Endocrine genetics : proceedings of a symposium held in Churchill College, University of Cambridge, on 29, 30 and 31 March 1966 / edited on behalf of the Society for Endocrinology by the late S.G. Spickett ; with the assistance of J.G.M. Shire.

  • Society for Endocrinology (Great Britain)
Date:
1967
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Licence: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)

Credit: Endocrine genetics : proceedings of a symposium held in Churchill College, University of Cambridge, on 29, 30 and 31 March 1966 / edited on behalf of the Society for Endocrinology by the late S.G. Spickett ; with the assistance of J.G.M. Shire. Source: Wellcome Collection.

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    HORMONAL CONTROL OF MACROMOLECULAR BIOSYNTHESIS 17 lating the synthesis of messenger RNA and hence cause increased bio¬ synthesis of protein. And, indeed, the results seemed to bear out this possibility. It was noted that growth hormone, for example, stimulated the labelling of RNA. Moreover, sucrose gradient centrifugation of the rat liver RNA, labelled after exposure to radioactive precursor for a short period of time, showed that material with a sedimentation coefficient which was thought to be characteristic of messenger RNA was labelled to a greater extent in rats treated with growth hormone (Korner, 1964). Wool & Munro (1963) found that when diaphragms were incubated with insulin, not only was more RNA synthesized but, in addition, a new radioactive peak appeared (in some experiments but not in all) which could have been messenger RNA. The polysome model of protein synthesis (Goodman & Rich, 1963) which offered good support for the idea of a template messenger RNA, also seemed to offer support for the messenger theory of hormone action. It was soon found (Korner, 1964) that the ribosome population of liver after hypophysectomy was deficient in polysomes compared with that from normal rat liver. It seemed reasonable, on the face of it, to argue that removal of growth hormone had inhibited messenger RNA production and resulted in there being less polysomes in the liver cells and hence less synthesis of protein. Meanwhile work with other hormones had revealed that they too, in their target organs, stimulated RNA and protein synthesis and that actinomycin inhibited the action of many hormones (see Karlson 1965 for review). The way was clear for a generalized statement of the messenger hypothesis of hormone action. Wool (19646) and Karlson (1963) have good statements of the idea that hormones act by a direct mechanism to de- repress a portion of the genome so that new, or more, messenger RNA molecules are produced. The intellectual attraction of the idea is clear. For insulin, as an example, it offered a clear way to explain all the effects of the hormone as secondary consequences of this one action. One could postulate (see Wool (19646) as an example) that specific messenger RNA molecules were synthesized by the de-repressing action of insulin so that specific proteins were synthesized which caused increased cellular accumu¬ lation of glucose, increased utilization of it, increased synthesis of glycogen and so on. Synthesis of a specific enzyme could be invoked to explain an action of insulin. But these arguments rest on poor logic. The messenger hypothesis set out to explain the mechanism of control of the kind of enzymes produced in bacteria, not the amount of enzyme produced. It is true that the power of the messenger hypothesis hypnotized many into believing that all 2 SEG