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
Catalogue details

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.

    42/358 (page 20)
    20 A. KORNER actinomycin yet the percentage of polysomes was not greatly affected (Earl & Korner, 1966). Evidence of a different kind is also available which suggests a mode of control of protein synthesis by growth hormone other than a direct effect on messenger RNA synthesis. It was noted that addition of polyuridylic acid to ribosomes of liver of hypophysectomized rats led to a stimulation of phenylalanine incorporation which was, in percentage terms, as great or greater than that seen with ribosomes of normal rat liver. But the absolute level of incorporation with ribosomes from hypophysectomized rats was not as great as with ribosomes from normal rat liver (Korner & Gumbley, 1966). These results mean that hypophysectomy has resulted in an alteration in the ability of the ribosomes to attach themselves to the synthetic messenger RNA. Recently (A. Korner, unpublished) similar results and conclusion were obtained when poly A and natural liver messenger RNA were used as template. Wool (1965) has reached a similar conclusion after experiments with insulin on muscle ribosomes : again the ability of the ribosomes to bind to messenger RNA is altered by the hor¬ mone status of the rat. We must conclude that we do not know which of the steps in protein synthesis is rate limiting nor do we know which ones are stimulated by insulin or by growth hormone. One could imagine a finely balanced situa¬ tion in which the stimulation by a hormone of the supply of the limiting component would alter the situation so that a different component now becomes limiting and might require stimulation by the same or by a different hormone. We will need patience to unravel this complex but fascinating situation. REFERENCES Ames, B. N. & Hartman, P. E. (1963). The histidine operon. Cold Spring Harb. Symp. quant. Biol. 28, 349. Attardi, G. H., Naono, S., Rouviere, J., Jacob, F. & Gros, F. (1963). Production of messenger RNA and regulation of protein synthesis. Cold Spring Harb. Symp. quant. Biol. 28, 363. Banting, F. G., Campbell, W. R. & Fletcher, A. A. (1922). Insulin in the treat¬ ment of diabetes mellitus. J. metab. Res. 2, 547. Beckwith, J. R. (1964). A deletion analysis of the Lac operator region in Escherichia coli. У. molec. Biol. 8, 427. Brenner, S., Stretton, A. O. W. & Kaplan, S. (1965). Genetic code : the nonsense triplets for Chain termination and their suppression. Nature, Lond., 206, 994. Butcher, R. W., Ho, R. J., Meng, H. C. & Sutherland, E. W. (1965). Adenosine 3', S'-monophosphate in biological materials. X biol. Chem. 240, 4515. Castles, J. J. & Wool, I. G. (1964). Effect of puromycin and insulin on amino acid accumulation by isolated intact rat diaphragm. Biochem. J. 91, 11 c. Chaikoff, I. L. & Forker, L. L. (1950). The antidiabetic action of insulin on nitrogen metabolism. Endocrinology, 46, 319,