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By Alan Carruth Stevenson and B. C. Clare Davison (Auth.)

ISBN-10: 0433315911

ISBN-13: 9780433315919

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However, 38 GENETIC COUNSELLING even if forward and back mutation rates are the same, the observed situation is that the number of mutated alleles determining harmful traits is very s m a l l relative to normal a l l e l e s in any population. The absolute number of changes in either direction w i l l therefore always be much greater from the more frequent to the less frequent a l l e l e . In practice, therefore, the phenomenon can probably safely be disregarded. Assuming again that there are only two possible a l l e l e s at a locus, Ai and A 2 , and that the frequency of A i is ρ and that of A 2 is then as there are no other alternatives/?

How^ever, as yet it is not possible to judge in how far risks to subsequent children should be reduced following the birth of several unaffected children after one affected. It cannot be done by a simple posteriori reasoning along the lines used in Chapter 3. In most of the conditions where it would appear that some multifactorial/threshold hypothesis is the most attractive, one sex is more frequently affected than the other. This observation is most plausibly explained in terms of there being different thresholds in the sexes.

E. the pheno­ type. If the determining genes are A 2 and B, as both can be identified, neither is dominant. However a person described as having blood group Ai may be of genotypes A i A i or A 1 A 2 , because A 2 antigen can­ not be recognised in combination with antigen Ai. So in sensu stricto Αι is dominant relative to A 2 , or A 2 can be described as recessive to Ai. However, both antigens can be identified if an individual is A 2 B so A 2 is recessive to Ai but not to B. This is probably a common situation at loci, different alleles having different degrees of dominance in different allelic combinations.

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Genetic Counselling by Alan Carruth Stevenson and B. C. Clare Davison (Auth.)


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