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General Information
Symbol
Dmel\Src42Ak10108
Species
D. melanogaster
Name
FlyBase ID
FBal0064225
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Src42Al(2)k10108, l(2)k10108, Src42K10108
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

P{lacW} insertion in the 5' untranslated region.

Insertion components
P{lacW}Src42Ak10108
Product class / Tool use(s)
Encoded product / tool
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 ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

In Src42Ak10108/+ 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.

Src42Ak10108/+ adults show a significantly impaired intestinal stem cell proliferation (regeneration) response in midguts after feeding flies with pathogenic bacteria.

Src42Ak10108 homozygous embryos hatch, but die as first instar larvae from defects in tail morphology, head involution, and tracheal necrosis.

Homozygotes die as first instar larvae. Src42Ak10108/Df(2R)nap9 animals show defects in head involution, tail morphology and tracheal necrosis.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Enhancer of
Statement
Reference
Suppressor of
NOT Suppressor of
Statement
Reference

Src42Ak10108 is a non-suppressor of lethal | pupal stage phenotype of Cskj1D8/CskS030003

Src42Ak10108 is a non-suppressor of lethal phenotype of Raf1

Other
Phenotype Manifest In
Enhanced by
Statement
Reference
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

Src42Ak10108 is a non-enhancer of eye phenotype of Ras85DV12.sev

Src42Ak10108 is a non-enhancer of ommatidium phenotype of Ras85DV12.sev

Suppressor of
Statement
Reference

Src42Ak10108 is a suppressor of eye phenotype of RetMEN2B.GMR

Src42Ak10108 is a suppressor of eye phenotype of RetMEN2A.GMR

Other
Additional Comments
Genetic Interactions
Statement
Reference

GluRIIASP16/GluRIIASP16 Cskc04256/Cskc04256 Src42Ak10108/+ third instar larvae show significant decreases in mEPSP (decreased quantal size) but do not show significant compensatory homeostatic increases in quantal content (similar to GluRIIASP16/GluRIIASP16 Cskc04256/Cskc04256 double mutants) at the NMJ. GluRIIASP16/GluRIIASP16 Src42Ak10108/+ third instar larvae look similar to GluRIIASP16/GluRIIASP16 larvae (significant decreases in mEPSP and compensatory homeostatic increases in quantal content) at the NMJ.

A Src42Ak10108 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.

Synthetic lethality is found in p130CAS1 homozygotes with a Src42Ak10108 heterozygous or homozygous background, with fewer than 46% of the double mutant embryos hatch. 90% of the cuticles of the double mutants have holes in or absence of the head cuticle and 10% of the double mutants exhibit additional germ band retraction defects.

Src42Ak10108/+; p130CAS1/Df(3L)Exel6083 mutants are semi-viable, emerging at approximately 50% of the rate of phenotypically normal adult siblings from the same cross.

The low percentage of Src42Ak10108/+; p130CAS1/p130CAS1 adult escapers manifest wing blister defects.

Approximately 90% of Src42Ak10108; p130CAS1 double mutants have holes in or completely absent head cuticles and 10% of these embryos exhibit germ band retraction cuticle defects.

Does not suppress the lethality of phl1.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Fails to complement three (unnamed) alleles of the SK2-4 complementation group.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (17)