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General Information
Symbol
Dmel\Dab1
Species
D. melanogaster
Name
FlyBase ID
FBal0247452
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
deletion
Comment:

Imprecise excision of the progenitor insertion, resulting in a 3070bp deletion.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Imprecise excision of the progenitor insertion, resulting in a 3070bp deletion which includes the 5' promoter region and the first exon (which includes the translation start site) of Dab.

3070bp deletion which begins 1980bp upstream of the Dab start codon and ends 1090bp downstream of the start codon.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

ISNb motor axons stall and fail to innervate their most distal target (muscle 12) in 46% of hemisegments in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab1 as the paternally derived copy of Dab). These embryos show a "stop short" phenotype in the dorsal branch of the SNa motor nerve, with the axons stopping short and failing to reach their muscle target in 39% of hemisegments.

ISNb motor axons stall and fail to innervate their most distal target (muscle 12) in 59% of hemisegments in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab2 as the paternally derived copy of Dab). These embryos show a "stop short" phenotype in the dorsal branch of the SNa motor nerve, with the axons stopping short and failing to reach their muscle target in 33% of hemisegments.

ISNb motor axons stall and fail to innervate their most distal target (muscle 12) in 9% of hemisegments in homozygous embryos. These embryos show a "stop short" phenotype in the dorsal branch of the SNa motor nerve, with the axons stopping short and failing to reach their muscle target in 9% of hemisegments.

Embryos lacking both maternal and zygotic Dab function (derived from a Dab1/Dab2 stock) show defects during cellularisation; anucleated pseudocells, incomplete pseudocleavage furrows and multinucleated cells are seen during cellularisation, with 92% of embryos having defective cells. The formation of the peri-nuclear tubulin baskets appears to be normal. Abnormal apical actin accumulation is seen throughout cellularisation in these embryos and variable lateral actin accumulation is also seen.

Embryos lacking both maternal and zygotic Dab function (derived from a Dab1/Dab2 stock) show defects in dorsal closure with occasional breaks of the leading edge, failure of cell elongation and disturbances in the "zippering" of the dorsal epithelia.

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

Dab1/Dab[+] is a non-suppressor of neuroanatomy defective | embryonic stage phenotype of enaGC5/enaGC1

Phenotype Manifest In
Enhanced by
Suppressed by
NOT Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The penetrance of the ISNb stall and SNa dorsal branch stop short phenotypes seen in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab1 as the paternally derived copy of Dab) is increased by In(3L)std11/+ to 77% and 69% respectively.

The penetrance of the ISNb stall and SNa dorsal branch stop short phenotypes seen in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab1 as the paternally derived copy of Dab) is increased by Df(3L)st100.62/+ to 65% and 57% respectively.

The penetrance of the ISNb stall and SNa dorsal branch stop short phenotypes seen in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab1 as the paternally derived copy of Dab) is increased by trio1/+ to 78% and 80% respectively.

The penetrance of the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab1 as the paternally derived copy of Dab) is increased by trio8/+ to 80%.

The penetrance of the ISNb stall and SNa dorsal branch stop short phenotypes seen in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab2 as the paternally derived copy of Dab) is increased by In(3L)std11/+ to 78% and 62% respectively.

The penetrance of the ISNb stall and SNa dorsal branch stop short phenotypes seen Dab1 homozygous embryos is increased by In(3L)std11/+ to 59% and 52% respectively.

The penetrance of the ISNb stall and SNa dorsal branch stop short phenotypes seen Dab1 homozygous embryos is increased by trio1/+ to 72% and 35% respectively.

The penetrance of the ISNb stall phenotype seen Dab1 homozygous embryos is increased by Df(3L)st100.62/+ to 54%.

The penetrance of the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab1 as the paternally derived copy of Dab) is decreased by enaGC5/+ to 26%.

The penetrance of the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab1 as the paternally derived copy of Dab) is decreased by enaGC1/+ to 36%.

The penetrance of the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab1 as the paternally derived copy of Dab) is decreased by expression of AblScer\UAS.cFa under the control of Scer\GAL4elav.PU to 29%.

The severe ISNb bypass phenotype seen in enaGC1/enaGC5 embryos is not suppressed by Dab1/+.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

Expression of DabScer\UAS.cWa under the control of Scer\GAL4elav.PU partially rescues the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab1 as the paternally derived copy of Dab).

Expression of DabScer\UAS.cWa under the control of Scer\GAL4sca-537.4 partially rescues the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab2 as the paternally derived copy of Dab).

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (2)