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Abstract:
Knowledge of the genetic control of human fetal growth is obtained indirectly from several different lines of evidence. Simply inherited pathological conditions indicate the number and effects of the corresponding normal alleles, and demonstrate the complexity of genetic factors in fetal growth, the interaction of quantitative and qualitative control, the large number of genes involved, and the pleiotropic effect of many. Information on genetic mechanisms shows that a cell at any one time responds to only a small proportion of its genes. Knowledge of human polymorphisms indicates that genetic control is exercised by switch mechanisms which bring into play a succession of genes producing different polypeptide chains. Implicit in this model is tissue specificity of isoenzymes, and temporal variation in their availability or activity during development, for both of which evidence is adduced. Such temporal changes do not coincide in different tissues, but vary according to physiological requirements of the tissues. Besides the sequential activation of genes, other mechanisms controlling the implementation of their instructions operate at all points from the replication of the genes, transcription, translation, to the final modification of their primary products.