2kb of upstream Abl promoter sequence drives expression of a mutated Abl coding region, which carries a K417N amino acid replacement in the kinase domain and also lacks the F-actin-binding domain (amino acid residues 1418-1520 are deleted). The protein is tagged at the C-terminal end with EGFP.

The near complete pupal lethality of Abl⁴/Df(3L)st-j7 animals is partially rescued by combination with Abl^{KDΔFABD.T:Avic\GFP-EGFP}, strongly restoring adult viability at 25 and to a lesser extent also at 18[o]C. It partially rescues the almost complete embryonic lethality and embryonic morphogenesis defects of progeny from Abl⁴/Df(3L)st-j7 mothers.

Abl^{KDΔFABD.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 are weakly, while mesoderm invagination and dorsal closure (uneven leading edge, zippering defects or aberrant shapes of cells at the leading edge) are strongly rescued.