leading edge cell phenotype
Src42A26-1, Src64BPI has tracheal branch primordium phenotype
Src42A26-1, Src64B[+]/Src64BPI has embryonic head phenotype
Src42A26-1, Src64B[+]/Src64BPI has Bolwig organ phenotype
Src42A26-1, Src64B[+]/Src64BPI has tracheal branch primordium phenotype
Src42A26-1, Src64BPI has mitotic domain 1 | extended germ band stage phenotype
Src42A26-1, Src64BPI has embryonic leading edge cell phenotype
Src42A26-1, Src64BPI has embryonic head phenotype
Src42A26-1, Src64BPI has Bolwig organ phenotype
Src42Amyri, Src64BPI has embryonic/first instar larval cuticle | dorsal phenotype
Src42A26-1/+ ; Src64BPI/+ double heterozygous embryos have normal cuticles.
Src42A26-1/+ ; Stat92E06346/+ double heterozygous embryos show defects in head formation and have segmentation and spiracle defects. This phenotype is enhanced if the embryos are also heterozygous for Src64BPI.
Src64BPI enhances the tracheal defects seen in Src42Amyri mutant embryos. Many dorsal branches fail to extend correctly, remaining in a multicellular state despite the progression of dorsal closure.
Significant overgrowth of the neuromuscular junction (NMJ) (increased bouton number per muscle area and increased NMJ length per muscle area) is seen in Src64BPI/+ FakN30/FakKG00304 third instar larvae.
Significant overgrowth of the NMJ (increased bouton number per muscle area) is seen in Src42AE1/+ ; Src64BPI/Src64BPI third instar larvae.
The overgrowth at the NMJ (increased bouton number per muscle area) seen in FakN30/FakK24 third instar larvae is enhanced if they are also carrying both Src42AE1/+ and Src64BPI/+.
drlR343 ; Src64BPI double heterozygotes show salivary gland guidance defects; the tips of the salivary glands curve ventromedially towards the central nervous system, instead of lying parallel to the midline as in wild-type embryos.
The salivary glands of drlR343 ; Src64BPI double homozygous embryos show a similar frequency of guidance defects as that seen in either of the single mutants alone.
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 Src64BPI homozygotes enhances the defective ovariole phenotype: 70% of ovarioles contain fused egg chambers in Btk29Ak05610/+; Src64BPI mutants.
34% of Src42A26-1; Src64BPI/+ embryos show a dorsal open phenotype and head involution defects. These embryos have misrouted longitudinal axons, but appear to have a normal number of neurons. The formation of Bolwig's organ and the trachea is significantly disrupted. Src42A26-1; Src64BPI embryos show more severe phenotypes than Src42A26-1; Src64BPI/+ embryos, with no germband retraction. The ovaries of Src42A26-1/+; Src64BPI/+ mutants show no nurse cell fusions. The nurse cell phenotype of Src64BPI ovaries is not enhanced in Src42A26-1; Src64BPI double mutants. Src42A26-1; Src64BPI/+ embryos exhibit almost normal cell-shape change at 9 hours AEL, but at later stages the leading edge is frequently kinked with partial dorsal-most epidermal cell deformation.
The small ring canal phenotype see in Src64BPI homozygous females is dominantly suppressed by Akap200k07118a.
Src42Amyri; Src64BPI double homozygous embryos have a mild but clear dorsal open phenotype.
Src64BPI is partially rescued by Src64BαTub67C.PD
Does not complement the cytoplasmic transfer defect of Src64BΔ17.
The reduction in female fertility and the defect in cytoplasmic transfer are reverted by excision of the P{lwB.D} element in the second intron.