no SECTIONAL ADDRESSES 



is at once uncovered in the case of the heterogametic individual, and so, 

 if in its action such a gene is disadvantageous, deleterious or lethal, to it 

 no time is allowed for the finding of modifying company and for the 

 pursuit of its own evolutionary development. It is expressed and tested 

 within a very short time of its first appearance, and should it cripple or 

 kill, it is the heterogametic sex that is affected. In this way the sex ratio 

 becomes modified, for the heterogametics either die before birth or else 

 their early post-natal mortality is greater than is that of the homogametics. 

 It is somewhat surprising that so few sex-linked lethals have so far been 

 discovered in mammals. It would seem that the differential segment of 

 the X is relatively insignificant and that the crossover portion, which 

 could not yield a differential mortality since its genes would not auto- 

 matically be expressed in the male, is relatively large. 



It is thus possible to look upon the inequality in capacity for continued 

 life between the sexes as being partly of the nature of an evolutionary over- 

 sight due to a lag in the development of a harmonious relationship between 

 the mechanisms of mutation and heterogamety. But this disharmony has 

 been repaired by the invention of a supplementary device which can 

 provide a compensatory primary sex ratio, high in those species with 

 male heterogamety, low in those in which the heterogametic sex is the 

 female. It is established that in many, though not in all, mammalian 

 stocks, the primary sex ratio is much higher than is the secondary, and it 

 is in such stocks that there is much sexually selective mortality operating 

 to the disadvantage of the heterogametic sex. This being so, it seems 

 reasonable to entertain the view that these three variables — ^the primary 

 sex ratio, a sexually selective pre-natal and early post-natal mortality 

 and the optimum reproductive sex ratio — -are somehow related, the dimen- 

 sions of the first being connected with the amount of the second. Should 

 this prove to be the case, then it would follow that in general the greater 

 the incidence of mutation, the more common the sex-linked recessive 

 lethals and the greater the difference in the sex incidence of mortality in 

 adolescence in a stock with male heterogamety, the higher will be the 

 primary sex ratio, and, conversely, the rarer mutation is, the fewer the 

 lethals and the less the difference in the sex incidence of mortality between 

 conception and reproductive prime, the nearer to equality will this primary 

 sex ratio be. 



This suggestion, of course demands that there should be genes which 

 affect the functioning of the heterogametic mechanism, and also that it 

 should be possible, by continued selection, to modify the primary sex 

 ratio of a stock. This will be equality when the heterogametic sex 

 elaborates its two kinds of gametes, X- and Y-chromosome-bearing 

 respectively, in equal numbers, and when both of these are equally 

 functional in fertilisation. Conversely, the primary sex ratio will be 

 removed more or less from equality if and when the two forms of gametes 

 are not produced by the heterogametic sex in equal numbers, or when, 

 between these two forms, there is functional inequality. The fact that 

 in those instances where the primary sex ratio is not equality it is the 

 Y-bearing gamete that is either produced in greater numbers or is greatly 

 advantaged in fertilisation, so that more XY than XX gametes are pro- 



