FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\FakCG1
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General Information
Symbol
Dmel\FakCG1
Species
D. melanogaster
Name
FlyBase ID
FBal0183605
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Fak56DCG1, Fak56CG1, DFakCG1
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description

Imprecise excision of the P{SUPor-P} element that removes the entire element and 1887bp of the Fak56D gene. This removes the first 1263bp of coding sequence, corresponding to the first 421 amino acids of Fak56D.

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 ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 1 )
 

FakCG1 exacerbates the phenotypes seen in RetMEN2A.Scer\UAS when heterozygous with Fak5-SZ-3124.

Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

FakCG1/+ larvae do not display increased dendrite crossing in the class IV dendrite arborizing neurons.

Eyes from FakCG1 null mutants display normal patterning.

Synapse number is highly variable in Fak56DCG1 mutant larvae. There is a tendency for synapse number to decrease, rather than increase, compared to wild-type.

Boutons in Fak56DCG1 mutants often appear to be larger in size than wild-type.

Expression of Fak56DScer\UAS.T:Ivir\HA1 in motor neurons under the control of Scer\GAL4D42 in a Fak56DCG1 background increases axon diameter.

Fak56DCG1 larvae show an increased rate of onset of long term facilitation. EJP amplitude at 0.15mM and 0.2mM Ca[2+] concentrations is significantly increased but is not significantly different from wild-type amplitudes at 0.1mM Ca[2+] concentration in this mutant.

Miniature EJPs are unaffected in these mutants.

Expression of Fak56DScer\UAS.T:Ivir\HA1 in motor neurons under the control of Scer\GAL4D42 in a Fak56DCG1 background does not affect miniature EJP amplitude.

The neuromuscular junction is overgrown and shows an increase in bouton number in mutant third instar larvae.

Photoreceptor axons fail to form a bundle at the optic stalk in homozygous mutants. In addition, the optic stalk itself is also severely disrupted, with about 80% of animals showing significant defects in optic stalk morphogenesis (the length of the stalk is less than or only equal to the diameter of the stalk, in contrast to the wild type where the length of the stalk is at least two times bigger than the diameter). These optic stalk defects are not detected until the early third larval instar and they become progressively more severe as development proceeds through the third larval instar.

Surface glia (SG) cells of the optic stalk fail to form a tubular structure in mutants, but instead spread over the surface of the optic lobe. This defect in CG cell localisation occurs before photoreceptor cell axon innervation. The SG cells show the same elongated morphology as wild type. However, analysis of small marked clones indicates that SG cells in mutant animals disperse along the anterior-posterior axis to a lesser extent than wild-type cells examined under the same conditions.

Homozygous embryos show no obvious muscle disruption phenotypes compared to wild-type embryos. and no obvious defects in the migration of primordial midgut cells are seen.

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

FakCG1 has embryonic/larval optic stalk phenotype, enhanceable by mys1/mys[+]

FakCG1 has embryonic/larval optic stalk phenotype, enhanceable by mys11/mys[+]

Enhancer of
Statement
Reference

FakCG1/Fak[+] is an enhancer of eye phenotype of RetGMR.PR

FakCG1 is an enhancer of eye phenotype of RetGMR.PR

FakCG1/Fak56D[+] is an enhancer of embryonic/larval optic stalk phenotype of mys1

FakCG1/Fak56D[+] is an enhancer of embryonic/larval optic stalk phenotype of mys11

FakCG1/Fak56D[+] is an enhancer of embryonic/larval optic stalk phenotype of CdGAPrNP3053

NOT Enhancer of
Suppressor of
NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

FakCG1,Df(2R)Sema-2b-C4 double mutant larvae do not display increased dendrite crossing in the class IV dendrite arborizing neurons.

Heterozygous FakCG1 enhances the ommatidial mis-patterning seen in eyes expressing RetGMR.PR. Homozygous FakCG1 causes a smaller eye due to a completely disrupted ommatidial pattern. This enhancement is reversed upon co-expression of either FakScer\UAS.T:Ivir\HA1 or FakY430F.Scer\UAS under the control of Scer\GAL4GMR.PU.

The retinas of pupae (42 hours after pupal formation) expressing RetGMR.PR in a homozygous FakCG1 mutant background lack the hexagonal array and identifiable ommatidial units. Numerous ct-positive cone cells are seen. Some bristle cells and a few cells recognisable as primary pigment cells remain, but there are no detectable cells with the appearance of normal interommatidial cells. Ommatidial units with extranumerary cone cells are also seen at early stages of development (4 hours after pupal development). Eye discs contain normal number of photoreceptors, albeit some clusters have rotation defects.

FakCG1/Fak5-SZ-3124 enhances the partial lethality and wing disc defects seen when RetMEN2A.Scer\UAS is expressed under the control of Scer\GAL4dpp.PU. The proportion of surviving flies rises from 46% to 92%.

A Fak56DCG1 background completely suppresses the increased synapse number conferred by CaMKIIT287D.Scer\UAS expression. Synapse number in these double mutants is indistinguishable from that in Fak56DCG1 single mutants.

The increase in synapse number seen in larvae expressing Pi3K92EScer\UAS.T:Hsap\MYC,T:Hsap\CAAX in motor neurons under the control of Scer\GAL4D42 is unaffected by a Fak56DCG1 background.

The axon diameter increase seen upon expression of CaMKIIT287D.Scer\UAS under the control of Scer\GAL4D42 is suppressed by a Fak56DCG1 mutant background.

The axon diameter increase seen upon expression of Pi3K92EScer\UAS.T:Hsap\MYC,T:Hsap\CAAX under the control of Scer\GAL4D42 is unaffected by a Fak56DCG1 mutant background.

Fak56DCG1/+; p130CAS1/Df(3L)Exel6083 adults do not emerge, indicating complete lethality. Analysis of the Fak56DCG1/Fak56DCG1; p130CAS1/+ lethal phenotype indicates that most (95%) of the embryos do not hatch. The few escapers survive to pupal stages, but do not emerge. Only 5% of Fak56DCG1; p130CAS1 double homozygotes produce cuticles and almost all are marked by dorsal and/or ventral holes, indicating dorsal closure defects. These cuticles also show fused or missing denticle belts.

CdGAPrNP3053 Fak56DCG1 double heterozygotes show severe defects in optic stalk morphology, in contrast to either single heterozygote, which show only slight defects in optic stalk formation.

CdGAPrEY13451 Fak56DCG1 double heterozygotes show severe defects in optic stalk morphology, in contrast to either single heterozygote, which show only slight defects in optic stalk formation.

Fak56DCG1 mys1 double heterozygotes show more severe defects in optic stalk morphology than either single heterozygote, which each show only slight defects in optic stalk formation.

Fak56DCG1 mys11 double heterozygotes show more severe defects in optic stalk morphology than either single heterozygote, which each show only slight defects in optic stalk formation.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Not rescued by
Comments

Expression of Fak56DScer\UAS.T:Ivir\HA1 in motor neurons under the control of Scer\GAL4D42 restores normal glutamate sensitivity to Fak56DCG1 mutants.

Expression of Fak56DScer\UAS.T:Ivir\HA1 in motor neurons under the control of Scer\GAL4D42 restores wild-type levels of long term facilitation in Fak56DCG1 mutants.

The increased EJP amplitude found in Fak56DCG1 mutants is rescued by motor neuron-dependent expression of Fak56DScer\UAS.T:Ivir\HA1.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (12)