Animal genetics / Frederick B. Hutt.

  • Frederick Hutt
Date:
[1964]
Catalogue details

Licence: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)

Credit: Animal genetics / Frederick B. Hutt. Source: Wellcome Collection.

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    BIOCHEMICAL GENETICS 453 For example, by an analysis like that just given, Horowitz was able to show that there are at least three distinct steps in the synthesis of the amino acid methionine from cysteine. The conversion proceeds as follows : cysteine —^ cystathionine —> homocysteine —> methionine For each step in the process, a specific gene is needed, and mutation of any one of those three genes to a mutant allele effectively blocks formation of the end-product. From studies like this it has been possible to determine many of the previously unknown chains of reaction by which complex compounds are built up from simple ones. It is appropriate, therefore, that while Neurospora may be viewed by bakers and handlers of bread only as an unmitigated nuisance, geneticists and biochemists should both be grateful to it, not only for its contributions to their two sciences, but also for bringing those two closer together. Let us not forget, either, that the contribution of Neurospora to science was made possible because its special poten¬ tialities for revealing mutations affecting biochemical processes were recognized and utilized by Beadle and Tatum. Blocks in the Catabolism of Phenylalanine Any synthesis of essential nutrients by animals is on a small scale compared with that in plants. In general, animals use complex sub¬ stances that have been built up by plants, and do so by breaking them down to simpler substances. Before proceeding to considera¬ tion of genetic blocks in catabolism in domestic animals, we might consider briefly, as perhaps the best known examples of such defects, some of the conditions caused in man by genetic blocks in the utili¬ zation of phenylalanine. That amino acid is used to some extent for formation of proteins, but much of it is oxidized to tyrosine, and to derivatives therefrom such as melanin, adrenaline, and thyroxine. Four blocks in the catabolism of phenylalanine are shown in Fig. 20-1. Phenylketonuria. Individuals homozygous for this condition lack the enzyme phenylalanine hydroxylase which normally converts phenylalanine to tyrosine. Because the phenylalanine cannot be oxidized to tyrosine, it accumulates in the blood, and a derivative of it, phenylpyruvic acid ( A ), is excreted in abnormally large amounts in the urine ( from which it is absent in normal persons ). This met¬ abolic disorder, which was first recognized by F0lling in Norway, causes a form of idiocy which was originally called phenylpyruvic oligophrenia, and it has been variously estimated to be responsible
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