The development of animals homozygous for a mutation causing periodic albinism (ap) in Xenopus laevis.
This paper describes the development of a mutant strain associated with periodic albinism (ap) in the clawed toad Xenopus laevis. The most outstanding feature of this mutation is the instability of the albino state. In the course of the development there is a succession of three periods of pigment expression: (1) complete absence of melanin pigment, (2) appearance of melanin in the pigmented epithelium of the eyes and in small quantities in skin melanophores, (3) disappearance of most pigment granules. Repeated spawnings show that the mutant syndrome is inherited as a recessive trait. Possible ways of analysing pigment cell differentiation with the use of the mutation described are discussed.
D000417:Albinism / Q000196:embryology / Q000235:genetics*; D000818:Animals; D002454:Cell Differentiation; D005808:Genes, Recessive; D006720:Homozygote; D007814:Larva; D008543:Melanins / Q000096:biosynthesis; D008547:Melanophores / Q000378:metabolism; D009154:Mutation; D010857:Pigment Epithelium of Eye / Q000378:metabolism; D010858:Pigmentation; D012867:Skin / Q000196:embryology / Q000378:metabolism; D014981:Xenopus / Q000196:embryology / Q000254:growth & development*
D008543:Melanins