Homozygotes survive to the late third larval instar stage, developing to early metamorphosis before dying, mod(mdg4)^bpdEX1/Df(3R)e-BS2 hemizygotes die during early larval or late embryonic stages. The morphology of the nerve terminals at muscle 12 is abnormal in 62% of abdominal segments, with four categories of phenotype being observed: overgrowth of nerve terminals to neighbouring muscles ("back branching", 55%), the presence of multiple branch points (25%), defasciculation at the branch point before reaching the muscle (35%), and/or detachment of the nerve branch point from the muscle (48%). Recurrent innervation is seen where the 3 different axons of muscle 13 branch out over the muscle and form boutons, only to refasciculate and cross over to muscle 6 where they make an ectopic set of contacts. Besides the defects at the neuromuscular junction, no major morphological abnormalities in the central nervous system or other organs are seen in mod(mdg4)^bpdEX1 larvae. Homozygous larvae show alterations in the organisation of the synaptic boutons at the neuromuscular junction. The subsynaptic reticulum (SSR) is dramatically altered, in contrast to wild type it is spread in a wide area around the synaptic bouton, and the boundary between the SSR and the rest of the muscle cell is poorly defined. Large areas of muscle tissue that are devoid of SSR also interrupt the mutant SSR. In the most extreme cases, type I synaptic boutons completely lack the SSR. The density of the SSR is approximately 50% lower than wild type in homozygous or mod(mdg4)^bpdEX1/mod(mdg4)^bpdEX5 animals. The number of SSR layers is reduced and the SSR is increased in thickness (in mod(mdg4)^bpdEX1/mod(mdg4)^bpdEX5 animals). The length of the SSR and index of convolution is unaltered.