The presence of skeletal anomalies in farmed teleost fish is currently a major problem in aquaculture, entailing economical, biological and ethical issues. The common occurrence of skeletal abnormalities in farmed fish and the absence of effective solutions for avoiding their onset or definitely culling out the affected individuals as early as possible from the productive cycle, highlight the need to improve our knowledge on the basic processes regulating fish skeletogenesis and skeletal tissues differentiation, modelling and remodelling. Severe skeletal anomalies may actually occur throughout the entire life cycle of fish, but their development often begins with slight aberrations of the internal elements. Comprehensive investigation efforts conducted on reared larvae and juveniles could provide a great contribution in filling the gap in knowledge, as skeletogenesis and skeletal tissue differentiation occur during these early life stages. The aim of this review is to provide a synthetic but comprehensive picture of the actual knowledge on the ontogeny, typologies and occurrence of skeletal anomalies, and on the proposed causative factors for their onset in larvae and juveniles of European farmed fish. The state-of-art of knowledge of these issues is analysed critically intending to individualize the main gaps of knowledge that require to be filled, in order to optimize the morphological quality of farmed juveniles.

This critical review summarizes the knowledge about fish skeletal tissues and inherent normal and anomalous development. Particular emphasis is given to existing literature on reared European fishes. The aim was to identify the main gaps of knowledge that require to be filled, in order to precociously identify anomalous developmental patterns that lead to skeletal anomalies in reared finfish larvae and juveniles. The review also aims to extend our knowledge about the factors that are possibly involved in the onset of skeletal anomalies. The final goal is the optimization of the morphological quality of farmed juvenile fish.

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Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors belonging to the nuclear hormone receptor superfamily that functions as critical regulators of lipid and energy homeostasis. Although intensively studied in mammals, their basic biological functions are still poorly understood. The objective of this work was to characterize PPARb subtypes in a fish, the Atlantic salmon (Salmo salar), in order to address PPAR function and the regulation of lipid homeostasis in lower vertebrates. The screening of an Atlantic salmon genomic library revealed the presence of four genes for PPARb subtypes. Based on comparisons of exons and exon-flanking regions, these genes were assigned into two families, ssPPARb1 and ssPPARb2, each family containing two isotypes: ssPPARb1A and b1B and ssPPARb2A and b2B. Two full-length cDNAs for ssPPARb1A and ssPPPARb2A were isolated. Transcripts for ssPPARb1A and ssPPARb2A have distinct tissue expression profiles, with ssPPARb1A predominating in liver and ssPPARb2A predominating in gill. Expression levels of mRNA of either isotypes were up to tenfold lower in kidney, heart, spleen, muscle, and brain. In cellular transfection assays, ssPPARb1A is activated by monounsaturated fatty acids, 2-bromopalmitate, and mammalian PPARb-specific ligand GW501516. In contrast, PPARb2A was not activated by any of the compounds tested. Furthermore, ssPPARb2A repressed both the basal reporter gene activity and the GW501516-induced activity of ssPPARb1A. The results indicate unexpected levels of variety and complexity in PPAR subtype and mechanism of action in lower vertebrates.

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