P{hsneo} insertion within the transcribed leader region, 13bp downstream of the transcription start site.
Embryonic muscle loss is due to defects in early somatic differentiation. Severe abnormalities are observed in a subset of pericardial cells.
Embryos fail to build the normal pattern of somatic muscles.
Some somatic muscles are missing and the chordotonal organs of the PNS are distorted, visceral mesoderm and the dorsal vessel are not disturbed. Pattern formation of the cuticle is normal suggesting the observed muscle phenotype is not a consequence of epidermis defects.
Mobilisation of the P{hsneo} insertion reverts the lethal phenotype to viable, insertion is thought to be responsible for the mutation.