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General Information
Symbol
Dmel\dock3
Species
D. melanogaster
Name
FlyBase ID
FBal0049422
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
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

510bp region extending from base pair 48 in the first exon to the P{PZ} insertion site of dock04723 is deleted and replaced by a 15bp sequence of unknown origin.

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

dock3 mutants display a delay in neuromuscular junction formation by the RP3 motorneuron on the muscle 6/7 pair. No defects are associated with loss of one copy of dock.

About 5% of heterozygotes exhibit some Bolwig's nerve targeting defects. About 44% of Df(2R)EW60/dock3 embryos exhibit some Bolwig's nerve targeting defects.

In dock13421/dock3 mutant embryos longitudinal connectives are more wavy and more varied in thickness than wild type and the outermost one is occasionally interrupted. There are low penetrance defects in muscle organization. The muscle phenotype is not affected further in embryos lacking both maternal and zygotic dock activity. dock13421/dock3 mutant embryos (and homozygotes of both alleles) show a variable absence of the synapse between RP3 and muscles 7 and 6. Outgrowth of RP3 from the CNS is normal. Synapse formation eventually occurs, but is delayed. No ectopic synapses occur. This phenotype is identical to that of lbmY13.

Some homozygotes survive to adulthood. These flies are sluggish and uncoordinated, dying within a few days after eclosion. Homozygous third instar larvae exhibit defects in receptor cell fasciculation, targeting and retinotopy.

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

dock3 is an enhancer of abnormal neuroanatomy phenotype of robo15, sli1

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

dock3 has phenotype, non-enhanceable by lbmY13

NOT suppressed by
Statement
Reference

dock3 has phenotype, non-suppressible by lbmY13

Enhancer of
Statement
Reference

dock3 is an enhancer of Bolwig nerve phenotype of Dscam105518

NOT Enhancer of
Statement
Reference

dock3 is a non-enhancer of ommatidium phenotype of dshhs.sev.B

dock3 is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, msnEP549

NOT Suppressor of
Statement
Reference

dock3 is a non-suppressor of ommatidium phenotype of dshhs.sev.B

dock3 is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, msnEP549

Other
Additional Comments
Genetic Interactions
Statement
Reference

ISNb pathfinding is delayed in approximately 23% of dock3 cknK.Δ324-331 double heterozygotes.

A heterozygous cknK.Δ324-331 background enhances ISNb pathfinding defects in dock3 homozygotes, from 6% to 43% of hemisegments.

dock3 cknK.Δ324-331 double homozygotes exhibit delayed 'immature' ISNb axons in 65% of hemisegments. Motor axons in the affected nerves are loosely organised with multiple projections and resemble wild-type axons at earlier stages. Furthermore, the ISNd branch is frequently absent or reduced in size. Examination of the ISNb/d choice point reveals defects in ISNb/d branch segregation. The lateral two longitudinal Fas2-positive fascicles are poorly fasciculated and discontinuous in these double mutants.

When enaGC5/enaGC1 and homozygous dock3 are combined only a mild additive effect is see on the longitudinal exon guidance phenotype. Heterozygous dock3 enhances the longitudinal axon ectopic midline crossing defect seen in transheterozygous sli1, robo5 mutants. An average of 5.7 defects are seen per animal. 52% of segments (calculated as number of defects/segments) show defects.

About 42% of Dscam05518/dock3 embryos exhibit some Bolwig's nerve targeting defects.

The ommatidial polarity defects seen in dshhs.sev.B flies grown at 29oC are not affected by the addition of dock3. Has no effect on the ommatidial polarity phenoptype seen in flies with msnEP549 driven by Scer\GAL4hs.2sev.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (7)