FB2024_03 , released June 25, 2024
Allele: Dmel\Src64Bko
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General Information
Symbol
Dmel\Src64Bko
Species
D. melanogaster
Name
FlyBase ID
FBal0193616
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
src64KO
Key Links
Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description

5550bp of genomic sequence (extending from -802bp to +971bp relative to the Src64B start and stop codons respectively) has been replaced by a w+mW.hs marker.

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

In Src64Bko/+ wandering third instar larvae CadN-immunopositive adherens junctions between photoreceptor precursor cells R3 and R4 in row 5 have similar lengths as wild-type controls.

Src64Bko/+ does not significantly alter baseline neurotransmission at the NMJ of third instar larvae.

Src64Bko mutant nephrocytes exhibit morphological changes, the most significant of which is a shortening and reduction in numbers of labyrinthine channels with the consequent displacement of vacuoles and organelles towards the periphery of the cell and nephrocyte agglutination. Regions are seen that are practically devoid of filtration diaphragms and more than one diaphragm can be seen closing the entrance of the labyrinthine channels. The formation of ectopic diaphragms is observed at internal protrusions from the membrane, and this is never observed in wild type. Electron-dense material, reminiscent of adherens junctions, is seen at the membrane in regions of nephrocyte apposition.

Homozygous females lay significantly fewer eggs than wild type. 15% of these eggs hatch.

Src64BD404N/Src64Bko females lay significantly fewer eggs than wild type. 28% of these eggs hatch.

Src64BΔ17/Src64Bko females lay significantly fewer eggs than wild type. 43% of these eggs hatch.

Eggs laid by Src64BP190L/Src64Bko, Src64BG208E/Src64Bko, Src64BR217C/Src64Bko, Src64BD372N/Src64Bko or Src64BR403C/Src64Bko females hatch at a normal rate.

Ring canal diameter in homozygous egg chambers significantly smaller than wild type. Nurse cell fusion is seen in the mutant egg chambers.

Ring canal diameter in Src64BD404N/Src64Bko egg chambers significantly smaller than wild type.

Homozygous embryos derived from homozygous females show defects during cellularisation. The microfilament rings show significantly more deviation from circularity than in wild-type embryos during both early and late cellularisation.

Src64Bko females display severe fertility defects; these include severely reduced egg lay and hatch rates.

The egg chambers of Src64Bko females contain aberrantly small ring canals (on average 5.1μm diameter vs 9.1μm in wild-type females). Src64Bko ring canals exhibit defects in attaching to the cortical membrane.

Src64Bko egg chambers have aberrant cell numbers. Egg chambers with too many or too few germ cells are occasionally neighbors, and, on rare occasions, there are entirely fused ovarioles. The total number of germ cells is usually a multiple of the wild-type number of 16. In cases where adjacent egg chambers are abnormal, the sum of the two is uaually a multiple of 16 with a 15:1 ratio of nurse cells to egg chambers. For example, egg chambers have been observed with 22 nurse cells and one oocyte next to an egg chamber containing 8 nurse cells and 1 oocyte and egg chambers have also been observed with 24 nurse cells and 2 oocytes next to an egg chamber containing 6 nurse cells. The penetrance of the phenotype increases with age and temperature. Most Src64Bko egg chambers exhibit severe ring canal attachment defects, including floating ring canals and cortical membrane collapse, making it difficult to accurately score ring canal number in defective egg chambers.

Oocyte specification occurs normally in most mispackaged Src64Bko egg chambers; in most cases, oocyte absence is correlated with membrane collapse.

Src64Bko germ cells are indistinguishable from wild-type in terms of size and localization of adhesion molecules in the germarium. However, in many cases nurse cell morphology is subsequently affected by detachment of ring canals from the cortical membrane as early as stage 1. Gaps in the follicle cell layer and follicle cell polarity defects are not observed and polar and stalk cell differentiation is normal in Src64Bko ovarioles. Src64Bko egg chambers are always separated by stalks, even when egg chambers are mispackaged.

In Src64Bko germaria, cysts with aberrant cell numbers are frequently observed and, in rare cases, cells are separated from the rest of the cyst. The follicle cells in these germaria extend projections and migrate to fully surround the germline cysts. Germline cysts in Src64Bko germaria often fail to flatten in region 2B, resulting in the simultaneous packaging of side-by-side cysts. There is a higher penetrance of packaging defects in germaria versus vitellaria.

Src64BΔ17/Src64Bko transheterozygous females show egg chamber packaging defects.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference
Suppressor of
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference

Src64Bko has egg chamber phenotype, non-suppressible by Csk[+]/Cskunspecified

Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

Src64Bko is a non-enhancer of fascicle phenotype of Src42AE1

Suppressor of
Statement
Reference

Src64B[+]/Src64Bko is a suppressor of embryo | maternal effect phenotype of Cul5GM163/Cul5GM130

Src64B[+]/Src64Bko is a suppressor of larval EW neuron phenotype of fra6/fra3

Src64B[+]/Src64Bko is a suppressor of larval posterior commissure phenotype of fra6/fra3

Src64Bko/Src64Bko is a suppressor of eye phenotype of ASPP8

NOT Suppressor of
Statement
Reference

Src64Bko is a non-suppressor of fascicle phenotype of Src42AE1

Other
Additional Comments
Genetic Interactions
Statement
Reference

GluRIIASP16/GluRIIASP16 Cskc04256/Cskj1D8 Src64Bko/+ third instar larvae show significant decreases in mEPSP (decreased quantal size) partially restores significant compensatory homeostatic increases in quantal content (unlike GluRIIASP16/GluRIIASP16 Cskc04256/Cskj1D8 double mutants, which do not show significant increases in quantal content) at the NMJ. GluRIIASP16/GluRIIASP16 Src64Bko/+ third instar larvae look similar to GluRIIASP16/GluRIIASP16 larvae (significant decreases in mEPSP and compensatory homeostatic increases in quantal content) at the NMJ.

In the tracheal dorsal trunk of stage 17 Src42AE1 Src64Bko double homozygous embryos, tanedial folds are similar to controls.

A Src64Bko heterozygous background suppresses the EW axon midline crossing defects found in fra3/fra6 hypomorphic mutants.

A Src64Bko heterozygous background suppresses the EW axon midline crossing defects found in Df(1)NetABΔ mutants.

A Src64Bko heterozygous background partially suppresses the eg-positive neuron midline crossing defects found upon expression of fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360.

A Src42Ak10108/+ ; Src64Bko/+ trans-heterozygous background partially suppresses the eg-positive neuron midline crossing defects found upon expression of fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360.

Src42Ak10108/+;Src64Bko heterozygous background suppresses the eg-positive neuron midline crossing defects found upon expression of fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360.

Src42AE1/Src42Ak10108 ; Src64Bko/+ mutants display occasional wandering/defasciculation in commissural axon pathfinding but remain ipsilateral in the embryonic central nervous system.

Src42AE1/Src42Ak10108 ; Src64Bko/Src64Bko double mutants exhibit severe defects in Fas2-positive axons, with Fas2-positive ipsilateral axons often crossing the midline inappropriately. eg-positive commissural neurons do not exhibit defects in these mutants.

Src42AE1+; Src64Bko mutants display occasional wandering/defasciculation in commissural axon pathfinding but remain ipsilateral in the embryonic central nervous system.

The eye phenotype of ASPP8 homozygotes is suppressed by Src64Bko/Src64Bko.

The penetrance of egg chamber packaging defects of Src64BΔ17/Src64Bko transheterozygotes is somewhat reduced in Src64BΔ17/Src64Bko, Cskunspecified/+ females, while the penetrance of the Src64Bko phenotype is not significantly reduced in Src64Bko, Cskunspecified/+ females.

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

Expression of Src64Bosk.PO partially rescues the ring canal size defects of Src64Bko mutants, although rescued ring canals are not as large as wild type.

The egg chamber packaging defects of Src64Bko females are fully rescued by Src64Bosk.PO expression.

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Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (12)