Single-nucleotide polymorphisms responsible for pseudo-albinism and hypermelanosis in Japanese flounder (Paralichthys olivaceus) and reveal two genes related to malpigmentation

Identification of Potential Blind-Side Hypermelanosis-Related lncRNA–miRNA–mRNA Regulatory Network in a Flatfish Species, Chinese Tongue Sole (Cynoglossus semilaevis)

“…Recently, studies in both tongue sole and Japanese flounder (Paralichthys olivaceus) that employed RNA sequencing and bioinformatics analysis found that hypermelanosis-related genes involved in tyrosine metabolism, melanogenesis, and thyroid synthesis pathways play important roles in blind-side hypermelanosis (Peng et al, 2020;Li et al, 2021a). Moreover, a recent study on Japanese flounder suggests that single-nucleotide polymorphism mutations are responsible for malpigmentation (Zhang et al, 2021). Current views support that the blind-side hypermelanosis trait in flatfish is controlled by polygenic genes, which can be affected by environmental factors; moreover, improvement by selective breeding is feasible.…”

Understanding asymmetrical malpigmentation in flatfishes and improvement measures for aquaculture

“…maximus , 89 molecular mechanism of P . olivaceus asymmetric development, 32 and benthic adaptation and metamorphosis of V. variegates 4 can be explained from the perspective of genome‐level data and evolutionary biology. The genomes of 11 other flatfish species, representing nine of the 14 Pleuronectiform families, also have been reported for phylogenetic and evolutionary studies 90 .…”

“…A normal flatfish shows left/right (ocular/blind side) asymmetrical pigmentation with the dark brown ocular side and the white blind side. This asymmetrical pigmentation happens as a result of normal development and is established post metamorphosis 2–4 . Under hatchery‐rearing conditions, however, pigmentation abnormalities are frequently expressed by flatfishes, including excess blind‐side pigmentation (ambicolouration, spotting, or staining) or pigment cell deficiency on portions of the ocular side (pseudoalbinism) (Figure 1).…”

“…of normal development and is established post metamorphosis. [2][3][4] Under hatchery-rearing conditions, however, pigmentation abnormalities are frequently expressed by flatfishes, including excess blind-side pigmentation (ambicolouration, spotting, or staining) or pigment cell deficiency on portions of the ocular side (pseudoalbinism) (Figure 1). The distinct appearances of pseudoalbino, ambicoloured, and stained fish correlate with differences in the populations of melanophores and xanthophores.…”

“…Through the investiga-tion of some key genes and mutation sites in nutrition and bodycolour signalling pathways, researchers have identified some key SNP screening sites, where mutation rate of these sites is higher in abnormal body-colour groups than in normal fish, which may have a certain impact on aquaculture.Recently, four high-quality Pleuronectiform genomes, including those of members of families Cynoglossidae (half-smooth tongue sole, C. semilaevis), Scophthalmidae (turbot, S. maximus), Bothidae (Japanese flounder, P. olivaceus), and Pleuronectidae (spotted halibut, Verasper variegatus), have been reported for interpretation of important biological mechanisms. Supported by genomic information, evolution of sex chromosomes in C. semilaevis,88 benthic adaptation in S. maximus,89 molecular mechanism of P. olivaceus asymmetric development,32 and benthic adaptation and metamorphosis of V. variegates4 can be explained from the perspective of genome-level data and evolutionary biology. The genomes of 11 other flatfish species, representing nine of the 14 Pleuronectiform families, also have been reported for phylogenetic and evolutionary studies 90.…”