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.For what I called 'version of the code-script' -be it the original one or a mutant one -the term 'allele' has been; adopted.When the versions aredifferent, as indicated in Fig.8, the individual is called heterozygous, with respect to that locus.When theyare equal, as in the non-mutated individual or in the case of Fig.10, they are called homozygous.Thus arecessive allele influences the pattern only when homozygous, whereas a dominant allele produces thesame pattern, whether homozygous or only heterozygous.Colour is very often dominant over lack ofcolour (or white).Thus, for example, a pea will flower white only when it has the 'recessive alleleresponsible for white' in both chromosomes in question, when it is 'homozygous for white'; it will thenbreed true, and all its descendants will be white.But one 'red allele' (the other being white; 'heterozygous')will make it flower red, and so will two red alleles ('homozygous').The difference of the latter two caseswill only show up in the offspring, when the heterozygous red will produce some white descendants, andthe homozygous red will breed true.The fact that two individuals may be exactly alike in their outwardappearance, yet differ in their inheritance, is so important that an exact differentiation is desirable.Thegeneticist says they have the same phenotype, but different genotype.The contents of the precedingparagraphs could thus be summarized in the brief, but highly technical statement: A recessive alleleinfluences the phenotype only when the genotype is homozygous.We shall use these technical expressionsoccasionally, but shall recall their meaning to the reader where necessary.THE HARMFUL EFFECT OFCLOSE-BREEDINGRecessive mutations, as long as they are only heterozygous, are of course no working-ground for naturalselection.If they are detrimental, as mutations very often are, they will nevertheless not be eliminated,because they are latent.Hence quite a host of unfavourable mutations may accumulate and do noimmediate damage.But they are, of course, transmitted to that half of the offspring, and that has animportant application to man, cattle, poultry or any other species, the good physical qualities of which areof immediate concern to us.In Fig.9 it is assumed that a male individual (say, for concreteness, myself)carries such a recessive detrimental mutation heterozygously, so that it does not show up.Assume that mywife is free of it.Then half of our children (second line) will also carry it -again heterozygously.If all ofthem are again mated with non-mutated partners (omitted from the diagram, to avoid reed confusion), aquarter of our grandchildren, on the average, will be affected in the same way.No danger of the evil everbecoming manifest arises, unless of equally affected individuals are crossed with each other, when, as aneasy reflection shows, one-quarter of their children, being homozygous, would manifest the damage.Nextto self-fertilization (only possible in hermaphrodite plants) the greatest danger would be a marriagebetween a son and a daughter of mine.Each of them standing an even chance of being latently affected ornot, one-quarter of these incestuous unions would be dangerous inasmuch asone-quarter of its children would manifest the damage.The danger factor for an incestuously bred child isthus 1: 16.In the same way the danger: factor works out to be 1 :64 for the offspring of a union betweentwo ('clean-bred') grand- children of mine who are first cousins.These do not seem to be but overwhelmingodds, and actually the second case is usually tolerated.But do not forget that we have analysed theconsequences of only one possible latent injury in one partner of the ancestral couple ('me and my wife').Actually both of them are quite likely to harbour more than one latent deficiency of this kind.If you knowthat you yourself harbour a definite one, you have to reckon with l out of 8 of your first cousins sharing it!Experiments with plants and animals seem to indicate that in addition to comparatively rare deficiencies ofa serious kind, there seem to be a host of minor ones whose chances combine to deteriorate the offspring ofclose-breeding as a whole.Since we are no longer inclined to eliminate failures in the harsh way theLacedemonians used to adopt in the Taygetos mountain, we have to take a particularly serious view aboutthese things in the case of man, were natural selection of the fittest is largely retrenched, nay, turned to thecontrary.The anti-selective effect of the modern mass slaughter of the healthy youth of all nations is hardlyoutweighed by the consideration that in more primitive conditions war may have had a positive value inletting the fittest survive.GENERAL AND HISTORICAL REMARKSThe fact that the recessive allele, when heterozygous, is completely overpowered by the dominant andproduces no visible effects at all, is amazing.It ought at least to mentioned that there are exceptions to thisbehaviour.When a homozygous white snapdragon is crossed with, equally homozygous, crimsonsnapdragon, all the immediate descendants are intermediate in colour, i.e.they are pink (not crimson, asmight be expected).A much more important case of two alleles exhibiting their influence simultaneouslyoccurs in blood-groups -but we cannot enter into that here.I should not be astonished if at long lastrecessivity should turn our to be capable of degrees and to depend on the sensitivity of the tests we apply toexamine the phenotype.This is perhaps the place for a word on the early history of genetics.Thebackbone of the theory, the law of inheritance, to successive generations, of properties in which the parentsdiffer, and more especially the important distinction recessive-dominant, are due to the now world famousAugustininan Abbot Gregor Mendel (1822-84).Mendel knew nothing about mutations and chromosomes
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