FB2024_03 , released June 25, 2024
Allele: Dmel\dock04723
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General Information
Symbol
Dmel\dock04723
Species
D. melanogaster
Name
FlyBase ID
FBal0008069
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dockP1, l(2)04723
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description

P{PZ} insertion in intron 1.

P{PZ} insertion in intron 1 of the CT42218 and CT12313 transcripts of dock, 798bp and 827bp downstream of the 5' end of the transcripts respectively.

P{PZ} insertion 18bp downstream of the first exon-intron boundary.

Allele components
Component
Use(s)
Inserted element
Encoded product / tool
Mutations Mapped to the Genome
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

antennal lobe & neuropil

eye photoreceptor cell & growth cone

glial cell & antennal lobe

neuron & antennal lobe

photoreceptor & axon

photoreceptor & axon | somatic clone

photoreceptor cell & axon

photoreceptor cell & axon (with dock4)

photoreceptor cell R1 & axon

photoreceptor cell R2 & axon

photoreceptor cell R3 & axon

photoreceptor cell R4 & axon

photoreceptor cell R5 & axon

photoreceptor cell R6 & axon

photoreceptor cell R7 & axon

photoreceptor cell R7 & axon | somatic clone

RP3 neuron & synapse

Detailed Description
Statement
Reference

dock04723 homozygous embryos show defects in dendritogenesis in the embryonic aCC motoneurons (misplacement of primary branches) compared to controls.

The muscle pattern appears similar to wild type in mutant embryos.

dock04723/+ mutant third instar larval eye discs do not show disrupted axon targeting from photoreceptor neurons to the brain optic lobes.

The initial stages of mesoderm spreading during mesoderm morphogenesis are normal in mutant embryos.

In dock04723 homozygous adults the antennal lobes are small and mis-shapen compared to wild-type, and have amorphous neuropil. Antennal glomeruli DM2 and DM3 are severely mis-shapen or split into smaller structures that are scattered randomly around the antennal lobe. The integrity and position of VA11m is unaffected, but it is enlarged and extends into the domains of surrounding glomeruli, in most cases completely engulfing the adjacent VA1d. Projection neurons and glial cells differentiate normally in antennal lobes of the mutants, but dendritic arborization of the projection neurons is more diffuse than in wild-type, and the number of glial processes is somewhat reduced. The development of neurons within the antennae appears normal. When somatic clones of dock04723 are induced in the eye-antennal disc, but not the brain (using Scer\FLP1ey.PN), the antennal lobes are severely mis-shapen and aglomerular, and olfactory neuron axons terminate in ectopic locations. In dock04723 homozygous pupae 30 hours after puparium formation (hAPF) the pattern of olfactory neuron projections from the antennae is normal. However, once in the antennal lobe, the axonal trajectories are clearly abnormal: instead of forming characteristic tracks, the fibers interweave to form a dense mat. Occasionally these axons leave the antennal lobe, and instead extend aberrantly into dorsal brain regions. Most axonal branches in the antennal lobe fail to reach their destination, instead terminating in ectopic mis-shapen glomeruli. Occasionally extra axon branches are seen, but they are short and not associated with ectopic glomeruli.

Mutant embryos that lack both maternal and zygotic dock, exhibit commissures that are generally thicker than wild-type, while longitudinals are reduced - many axons are seen to inappropriately cross the midline. An average of 70% of segments exhibit defects, and average of 7.7 defects are seen animal. 18% of embryos also exhibit defects in pCC/MP1.

In mosaic larvae in which homozygous clones have been induced in the eye, photoreceptor cell axons fail to target the optic lobe properly; gaps and clumps of axons are seen. The pattern of R7 and R8 projections in the medulla shows defects in mosaic adults in which homozygous clones have been induced in the eye; crossing of fibres, uninnervated regions and gaps in the R7 layer are seen. Heterozygotes have normal photoreceptor cell projections in the medulla.

When mutant somatic clones are made in the border cells no effect is seen.

14% of dock4/dock04723 animals show defects in photoreceptor axon projection, having a "medulla bypass" phenotype.

About 5% of heterozygotes exhibit some Bolwig's nerve targeting defects. In dock04723/dock13421 embryos, either the entire Bolwig's Nerve, or a subset of its axons project to ectopic positions. These defects have over a 90% penetrance.

The removal of dock04723 function in the eye by making clones in a Minute background causes the same phenotype as homozygosity for dock04723. The R7 and R8 axons in dock04723 mutants lack expanded growth cones and fail to form an even array in the medulla.

Mutant embryos 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. Maternal loss of dock expression enhances the CNS longitudinal axon defects, but not the RP3 synapse formation delay.

Many R1-R6 photoreceptor cell axons migrate ectopically into the medulla in homozygous larvae, passing their normal target (the lamina), generating gaps in the lamina R1-R6 termination site. Fasciculation and growth cone morphology of the photoreceptor cell axons is also altered. Abnormal large axon bundles are seen in both the lamina and medulla. The phenotype is completely penetrant.

R cell projections in both the lamina and medulla are disorganised. Large axon bundles form: bundles contain R1-R6 neurons that fail to terminate in the lamina.

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. The plexus of receptor cell terminals in the lamina is uneven. Bundles do project into the medulla where they establish an uneven array of terminals. Grouping of axons in the optic stalk is also aberrant. The pattern of proliferation of optic lobe neuroblasts and lamina precursors is indistinguishable from wild type. Lamina and neurons are disorganised, this is a likely consequence of defects in receptor cell innervation rather than an intrinsic defect in neurons or glia. Structure of the medulla neuropile is abnormal. Mosaic heads reveal that projections of mutant fibres in the medulla terminal field are abnormal, gaps are present in the R7 terminal field and fibres cross between columns. Some R1-R6 axons underlying mutant patches project into the medulla. Most ommatidia in mosaic patches are indistinguishable from wild type. A small number of receptor cells are missing, this may reflect a weak defect in cell survival due to abnormal innervation.

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

dock04723 is a non-suppressor of visible phenotype of RetMEN2B.GMR

Other
Phenotype Manifest In
Enhanced by
Statement
Reference

dock04723 has fascicle phenotype, enhanceable by sli2

dock4/dock04723 has phenotype, enhanceable by trio8/trio[+]

dock4/dock04723 has photoreceptor cell & axon phenotype, enhanceable by trio8/trio[+]

dock4/dock04723 has phenotype, enhanceable by trio4/trio[+]

dock4/dock04723 has photoreceptor cell & axon phenotype, enhanceable by trio4/trio[+]

dock04723 has photoreceptor & axon phenotype, enhanceable by msn102

NOT Enhanced by
Statement
Reference

dock04723 has phenotype, non-enhanceable by lbmY13

Suppressed by
Statement
Reference

dock04723 has eye photoreceptor cell & axon phenotype, suppressible by msnEP549/Scer\GAL4GMR.PF

dock04723 has eye photoreceptor cell & growth cone phenotype, suppressible by msnEP549/Scer\GAL4GMR.PF

NOT suppressed by
Statement
Reference

dock04723 has photoreceptor & axon phenotype, non-suppressible by msnF.UAS.Tag:M(Far-Unk)/Scer\GAL469B

dock04723 has photoreceptor & axon phenotype, non-suppressible by Scer\GAL4elav-C155/msnF.UAS.Tag:M(Far-Unk)

dock04723 has phenotype, non-suppressible by lbmY13

Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

dock[+]/dock04723 is a non-enhancer of egg | maternal effect phenotype of Scer\GAL4nanos.PG, msnHMJ02084

dock[+]/dock04723 is a non-enhancer of heart primordium phenotype of sli2

dock04723 is a non-enhancer of eye phenotype of RetMEN2B.GMR

Suppressor of
Statement
Reference

dock[+]/dock04723 is a suppressor of eye phenotype of Scer\GAL4GMR.PF, fruNP0021

NOT Suppressor of
Statement
Reference

dock04723 is a non-suppressor of eye phenotype of RetMEN2B.GMR

dock04723 is a non-suppressor of photoreceptor & axon phenotype of Scer\GAL4elav-C155, msnUAS.cSa

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

dock04723;Dscam121 double heterozygous mutants display defects in dendritogenesis in the embryonic aCC motoneurons (decreased number of dendritic tips), which are not seen in either of the single heterozygotes.

A dock04723 heterozygous mutant background modifies the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing CskGD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4ptc-559.1.

dock04723 drke0A double mutant embryos do not show defects in myoblast fusion.

dock04723 hbs459 double mutant embryos have severe defects in myoblast fusion.

The number of unfused myoblasts in sns4.3 embryos is enhanced if they are either heterozygous or homozygous for dock04723.

Expression of kirreVDRC.cUa under the control of Scer\GAL4Mef2.PR in a dock04723 background results in severe myoblast fusion defects in embryos.

The muscle pattern of rst6 dock04723 embryos is similar to that of rst6 single mutants.

A dock04723 background suppresses the rough eye phenotype related to fru isoform A, found upon expression of fruNP0021 under the control of Scer\GAL4GMR.PF.

dock04723 cknC.Δ750-806 double homozygotes exhibit delayed 'immature' ISNb axons in 59% 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.

dock04723/+; Dys8-2/+ double heterozygous mutant third instar larval eye discs do not show disrupted axon targeting from photoreceptor neurons to the brain optic lobes.

dock04723/+; Df(3R)Dl-X43/+ double heterozygous mutant third instar larval eye discs do not show disrupted axon targeting from photoreceptor neurons to the brain optic lobes.

Dg323/dock04723 double heterozygous mutant third instar larval eye discs show disrupted axon targeting from photoreceptor neurons to the brain optic lobes.

dock04723/+, sli2/+ embryos do not show defects in heart formation.

The antennal lobes of dock04723/+; Pak4/+ animals exhibit normal axon trajectories and glomerular subdivisions.

Heterozygous dock04723 enhances the longitudinal axon guidance and pCC/MP1 defects seen in transheterozygous sli1, robo5 mutants. An average of 7.4 defects are seen per animal. 67% of segments (calculated as number of defects/segments) show defects, and 72% of embryos show defects in pCC/MP1.

dock04723/+ ; InRex15/+ double heterozygotes show defects in photoreceptor axon projections in the medulla; gaps in the R7 terminal array and uninnervated areas are seen. These defects are seen in larvae and adults.

Embryos with a single copy of sli2 and dock04723 have midline guidance errors in 77% of embryonic segments, sometimes involving all axon fascicles (as assayed with Fas2).

Moderate dominant enhancer of the Ras85Dix12a eggshell phenotype; 31-40% of dorsal appendages are wild type.

More than 80% of dock4/dock04723 animals which are also heterozygous for either trio4 or trio8 show defects in photoreceptor axon projection, having a "medulla bypass" phenotype.

The dock04723 phenotype is identical to that of lbmY13. Double mutants show no enhanced phenotype compared to that of the single mutants.

The phenotype is largely suppressed by msnEP549 expressed under the control of Scer\GAL4GMR.PF; the number of photoreceptor cell axons in the medulla is dramatically reduced. The premature termination of many photoreceptor cell growth cones within the optic stalk is also seen in these larvae (this phenotype is not seen in larvae expressing msnEP549 under the control of Scer\GAL4GMR.PF in a wild-type background).

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

The dendritogenesis defects (reduced number of dendritic tips, abnormal positioning of the remaining dendrites) in the embryonic aCC motoneurons characteristic for dock04723 homozygotes are rescued by expression of dockScer\UAS.T:Zzzz\SNAP-m under the control of Scer\GAL4eve.RN2 in the mutant background.

Scer\GAL4SG18.1; dockScer\UAS.cRa (gives expression in olfactory neurons, but not in the brain) rescues the development of most glomeruli in the antennal lobes of dock04723 homozygous flies.

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

A. Spradling.

Comments
Comments

Complements: ex01270. Complements: l(2)0185501855. Complements: Gsc05341. Complements: α-Adaptin06694. Complements: capt06955. Complements: S07056. Complements: dbek00108. Complements: dbek05428. Complements: dbek05447. Complements: dbek06708.

Precise excision of the P{PZ} element reverts both the lethality and the receptor cell connectivity defects.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (9)
References (37)