Complements: Df(3R)by10.
Complements: T(2;3)G16DTE35B-3P.
Fails to complement: Df(3R)by62.
Fails to complement: Df(3R)mr73.
Fails to complement: Df(3R)mrO1.
41.9% of hemisegments in Df(4)C3/+ ; Df(3R)swp2MICAL/+ double heterozygotes show defects in muscle 6/7 innervation and 33.0% show defects in muscle 12/13 innervation (these defects in ISNb axons include axons stalling, bypassing targets and absent or decreased muscle innervation). 44.6% of hemisegments show SNa pathway defects, failing to make the two characteristic turns between muscles 22 and 23 and muscles 23 and 24.
Homozygous embryos show guidance and innervation defects in the SNa pathway (46.2% of hemisegments show defects compared to 11.2% in wild-type embryos).
Homozygotes survive to larval stages and have no obvious morphological abnormalities. There are no obvious somatic muscle defects and the overall architecture of the PNS and CNS is normal.
Homozygotes survive to larval stages and have no obvious morphological abnormalities.
68.9% of homozygous hemisegments show defects in muscle 6/7 innervation and 57.3% show defects in muscle 12/13 innervation (these defects in ISNb axons include axons stalling, bypassing targets and absent or decreased muscle innervation). 81.2% of homozygous hemisegments show SNa pathway defects, failing to make the two characteristic turns between muscles 22 and 23 and muscles 23 and 24. Prominent guidance defects are also seen in axons that give rise to the ISNd, SNc, TN and the third most lateral Fas2-positive longitudinal connective in the CNS.