Df(2R)Jp6 mutant embryos show normal cardiac cell alignment.

The Df(2R)Jp6 chromosome acts as a dominant weak suppressor of telomeric silencing (assayed using the effect of the chromosome on the eye colour phenotype of flies carrying "P{w^var}KR3-2", a stable "brown-red" variant of the P{3'WP-2,w^var}2Lt insertion).

Khc⁶/Df(2R)Jp6 larvae exhibit early loss of motor activity in the ventral posterior segments causing an inbalance in bodywall contractions such that larvae rhythmically flip their tails upward during locomotion. Mutation causes organelle-filled axonal swellings that exhibit abnormal accumulation of nerve terminal proteins, Syt1, Csp, Syx1A and Fas3. Slow axonal transport does not make a substantial contribution to the swellings. Mutation causes dystrophic neuromuscular junctions; the number of synaptic boutons per muscle 6/7 junction in segments A2 and A6 in wandering third instar larvae is reduced threefold and fivefold respectively. The terminal phenotype is completely rescued by a single copy of P{Khc7.5}.