Human Gene Evolution (Human Molecular Genetics) by David Cooper
By David Cooper
The tale of our evolutionary earlier is advised in our genome series. Human Gene Evolution bargains with the origins of human genes, describes their constitution, functionality, enterprise and expression. The textual content integrates our rising wisdom of chromosome and genome constitution, and discusses the character of the mutational mechanisms underlying evolutionary switch.
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Extra resources for Human Gene Evolution (Human Molecular Genetics)
A first estimate of the in vivo rate at which 5mC is deaminated and fixed as thymidine was arrived at by extrapolation from in vitro data (Cooper and Krawczak, 1989). To this end, the deamination rate of 5mC as measured under laboratory conditions in single stranded DNA, was modified so as to be consistent with the observed spectrum of point mutations found to have caused human genetic disease. 66 × 10–16sec–1 was consistent with the rate calculated from the evolutionary pattern of CpG substitution exhibited by β-globin gene and pseudogene sequences in human, chimpanzee and macaque (Cooper and Krawczak, 1989).
2). e. the reverse transcription of the mRNA and the integration of the resulting cDNA). g. β-globin, actin, HLA, interferons, snRNAs, keratins, T-cell receptors, immunoglobulin gene clusters; see Chapter 6). g. prohibitin, PHB, four pseudogenes; argininosuccinate synthetase, ASS, 14 pseudogenes). Promoter elements. e. 3). g. 4; reviewed by Ayoubi and van de Ven, 1996). g. 3. 3) and metallothionein 2A (MT2A; 16q13) genes. The TATA, SP1, and CCAAT boxes bind transcription factors that are involved in constitutive transcription whilst the glucocorticoid response element (GRE), metal response element (MRE), heat shock element (HSE), and the AP1 and AP2 sites bind factors involved in the induction of gene expression in response to specific stimuli.
This theory might predict antagonistic coevolution between maternally and paternally derived genes for the control of fetal growth. However, contrary to the expectations of the conflict hypothesis, the rate of evolution of imprinted genes is not significantly different from that exhibited by non-imprinted genes encoding receptors (McVean and Hurst, 1997). , 1993). , 1997). , 1996; Haig, 1996). Whether this is an adaptation to allow these genes to be transcribed rapidly or whether it is merely a property of the chromosomal region in question is however unknown.