C-opsin, xenopsin and r-opsin are present in the bilaterian ancestor. Scenario A. In the bilaterian ancestor, c-opsin is employed by ciliary unpigmented brain PRCs not serving directional vision. Initially the only eye PRCs are of the r-opsin+ microvillar PRC type. In protostomes, c-opsin+ PRCs stayed in the brain and do not form part of the eye retina layer in recent arthropods and annelids, but became integrated into the eye retina of vertebrates. They were reduced in mollusks and brachiopods coincident with gene loss of c-opsin. One option preventing the assumption of multiple co-option of xenopsin by eye PRCs or emergence of completely new PRCs or eyes is that xenopsin was recruited once by r-opsin+ eye PRCs in the stem lineage of lophotrochozoans and entered sensory cilia. Such cells are still present in basal mollusks. In annelids except the basally branching Oweniidae (labelled with asterisk), xenopsin is lost and the eye PRCs are turned into purely microvillar cells. In brachiopod larvae, xenopsin is maintained and present in the purely ciliary eye PRCs. Scenario B. The evolution of ciliary c-opsin+PRCs is the same as in Scenario A.However, already the eyes of the bilaterian ancestor employed a very plastic mixed r-opsin+ and xenopsin+ rhabdomeric/ciliary PRC type. Distribution of PRC types and eye PRC organization in Bilateria is largely the result of lineage-specific loss of either xenopsin or c-opsin. Loss of xenopsin in vertebrates, arthropods and most annelids led to microvillar r-opsin+ PRCs. Though still present in the genome, r-opsin became downregulated in eye PRCs of brachiopods. Schemes are partly based on drawings and images from Rhode (1992) and Passamaneck et al. (2011).