CONTINUOUS VARIATION 



by their dirtcrences, cause discontinuities in the variation ot the 

 phcnotype and they will therefore be traceable by the mendelian 

 method. Included in this group are such genes as have a lethal eftect 

 when homozygous. At the other extreme are genes whose differences 

 cause effects so slight that they are obscured by the remaining 

 variation, both heritable and non-heritable. By itself, the etfect of 

 such a single gene might entirely escape detection, but a number rein- 

 forcing one another in action might produce quite a large difference 

 between the extreme genotypes. This difference will not, however, 

 create a discontinuity in variation, for two reasons. Between the 

 two extremes there will lie a graded series of genotypes; and the 

 environment will smooth out the small differences between the 

 members of this series. These genes cannot, therefore, be followed 

 individually in mendelian experiment; they must be handled as 

 groups by the biometrical method. 



Each character of the phenotype may show the effects ot gene 

 differences covering the whole range of the spectrum. Any example 

 of variation is likely to involve several, if not many, of the gene 

 differences of small effect, even where the major part of the 

 variation is due to one or more genes of large effect. Non-heritable 

 variation is also ubiquitous in its occurrence. It may indeed be 

 stated as a general rule that aU characters can and do show variation 

 due to genes of small effect, variation due to genes of large effect, 

 and variation due to non-heritable agencies. 



The susceptibility of a gene to detection by the mendelian method 

 is thus dependent, not on its mode of inheritance, but on the size 

 of its effect in relation to its fellows. We can in fact account for 

 continuous variation on the basis of the simultaneous operation of 

 a number of genes. These genes are inherited in the mendehan way, 

 but their differences have effects which are small in relation to those 

 of non-heritable agencies (or at least in relation to the total variation), 

 similar to one another and supplementary to one another (Fig. 15). 

 Such a set of genes constitutes a polygenic system, and its individual 

 members may be conveniently termed polygenes. 



Genes such as those with which Nilsson-Ehle was concerned have 

 two of the properties of polygenes. They are of similar and sup- 

 plementary' action. But they cannot be described as polygenes because 

 their effects are so large as to cause a sharp discontinuity in the 



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