The Tomita collection of medaka pigmentation mutants as a resource for understanding neural crest cell development

Abstract

All body pigment cells in vertebrates are derived from the neural crest. In fish the neural crest can generate up to six different types of pigment cells, as well as various non-pigmented derivatives. In mouse and zebrafish, extensive collections of pigmentation mutants have enabled dissection of many aspects of pigment cell development, including fate specification, survival, proliferation and differentiation. A collection of spontaneous mutations collected from wild medaka (Oryzias latipes) populations and maintained at Nagoya University includes more than 40 pigmentation mutations. The descriptions of their adult phenotypes have been previously published by Tomita and colleagues (summarised in Medaka (Killifish) Biology and Strains, 1975), but the embryonic phenotypes have not been systematically described. Here we examine these embryonic phenotypes, paying particular attention to the likely defect in pigment cell development in each, and comparing the spectrum of defects to those in the zebrafish and mouse collections. Many phenotypes parallel those of identified zebrafish mutants, although pigment cell death phenotypes are largely absent, presumably due to the different selective pressures under which the mutants were isolated. We have identified mutant phenotypes that may represent the Mitf/Kit pathway of melanophore specification and survival. We use in situ hybridisation with available markers to confirm a key prediction of this hypothesis. We also highlight a set of novel phenotypes not seen in the zebrafish collection. These mutants will be a valuable resource for pigment cell and neural crest studies and will strongly complement the mutant collections in other vertebrates.

Medaka double mutants for color interfere and leucophore free: characterization of the xanthophore–somatolactin relationship using the leucophore free gene

“…1) suggest the former. This result supports a study by Kelsh et al (2004), in which they observed a severe and consistent absence of leucophores in the lf (and lf-2) mutant (while there were variations in leucophore phenotype in all other medaka leucophore mutants they studied), and suggested a lack of the leucophore cell type in these mutants rather than a lack of pigmentation in the cells. Although we did not observe the skin of the adult lf mutants histologically because of the sparse distribution of leucophores (compare Figs.…”

Genetics, development and evolution of adaptive pigmentation in vertebrates

“…Since then, nearly 100 genes affecting pigmentation have been cloned in mice, but almost an equal number have yet to be identified (Bennett and Lamoreux, 2003), and new loci are accumulating as a result of chemical mutagenesis programs (Mouse Genome Database). In addition, complementary vertebrate systems, such as zebrafish, are providing additional pigmentation genes Odenthal et al, 1996;Kelsh et al, 2004), one of which (Slc24a5) has recently been linked to variation in human skin coloration (Lamason et al, 2006). Together, these loci provide excellent candidates for studying adaptive variation in natural populations of vertebrates.…”

Medaka Receptors for Somatolactin and Growth Hormone: Phylogenetic Paradox Among Fish Growth Hormone Receptors

“…The OLc08.02d clone is of Hd-rR. The ci are offspring of fish formerly transferred to our laboratory from Nagoya University (see Kelsh et al 2004), which have northern alleles at least around the ci locus (S. Fukamachi, unpublished data). All fish were bred at 27°and under 14 hr light/10 hr dark conditions.…”