A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\daw3

General Information
SymbolDmel\daw3SpeciesD. melanogaster
NameFlyBase IDFBal0211071
Feature typealleleAssociated geneDmel\daw
Allele classloss of function allele
Mutagenethyl methanesulfonate
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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
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Additional Notes
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Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Contains a 2bp deletion at 1893-1894, which results in a frame shift in the prodomain. This is predicted to result in a truncated protein at L515.
Cytology
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Statement
Reference
Homozygous embryos show stalling of ISNb axons at muscle 13 and incomplete extension with failure to form a synapse at muscle 12.
Photoreceptor axon targeting defects are not seen in daw3/daw4 larvae.
The majority (68%) of daw3 mutants die as white prepupae or as pharate adults and do not eclose. When reared at low density on nutritive agar plates, 7% eclose but most die shortly after eclosion. Rare escapers are fertile. The CNS of stage 16/17 daw3 embryos show occasional breaks and fusions of the longitudinal axon fascicles at the low incidence of 5%. The glial cell population shows no overt defects. Motorneuron pathfinding is disrupted in these embryos as although the ISNb and SNa axons exit the ventral nerve cord correctly and extend into their target field, they fail to advance far enough to innervate the appropriate muscle. The ISNb axons commonly stall at muscle 6 and fail to form synapses on muscles 12 and 13, or reach muscle 12 but are unable to form a synapse. The SNa usually extends into the target muscle but frequently exhibits the loss of one or both branches. In embryos from daw3/daw3 mothers mated to dawδ2/dawδ2 fathers, the incidence of ISNb and SNa defects is higher than in zygotic nulls.
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Statement
Reference
daw3 has neuroanatomy defective | embryonic stage phenotype, enhanceable by babo[+]/babo32
daw3 has neuroanatomy defective | embryonic stage phenotype, enhanceable by put88/put[+]
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Statement
Reference
daw[+]/daw3 is an enhancer of neuroanatomy defective | embryonic stage phenotype of babo32
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Statement
Reference
daw3 has intersegmental nerve phenotype, enhanceable by babo[+]/babo32
daw3 has intersegmental nerve phenotype, enhanceable by put88/put[+]
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Statement
Reference
daw[+]/daw3 is an enhancer of intersegmental nerve phenotype of babo32
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Statement
Reference
In daw3/+; babo32/+; double mutant embryos, 20% of hemisegments show ISNb pathfinding defects as opposed to only 2% in daw3/+ single mutants and 4% in babo32/+ single mutants. In daw3/+; put88/+ double mutant embryos, 14% of hemisegments show ISNb pathfinding defects as opposed to only 2% in daw3/+ single mutants and no defects in put88/+ single mutants.
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Fails to complement
Rescued by
Comments
Two copies of dawScer\UAS.cPa, under the control of Scer\GAL4repo or Scer\GAL4Mef2.PR, rescues the axon guidance defects of daw3/dawδ1 embryos, while one copy provides partial rescue. Expression driven by Scer\GAL4OK6 also reverses the defects.
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hide References ( 3 )
Research paper
Pentek et al., 2009, genesis 47(4): 261--273
Follistatin preferentially antagonizes activin rather than BMP signaling in Drosophila. [FBrf0207743]
Zhu et al., 2008, Development 135(3): 513--521
Drosophila Activin-beta and the Activin-like product Dawdle function redundantly to regulate proliferation in the larval brain. [FBrf0202883]
Parker et al., 2006, Development 133(24): 4981--4991
The divergent TGF-beta ligand Dawdle utilizes an activin pathway to influence axon guidance in Drosophila. [FBrf0194818]