The origin and possible genetic control of new, stable pigment patterns in the poeciliid fish Xiphophorus maculatus.
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The common goldfish depigments its larval choroidal melanophores as well as the skin melanophores for about two to three months following hatching. Thereafter it begins to show a characteristic xanthic coloration. This depigmentation is under the control of depigmentation genes Dp1 and Dp2. The larval choroidal melanophores of the common goldfish were cultured in vitro for more than four months without showing any sign of depigmentation. During the same period the skin and choroidal melanophores in the ACTH to the culture medium had no effect on depigmentation. The mechanisms of depigmentation in the goldfish are discussed.
The changes in cell shape of fish melanophores during pigment displacement, and the effects of colchicine and cytochalasin B on the surface morphology were studied by scanning electron microscopy. Dispersed melanophores are generally flat, with thick radiating dendritic processes. Aggregated melanophores are characterized by their swollen, hemispherical centrospheres and thin, collapsed dendrites. Colchicine induces a flattening of the entire surface of the cell while cytochalasin B elicits the swelling of the centrosphere accompanied by a partial migration (aggregation) of melanosomes.
The genotype of albino goldfish is represented by pp,cc, and the non-albino fish is PP,CC. The P gene begins to control the melanosome formation of retinal pigment cells at St-21; and the C, which is epistatic to P and p, governs melanosome formation in the dermal melanophores and in retinal pigment cells after St-22. Then in the pp,CC fish, between St-21 and St-22, melanosomes of the pigmented retina are albino in type, but after St-22 they become non-albino in type. From ultrastructural observations on the melanosomes of these late-melanizing fish, it is apparent that the imcompletely melanized albino pigment granules can differentiate into normal melanosomes under the control of the C gene. The processes of melanosome maturation in the late-melanizing goldfish are evident from these observations.
Hormone-induced pigment translocation studies were conducted at both the light and electron microscopic levels on cultured dermal iridophores from the Mexican leaf frog, Pachymedusa dacnicolor. Two distinct types of dermal iridophores were characterized which differed in (1) their in vivo locations, (2) their overall morphologies in vitro, (3) their responses to alpha-MSH, ACTH, c-AMP or theophylline, (4) their physical alterations of light, and (5) certain ultrastructural features. One iridophore (Type I) was found to be physiologically responsive to the above hormones or agents by a reversible retraction of cellular processes and a thickening of the cell body, an event which is inhibited by cytochalasin B. The other iridophore (Type II) appeared to be unresponsive. Type I iridophores contain cube-like pigmentary organelles, refractosomes, while Type II iridophores contain larger, bar-shaped refractosomes. In addition, both iridophore types contain 60 and 100 A microfilaments as well as microtubules. By in large, micorfilaments were found within microvilli, beneath and parallel to the plasma membrane and in the perinuclear region. Occasionally, bundles of 100 A microfilaments were found between layers of refractosomes in Type I iridophores. These results are discussed in relation to hormone-induced changes in cell shape.
A study has been made of the normal development and of the regeneration after excision of the groups of large pigment cells which form the spotted skin pattern of the gecko Eublepharis macularius, together with the effects of neonatal graft transplantation on this pattern. The results all indicate strongly that such groups of specialized pigment cells are not clones but the product of an induction process. This is then compared with the neural reflex mechanism by which the skin pattern of Chamaeoleo dilepis is formed.
Recent studies using zebrafish and its relatives have provided insights into the development and evolution of adult pigment patterns. In this review, I describe how an iterative approach using a biomedical model organism and its close relatives can be used to elucidate both mechanistic and organismal aspects of pigment pattern formation. Such analyses have revealed critical roles for post-embryonic latent precursors as well as interactions among different pigment cell classes during adult pigment pattern formation and diversification. These studies also have started to reveal homologous and novel features of the underlying developmental processes.
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