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.
Deletion of nucleotides 1893-1894 (CA) of the cDNA leads to a frameshift at amino acid 450 and early translation termination.
Homozygous embryos show stalling of ISNb axons at muscle 13 and incomplete extension with failure to form a synapse at muscle 12.
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.
daw3 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by babo[+]/babo32
daw3 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by put88/put[+]
daw[+]/daw3 is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of babo32
daw3 has larval intersegmental nerve phenotype, enhanceable by babo[+]/babo32
daw3 has larval intersegmental nerve phenotype, enhanceable by put88/put[+]
daw[+]/daw3 is an enhancer of larval intersegmental nerve phenotype of babo32
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.
dawΔ1/daw3 is rescued by dawUAS.cPa/Scer\GAL4repo
dawΔ1/daw3 is rescued by dawUAS.cPa/Scer\GAL4Mef2.PR
dawΔ1/daw3 is rescued by dawUAS.cPa/Scer\GAL4RapGAP1-OK6
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.