Opsin genes and absorbance spectra of corresponding visual pigments from the genus Mysis were analyzed. Nucleotide sequences were obtained from 45 populations of 12 species from arctic marine waters, coastal littoral habitats, freshwater lakes and the Caspian Sea, representing a wide range of different separation histories and light conditions. All appear to have a single opsin encoded by a single gene. Extensive sequence variation was found, with a maximum 5.5% nucleotide sequence divergence within the genus and 12 % of amino-acid residues showing variation. The levels of intraspecies variation varied widely among the species but showed only weak correlation with previous estimates of mtDNA diversities. Likewise, the opsin gene phylogeny only partly corresponded with that from other data. In the main cluster of species, comprising seven continental and two coastal marine taxa, two main allelic lineages differing at several amino-acid sites were found. Of species from the M. relicta group, M. salemaai and M. segerstralei were represented in both. Statistical testing could not reject the null hypothesis that opsin evolution is neutral, showing no effects of selection. Yet it is almost self-evident that the opsin gene of visual animals inhabiting dim-light aquatic habitats is under a strong selection pressure favouring pigments that afford high visual sensitivity. Visual-pigment absorbance spectra were recorded and related to opsin amino-acid substitutions in 9 populations of 3 species of the M. relicta group from the Baltic Sea and Fennoscandian lakes with different spectral transmittance. The spectra of all lake populations were long-wavelength-shifted by 20-40 nm ((_max range 554-562 nm) compared with all sea populations ((_max range 521-535 nm), both within and between species. This distinction did not coincide with the allelic lineages, and the shifts were realized by partly different changes in the opsin genes. The results suggest that different but spectrally convergent lines of adaptive evolution have occurred repeatedly and sometimes rapidly on a statistically dominant background of neutral molecular divergence. Mechanisms apparently include loss of either of two ancestral alleles (I and II) as well as mutations within each of the alleles.