FB2024_03 , released June 25, 2024
Allele: Dmel\Src64BPI
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General Information
Symbol
Dmel\Src64BPI
Species
D. melanogaster
Name
FlyBase ID
FBal0093202
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Src64BP1, Src64P1
Key Links
Nature of the Allele
Cytology
Description

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.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Enhancer of
Statement
Reference

Src42AE1, Src42A[+], Src64B[+], Src64BPI is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of FakK24/FakN30

Suppressor of
Statement
Reference

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

Other
Phenotype Manifest In
Enhanced by
Statement
Reference

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

NOT Enhanced by
Statement
Reference

Src64BPI has nurse cell phenotype, non-enhanceable by Src42A26-1

Suppressed by
Statement
Reference
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

Src64BPI is a suppressor of eye phenotype of RetMEN2B.GMR

Src64BPI is a suppressor of eye phenotype of RetMEN2A.GMR

Other
Additional Comments
Genetic Interactions
Statement
Reference

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.

Src64BPI capt10 double heterozygotes do not show significant midline crossing defects in the embryonic central nervous system.

Src42Amyri; Src64BPI double homozygous embryos have a mild but clear dorsal open phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Partially rescued by
Comments

Does not complement the cytoplasmic transfer defect of Src64BΔ17.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

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.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (17)