A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\Dab2

General Information
SymbolDmel\Dab2SpeciesD. melanogaster
NameFlyBase IDFBal0247453
Feature typealleleAssociated geneDmel\Dab
Allele classhypomorphic allele - molecular evidence
MutagenP-element activity
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Description
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FB2013_03
FB2013_02
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Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Imprecise excision of the progenitor insertion, resulting in a 1887bp deletion which includes the 5' promoter region and the first exon (which includes the translation start site) of Dab.
1887bp deletion which begins 1695bp upstream of the Dab start codon and ends 192bp downstream of the start codon.
Cytology
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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 Dab[1]/Dab[2] females and having Dab[1] 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 Dab[1]/Dab[2] females and having Dab[2] 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. Embryos lacking both maternal and zygotic Dab function (derived from a Dab[1]/Dab[2] 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 Dab[1]/Dab[2] 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.
Adult escapers are occasionally seen.
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Statement
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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 Dab[1]/Dab[2] females and having Dab[1] 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 Dab[1]/Dab[2] females and having Dab[1] 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 Dab[1]/Dab[2] females and having Dab[1] as the paternally derived copy of Dab) is increased by trio[1]/+ to 78% and 80% respectively. The penetrance of the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab[1]/Dab[2] females and having Dab[1] as the paternally derived copy of Dab) is increased by trio[8]/+ 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 Dab[1]/Dab[2] females and having Dab[2] as the paternally derived copy of Dab) is increased by In(3L)std11/+ to 78% and 62% respectively. The penetrance of the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab[1]/Dab[2] females and having Dab[1] as the paternally derived copy of Dab) is decreased by ena[GC5]/+ to 26%. The penetrance of the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab[1]/Dab[2] females and having Dab[1] as the paternally derived copy of Dab) is decreased by ena[GC1]/+ to 36%. The penetrance of the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab[1]/Dab[2] females and having Dab[1] as the paternally derived copy of Dab) is decreased by expression of Abl[Scer\UAS.cFa] under the control of Scer\GAL4[elav.PU] to 29%.
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Statement
Reference
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Partially rescued by
Comments
Expression of Dab[Scer\UAS.cWa] under the control of Scer\GAL4[elav.PU] partially rescues the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab[1]/Dab[2] females and having Dab[1] as the paternally derived copy of Dab). Expression of Dab[Scer\UAS.cWa] under the control of Scer\GAL4[sca-537.4] partially rescues the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab[1]/Dab[2] females and having Dab[2] as the paternally derived copy of Dab).
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Bloomington
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Reported As
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Research paper
Song et al., 2010, Development 137(21): 3719--3727
Disabled is a bona fide component of the Abl signaling network. [FBrf0212092]
Personal communication to FlyBase
Song, 2010.11.22, Dab[1] and Dab[2].
Dab[1] and Dab[2]. [FBrf0212475]