FlyBase Allele Report: Dmel\dock[3]

General Information

Symbol

Dmel\dock³

Species

D. melanogaster

Name

FlyBase ID

FBal0049422

Feature type

allele

Associated gene

Dmel\dock

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

amorphic allele - genetic evidence

Mutagen

Delta2-3 transposase

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Garrity et al., 1996)

Mutagen

Delta2-3 transposase

(Garrity et al., 1996)

Progenitor genotype

dock⁰⁴⁷²³

(Garrity et al., 1996)

Cytology

Description

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.

(Garrity et al., 1996)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

Bolwig nerve

(Schmucker et al., 2000)

Bolwig nerve (with Df(2R)EW60)

(Schmucker et al., 2000)

embryonic/larval somatic muscle cell

(Desai et al., 1999)

larval longitudinal connective

(Desai et al., 1999)

larval VL3/4 motor neuron | embryonic stage

(Weng et al., 2011)

neuromuscular junction | embryonic stage

(Weng et al., 2011)

photoreceptor cell & axon

(Garrity et al., 1996)

RP3 neuron & synapse

(Desai et al., 1999)

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.

(Weng et al., 2011)

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.

(Schmucker et al., 2000)

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 lbm^Y13.

(Desai et al., 1999)

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.

(Garrity et al., 1996)

External Data

Linkouts

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

(Fan et al., 2003)

NOT Enhancer of

Statement

Reference

dock³ is a non-enhancer of abnormal planar polarity phenotype of dsh^hs.sev.B

(Paricio et al., 1999)

dock³ is a non-enhancer of abnormal planar polarity phenotype of Scer\GAL4^hs.2sev, msn^EP549

(Paricio et al., 1999)

NOT Suppressor of

Statement

Reference

dock³ is a non-suppressor of abnormal planar polarity phenotype of Scer\GAL4^hs.2sev, msn^EP549

(Paricio et al., 1999)

dock³ is a non-suppressor of abnormal planar polarity phenotype of dsh^hs.sev.B

(Paricio et al., 1999)

Other

Statement

Reference

ckn^K.Δ324-331, dock³ has abnormal neuroanatomy | embryonic stage phenotype

(Weng et al., 2011)

Phenotype Manifest In

Enhanced by

Statement

Reference

dock³ has larval intersegmental nerve branch ISNb of A1-7 phenotype, enhanceable by ckn^K.Δ324-331/ckn[+]

(Weng et al., 2011)

dock³ has larval intersegmental nerve branch ISNb of A1-7 phenotype, enhanceable by ckn^K.Δ324-331

(Weng et al., 2011)

dock³ has Bolwig nerve phenotype, enhanceable by Dscam1⁰⁵⁵¹⁸

(Schmucker et al., 2000)

NOT Enhanced by

Statement

Reference

dock³ has phenotype, non-enhanceable by lbm^Y13

(Desai et al., 1999)

NOT suppressed by

Statement

Reference

dock³ has phenotype, non-suppressible by lbm^Y13

(Desai et al., 1999)

Enhancer of

Statement

Reference

dock³ is an enhancer of larval longitudinal connective phenotype of robo1⁵, sli¹

(Fan et al., 2003)

dock³ is an enhancer of Bolwig nerve phenotype of Dscam1⁰⁵⁵¹⁸

(Schmucker et al., 2000)

NOT Enhancer of

Statement

Reference

dock³ is a non-enhancer of ommatidium phenotype of dsh^hs.sev.B

(Paricio et al., 1999)

dock³ is a non-enhancer of ommatidium phenotype of Scer\GAL4^hs.2sev, msn^EP549

(Paricio et al., 1999)

NOT Suppressor of

Statement

Reference

dock³ is a non-suppressor of ommatidium phenotype of Scer\GAL4^hs.2sev, msn^EP549

(Paricio et al., 1999)

dock³ is a non-suppressor of ommatidium phenotype of dsh^hs.sev.B

(Paricio et al., 1999)

Other

Statement

Reference

ckn^K.Δ324-331, dock³ has larval intersegmental nerve branch ISNd of A1-7 phenotype

(Weng et al., 2011)

ckn^K.Δ324-331, dock³ has lateral longitudinal fascicle | embryonic stage phenotype

(Weng et al., 2011)

ckn^K.Δ324-331, dock³ has intermediate longitudinal fascicle | embryonic stage phenotype

(Weng et al., 2011)

Additional Comments

Genetic Interactions

Statement

Reference

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

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

dock³ ckn^K.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.

(Weng et al., 2011)

When ena^GC5/ena^GC1 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.

(Fan et al., 2003)

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

(Schmucker et al., 2000)

The ommatidial polarity defects seen in dsh^hs.sev.B flies grown at 29^oC are not affected by the addition of dock³. Has no effect on the ommatidial polarity phenoptype seen in flies with msn^EP549 driven by Scer\GAL4^hs.2sev.

(Paricio et al., 1999)

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

Symbol Synonym

dck3

(Paricio et al., 1999)

dck³

(Paricio et al., 1999)

dock³

(Weng et al., 2011, Yang and Bashaw, 2006)

Name Synonyms

Secondary FlyBase IDs

References (7)

Report Sections

Open Close