Abstract
Fin abnormalities are common in reared fish. They mainly consist of partial to complete lack of rays and severe abnormalities of fin-supporting skeletal elements, which develop during the larval stage, up to the completion of fin skeleton ontogeny. This study reports a new abnormal condition, ray-resorption syndrome (RSS), which developed after the completion of fin ontogeny in initially normal European seabass larvae, leading to extensive loss of fin rays. At 49 days post-fertilisation (dpf) (15 mm standard length, SL) all fish presented normal fins. However, nineteen days later (21 mm SL), significant fin damage, characterised by ray loss or fractures, was observed in all studied populations. The dorsal fin was most affected (55%-84%), followed by the pelvic (27%-53%) and anal fins (7%-17%). Microscopically, multiple non-mineralised areas resembling resorption lacunae were evident along all fin lepidotrichia. By 98 dpf (40 mm SL), the fin-ray loss had advanced, reaching its higher frequency in the dorsal (74%-83%) and caudal fins (71%-94%). Gene expression analysis revealed a significant upregulation of bglap (osteoblast maturation marker), acp5a (osteoclast maturation marker) and mmp13a (extracellular-matrix remodelling marker) in RSS specimens. The results are discussed in respect of the possible causative factors of RSS.
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