ABSTRACT
While fish had been comfortable with this complex issue for millions of years, research has evolved at a different time scale. In a quarter of a century, it has gone from a seemingly simple to an amazingly intricate complex with a multitude of internal and external regulatory systems. Disregarding control mechanisms, the vitellogenic system itself has developed away from a single Vtg under the control of the straightforward estradiol, one type of nuclear estrogen receptor and a receiving oocyte. The current model involves multiple vitellogenin genes, each with unique promoter regions and varying sensitivity to induction by estradiol, and multiple Vtg proteins themselves, with variable degrees of posttranslational modification. Further, the existence of three subtypes and variants of nuclear estrogen receptors, membrane actions of estradiol and at least two types of Vtg receptors fails to introduce any element of simplicity. And all this is before considering the potential of the effects of recent genome duplications found in quite a few of our finned friends or their ancient genome duplication. The only component of the system that may be as straightforward now as it was a quarter of a century ago is estradiol, the key steroid produced by the ovarian follicle cells in response to diverse inputs. However, even for estradiol, the picture has been complicated by the description of sex steroid binding globulins and other steroid-binding proteins that are likely to influence the availability of free estradiol and the uptake of the steroid into target organs and, not least, the dynamics of its removal from the circulation. To round this off, it is now obvious that estradiol is certainly not the only steroid inducing Vtg synthesis. Furthermore, for vitellogenesis, interesting interactions with other hormones, including other steroids, abound. A concise, by no
means complete, picture of the various components is presented in Fig. 4.1.
