Skin structure studies and molecular identification of the Atlantic cod Gadus morhua L. of unique golden pigmentation from the Svalbard Bank

Abstract

Summary An Atlantic cod, Gadus morhua L., with unique golden pigmentation was caught during a commercial trawl on the Svalbard Bank. Stomach content analysis excluded the possibility of golden pigmentation resulting from diet. Skin morphology, mitochondrial and molecular species markers and also the concentration of melatonin (MEL) were examined. Skin samples from five areas below and above the lateral line contained correctly developed melanophores, but their distribution was different from those observed in the skin samples of standard coloured cod. Only the difference between the numbers of melanophores below the lateral line was statistically significant (8 vs 19.8 in standard coloured cod). DNA analyses allowed exclusion of the possibility of interspecies hybridisation with haddock Melanogrammus aeglefinus. MEL concentrations in the skin sample of the golden cod compared to the control sample of standard coloured cod were similar and with no statistically significant differences. Some abnormalities observed in the detailed morphology and melanophore distribution suggest a genetic or hormonal nature in the golden pigmentation of the cod. Some of these, e.g. mutations of TYR (tyrosinase) genes or of the MSH (melanophore‐stimulating hormone) level can be tested in further analyses.

Understanding the ultrastructural aspects of berberine-induced skin-darkening activity in the toad, Bufo melanostictus, melanophores

“…The light-microscope examination of the semithin vertical sections of the dorsal skin melanophores of B. melanostictus indicated that melanophores are present dominantly in the subepidermis, called as subepidermal melanophores. Dermal melanophores in this species have been found in very less number and remain situated just below the subepidermal layer, although some melanophores occur deeper in the dermis, as revealed by Kijewska et al [ 27 ] in the Atlantic cod, Gadus morhua . We have examined the effects of berberine per se , and with its specific antagonists and agonists on toad-skin subepidermal melanophores using the electron microscope, and found that berberine stimulated the process of melanization, as well as increased the number of melanin-loaded dendrites of the subepidermal melanophores of the toad, B. melanostictus .…”

First records of xanthochromism in three-bearded rocklingGaidropsarus vulgaris(Cloquet, 1824) and pollackPollachius pollachius(Linnaeus, 1758)

“…The aetiology of abnormal xanthochromism in fish is not always clear. For example, the condition has been observed in association with overt skin pathologies (chromatophoromas and chromatophore hyperplasia) in yellowtail rockfish S. flavidus (Ayres, 1862) (Okihiro, Whipple, Groff, & Hinton, 1993) and flag rockfish S. rubrivinctus (Jordan & Gilbert, 1880) (Phillips, 1957), a diet rich in carotenoids (Leclercq, Taylor, & Migaud, 2010), hormonal imbalance (Burton, 2010), and possibly interspecific hybrids (Kijewska, Wiecaszek, Kalamarz-Kubiak, Szulc, & Sobecka, 2012). However, in the vast majority of cases, the condition is generally thought to be caused by a non-pathological genetic mutation.…”

​Xantismo en peces cíclidos (Cichliformes: Cichlidae) costarricenses, y variación ontogenética en Parachromis dovii

“…Entre las posibles causas de esta alteración/aberración se han sugerido, tanto en peces como en otros grupos de organismos, aspectos ecológicos [e.g., una dieta rica en carotenoides (Leclercq et al, 2010) o deficiente en vitaminas C y E (Simon, Joyeux, & Gasparini, 2011), así como la hibridización interespecífica (Kijewska, Wiecaszek, Kalamarz-Kubiak, Szulc, & Sobecka, 2012)], patológicos [cromatoforomas (tumores compuestos por cromatóforos) o cromatóforos hiperplásicos (e.g., Okihiro, 1993;Noga, 2010)], fisiológicos [e.g., desbalances hormonales (Burton, 2010), siendo la epinefrina una de las más importantes (Irigoyen-Arredondo et al, 2018) y otros desordenes neuroendocrinos (Noga, 2010)] y genéticos [i.e., mutaciones diversas y, usualmente, múltiples en uno o varios de los genes (usualmente recesivos) involucrados en (1) la formación, desarrollo y regulación de células pigmentarias, (2) la síntesis y producción de los diversos pigmentos cutáneos, y (3) la translocación y expresión de estos pigmentos, entre otros (Odenthal et al, 1996;Leclercq, 2010 et al;Kijewska et al, 2012)]. Otros factores que han sido señalados como posibles causas o desencadenantes de tal afectación son las infecciones parasíticas (Irigoyen-Arredondo et al, 2018), la presencia de contaminantes (Macieira, Joyeux, Chagas, 2006;Irigoyen-Arredondo et al, 2018) o la presencia de heridas provocadas por otros organismos durante interacciones antagónicas (Colman, 1972), no obstante, no se ha probado una correlación directa entre estas y la anomalía pigmentaria en cuestión.…”