Marine fish larvae undergo major functional and morphological changes during the developmental stages and several factors can interfere with the normal development of larvae and affect fry quality. Skeletal malformations, such as spinal malformation-scoliosis, lordosis, coiled vertebral column-, missing or additional fin rays, bending opercle or jaw malformations, are frequently observed in hatchery-reared larvae. This paper reviews the effects of some nutritional components on skeletal development in larvae of a number of fish species. In the dietary lipid fraction, for instance, it was proven that the phospholipid concentration affected the spinal malformation rate in sea bass fed a compound diet from mouth opening onwards. Phosphatidylinositol, in particular, seems to prevent skeletal deformities. Highly unsaturated fatty acids, and particularly DHA enrichment in live prey, induce a decrease of opercular deformities in milkfish. It is known that highly unsaturated fatty acids have profound effects on gene expression, leading to changes in metabolism, growth and cell differentiation, and these effects are worth investigating in developing fish. The nature of the dietary protein fraction also affects the quality of fish larvae development. It appears that dietary incorporation of 20 amino acid peptides or di-and tripeptides leads to a reduction of spinal malformations in sea bass. Among vitamins, the teratogenic effect of retinoic acid is now well documented in vertebrates. High dietary retinoic acid levels result in higher incidence of bone deformities, such as vertebral curvature, central fusion and compression of vertebra in Japanese flounder larvae. The teratogenic effect of retinoic acid observed in embryonic and postembryonic stages was explained by a depression of shh expression. As for vitamin C, opercular abnormalities in milkfish larvae, associated with distortion of gill filament cartilages, were reduced by 50% when feeding larvae with ascorbic acid enriched rotifers and Artemia, compared to control fish.

developmental plasticity ͉ germ cell transplantation ͉ sexual bipotency ͉ spermatogonia ͉ stem cell

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Our understanding of the molecular mechanisms of primordial germ cell (PGC) proliferation in fish is rudimentary, but it is thought to be controlled by the surrounding somatic cells. We assumed that growth factors that are specifically involved in PGC proliferation are expressed predominantly in the surrounding genital ridge somatic cells. In order to isolate these growth factors, we compiled a complementary DNA (cDNA) subtractive library using cDNA from the genital ridges of 40-dpf rainbow trout embryos as the tester and cDNA from embryos without genital ridges as the driver. This approach identified a novel cytokine, designated gonadal soma-derived growth factor (GSDF), which is a member of the transforming growth factor (TGF)-beta superfamily. GSDF was expressed in the genital ridge somatic cells surrounding the PGCs during embryogenesis, and in both the granulosa and Sertoli cells at later stages. Inhibition of GSDF translation by antisense oligonucleotides suppressed PGC proliferation. Moreover, isolated testicular cells that were cultured with recombinant GSDF demonstrated dose-dependent proliferation of type-A spermatogonia; this effect was completely blocked by antiserum against GSDF. These results denote that GSDF, a novel member of the TGF-beta superfamily, plays an important role for proliferation of PGC and spermatogonia.

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