Vitamin C (Ascorbic acid, AA) deficiency is one of the main factors explaining larval fish pathologies and juvenile mortality. Fish species are diversified regarding their vitamin C availability, because AA can be synthesised if the key enzyme, L- gulonolactone oxidase ( GLO ) is active.
This bio- synthetic pathway has been lost at different occasions during the course of evolution. Among the mammals, primates have lost this capacity because the gene coding GLO has accumulated large number of random mutations. In fish, it seems that all teleosts cannot synthetise AA while non teleost taxa have active GLO.
This could be the result of a single evolutionary event. To understand what drives the capacities of fish to synthesise AA, we propose to work on active GLO (bowfin, sturgeon) and non-active teleosts (rainbow trout, medaka), chosen for their phylogenetic links and the availability of molecular tools.