wing somatic clones exhibit mutant margin bristles. G-oα47A007
thoracic mutant clones exhibit bald regions with surviving bristles displaying polarity defects. Defects, due to aberrations in asymmetric division, including the absence of external cells, duplicated sockets and/or hairs, and bristles devoid of sockets or hairs are observed in G-oα47A007
mutant clones. Approximately 8% of G-oα47A007
bristles exhibit hair/socket duplications. Socket-only phenotypes occur in 5% of cases.
Only late induced somatic clones survive into the adult. Although homozygous early induced clones in the wing do not survive to the adult stage, clear polarity defects are seen in these wings in the adult, likely as a result of nonautonomous effects of clones that subsequently died. Homozygous late induced clones in the wing induce the loss of wing margin. In addition, these late induced clones often secrete multiple wing hairs, with up to five hairs per cell. These clones often cause nonautonomous defects on their proximal side. In addition, clones in the wing margin also result in nonautonomous defects in wing margin bristle polarity on the proximal side of the clone.
Homozygous embryos have defects in the heart and visceral muscles. Interruptions are seen in the dorsal vessel. Cardial cells are present and migrate properly to a dorsal position, but in some places they are not arranged as a continuous layer but appear as unorganised clusters of cells. The same types of defects are seen in the visceral mesoderm. Longitudinal axons of the nervous system are often pinched or sometimes missing and the axons of motoneurons are clearly misrouted.