Lack of external bristle structures are seen in mam2 somatic clones. they are correlated with a loss of internal cell types: typically, only solitary neurons are observed instead of neural hypertrophy or the wild-type thecogen/neuron pairs.
Embryonic CNS exhibits moderate disturbances and larval exhibit moderate cuticle loss.
Instead of forming distinct invagination folds, the mam mutant stomodeal nervous system anlage invaginates en masse.
Defects in neuroblasts, sensillum precursors, sensory neurons, peripheral glial cells, oenocytes, optic lobe, somatogastric nervous system, salivary gland, Malpighian tubules, trachea, somatic musculature and cardioblasts. Foregut, endoderm and larval midgut are wild type.
Homozygous clones in the eye have a severely disturbed ommatidial pattern, visible as a scar in the eye surface. Ommatidia are larger than wild-type and interommatidial bristles are missing. Each ommatidium contains more retinula cells and fewer pigment cells than wild-type. Each ommatidium contains more receptor cells than normal, and may contain up to 13 receptor cells. Homozygous clones in the cuticle lack all bristles.
Intermediate embryonic neurogenic phenotype. A segmented plate of dorsal cuticle is connected by means of two epidermal bridges to the remains of the cephalic cuticle. Posterior spiracles are still evident.