Malpigmentation is common in hatchery‐reared flatfishes, decreasing the market value of whole fish, and increasing the risk of predation for juveniles released to enhance wild stocks. Pigmentation development in flatfishes occurs in two phases. First, during embryonic and larval stages pigment cells differentiate on both sides of the body. Second, at metamorphosis larval melanophores disappear, and adult melanophores differentiate on the ocular but not on the blind side. Malpigmentation seems to result from disruptions of the second phase, and may take the form of albinism on the ocular side or darkening of the blind side. Both types of aberration may be related to aspects of the hatchery environment such as lighting, substratum, and diet. Larval nutrition appears to be a key factor and enrichment of larval diets with fatty acids and Vitamin A can greatly reduce malpigmentation rates; however, levels suffcient to prevent pigmentation defects frequently cause other abnormalities. Two developmental explanations for albinism have been proposed. The first is that differentiation of ocular‐side skin follows the normal blind‐side pathway and adult melanophores therefore fail to develop on the ocular side. The second hypothesis suggests that dietary deficiencies inhibit retinal development and the resulting visual defects lead to failure of a hormonal signal required for melanophore differentiation. These hypotheses may well be complementary; as yet neither has been thoroughly tested. Definitive tests will require a combination of manipulative techniques such as tissue transplantation and cell culture with nutritional, behavioural and hormonal assays. Such integrative studies will further the understanding both of normal pigmentation development and of the environmental factors that contribute to high rates of albinism in hatchery‐reared flatfish.
