A few maternal-zygotic stage 15 AblΔCR1.EGFP embryos display a range of CNS defects, from moderate axon patterning defects with frequent loss of commissures to more severe axon patterning defects.
AblΔCR1.EGFP partially rescues Abl4
AblΔCR1.EGFP partially rescues Abl4/Df(3L)st-j7
AblΔCR1.EGFP partially rescues Abl4
The near complete pupal lethality of Abl4/Df(3L)st-j7 animals is partially rescued by combination with AblΔCR1.T:Avic\GFP-EGFP, strongly restoring adult viability at 25 but only weakly at 18[o]C. It partially rescues the almost embryonic lethality and embryonic morphogenesis defects of progeny from Abl4/Df(3L)st-j7 mothers.
AblΔCR1.T:Avic\GFP-EGFP also partially rescues the lethality and to varying degrees also the multiple embryonic morphogenesis defects of progeny from females whose germlines are homozygous for Abl4 (created using the FLP/FRT/DFS system): the defective cellularization and disrupted axon scaffold at the ventral nerve cord as well as dorsal closure (uneven leading edge, zippering defects or aberrant shapes of cells at the leading edge) are weakly, while mesoderm invagination is strongly rescued.