Between the two compound eyes on the vertex on the adult head are the three simple eyes, ocelli. Transmission and scanning electron microscopy were used to investigate the corneal lenses, ocellar photoreceptors, and axonal projections in normal and mutant Drosophila melanogaster. In wild type flies, the cornea consists of about 45 lamellae. It has corneal nipples distally and is underlaid with a monolayer of corneagenous cells. Retinula cells have open rhabdomeres of about 2 microns (diameter) x 7 microns (length). Rhabdomeres extend to the distal extent of the cell and do not have caps. Microvilli have a rodlet within. Retinula cells are joined by belt desmosomes on the lateral borders. Eye color pigment granules are housed within the retinula cells of normal flies, not in accessory cells. The granules do not migrate in response to light. No screening pigment granules exist in the white mutant. Each ocellus has about 80 retinula cells whose axons project to corresponding ganglia from which 4 giant afferent interneurons (per ganglion) project to the brain. receptor terminals are invested with capitate projections from glia. Receptors synapse onto dyads of follower cells, usually interneuron processes, at sites of T shaped presynaptic ribbons. These "T bars" are surrounded by indistinct flattened vesicles. Interneurons make feed back synapses onto receptor terminals at T bars clustered with distinct round vesicles. Three mutants with abnormal ocelli were investigated. The none mutant has unusual compound eye and ocellar corneas. The compound eye is devoid of differentiated photoreceptors but some axons from undifferentiated cells from synapses. No receptors were found in the ocelli of none. The oc mutant has no ocelli, although sometimes an ocellar cornea like that of none is seen; the compound eye is normal. The rdo mutant is also specific to ocelli with smaller ocelli having half the wild type allotment of receptor cells; the number of giant afferents is unaffected. Mutants best known for their compound eye defects were examined. The norpA mutant loses its ocellar rhabdomeres with age but has normal feed forward and feed back synapses. This normal synaptology prevails despite the electrophysiological defects in norpA ocelli reported earlier. The rdgABS12 mutant has poorly formed ocellar receptors which show some degeneration with age but synapses survive. The trp. rdgBKS222 and rgdAPC47 mutants are essentially normal with respect to structure and survival of ocellar receptors and synapses.