D.— ZOOLOGY III 



duced, is of great interest in view of the observed fact that it is the XY 

 zygote that suffers more through the action of sex-linked lethals. 



It has been shown (King, 1919) to be possible, by continued selection 

 within an animal stock to produce high and low sex ratio strains, and 

 thus it would appear that there are genes which can be concentrated in 

 a genotype which, in their action, influence the heterogametic mechanism 

 affecting either the relative production of the two kinds of gametes pro- 

 duced by the heterogametic sex or else their relative functional ability. 

 If, as seems to be the case, the male in many forms and irrespective of 

 his chromosome constitution is the weaker sex, then in those instances 

 in which the male is homogametic, an excess of X-chromosome-bearing 

 ova is demanded from the hetero-gametic females or else there must be 

 some form of selective fertilisation, the X-ova being more often or more 

 readily fertilised. 



That genes which lead to the production of X- and Y-bearing gametes 

 in unequal numbers do exist is shown very clearly indeed by the work of 

 Sturtevant and others. One such gene was discovered as long ago as 

 1922 (Morgan, Bridges and Sturtevant, 1925) in a strain of Drosophila 

 affinis in which occasional males were found to produce families consisting 

 almost entirely of females. A definite X-borne gene was suspected. 

 Gershenson (1928) found a similar gene in Drosophila obscura, and showed 

 that it was indeed resident in the X-chromosome. A male carrying this 

 gene produces very few sons, regardless of the genetic nature of his mate. 

 More recently (1936) Sturtevant and Dobzhansky have found that his 

 gene has a very wide geographical distribution in both races of Drosophila 

 pseudo-obscura, that it is sex-linked, lying in the right arm of the X- 

 chromosome, and being associated with a small inversion. Cytological 

 study has shown that in these cases the X-chromosome undergoes equa- 

 tional division at each meiotic division, whilst the Y-chromosome de- 

 generates with the result that a male carrying this gene produces nearly 

 all X-sperm instead of the usual 50 per cent. It is to be expected, of 

 course, that a sex ratio gene of this kind would be discovered only if its 

 effects upon the sex ratio were profound. But the existence of such genes 

 permits us to assume that other genes of the same kind, having less severe 

 effects upon the heterogametic mechanism, also exist and are responsible 

 for minor distortions of the sex ratio. If such genes do exist, then of 

 course, they can be incorporated into, or extruded from a genotype, and 

 upon them selective agencies can work their will. These sex ratio genes 

 may perhaps provide a partial explanation of the observation that hybrid- 

 isation commonly is attended by marked distortions of the secondary 

 sex ratio. Such hybridisation in man (Pearl and Pearl, 1908), in the 

 mouse (von Guaita, 1898, 1900), and in the rat (King, 191 1), for example, 

 has given a secondary sex ratio much higher than those of the parental 

 stocks concerned, as might be expected if these had through time come to 

 possess different sex ratio gene complexes. It does not seem reasonable 

 to suppose that heterosis itself could produce such a result. 



But all this is so much speculation, and the only justification for toying 

 with such ideas is that criticism may be aroused and experimentation 

 launched. I have presented evidence to show that three possible causes 



