The Genetic Control of Mutation 



387 



some comes from certain natural popula- 

 tions, this cross ■ produces 93 to 99% (in- 

 stead of about 50% ) + progeny. More- 

 over, this atypical ratio is not associated with 

 any increase in egg mortality. It is con- 

 cluded, therefore, that the two kinds of male 

 gametes (H — h and cnbw) must be func- 

 tionally unequal in number at the time of 

 fertilization, suggesting that the segregation 

 ratio 1 -\ — \- : 1 en bw is somehow distorted 

 prior to gamete formation. Analysis of the 

 segregation distortion phenomenon reveals a 

 genetic factor, Segregation-Distorter , SD — 

 present in the otherwise wild-type II chro- 

 mosome — located in the heterochromatic re- 

 gion of the right arm near the centromere of 

 II. The en few-containing chromosome, 

 therefore, carries SD+. SD causes some 

 kind of genetic change, probably at or near 

 SD+ in the homologous chromosome, which 

 results either in the loss of the en few-con- 

 taining homolog or the inability of sperm 

 carrying that chromosome to be used in 

 fertilization. The net result is that the SD- 

 containing chromosome is recovered in ex- 

 cess in the F,. 



When, however, the SD + -containing chro- 

 mosome carries certain inversions involving 

 IIR absent in the homolog, the SD/SD + 

 male shows no segregation distortion. Con- 

 sequently, for SD to prevent the appearance 

 of SD+ in the progeny, SD and SD+ must 

 "pair." SD + alleles vary in their sensitivity 

 to any particular SD; SD alleles differ in their 

 ability to affect a given SD+ region. 



The original SD SD+ combination gives 

 a constant amount of distortion, indicating 

 that the SD line is stable. Every SD-bear- 

 ing chromosome recombinant for the (prob- 

 ably heterochromatic) tip of the right arm 

 of the II chromosome becomes less stable. 

 The decrease in stability is reflected by varia- 

 tions in ability to distort. Consequently, the 



3 As noted originally by Y. Hiraizumi and J. F. 

 Crow. 



stable line must have a modifying gene, 

 Stabilizer of SD, St(SD), at the tip of the 

 right arm of II. Stabilization occurs whether 

 St(SD) is in cis or trans position relative to 

 SD. 



Since the markers purple (pr) and en 

 closely span both the centromere and the 

 SD locus, one can study recombinants for the 

 regions near SD. The results show that a 

 locus is present in the right arm of II — near 

 SD but farther from the centromere — whose 

 presence is essential for SD operation. This 

 locus is Activator of SD, Ac(SD), which 

 must be in cis position for SD to function. 

 Since it is found that crossing over in the 

 SD-Ac(SD) region is reduced, it is hypothe- 

 sized that a small rearrangement exists in this 

 region. Usually, SD-Ac(SD) causes a ge- 

 netic change in the corresponding — presum- 

 ably nonrearranged — SD+ segment of the 

 homolog. An individual can be synthesized, 

 however, with one II chromosome, contain- 

 ing almost all the hypothesized rearrange- 

 ment without SD, whose homolog carries 

 SD, Ac(SD) and a segment of the nonrear- 

 ranged region. Under these conditions, seg- 

 regation distortion occurs against the SD- 

 containing chromosome instead of against 

 its homolog. 



Although the F, of the usual heterozygous 

 SD male occur in a distorted ratio (the 

 father distorts, or shows segregation distor- 

 tion via his progeny), the Fj from hetero- 

 zygous SD females do not. An SD SD + 

 male can distort when outcrossed to an at- 

 tached-X female. Surprisingly, when his 

 5X>-containing sons are tested (these re- 

 ceived the father's X), they do not distort. 

 It would appear that a distorting male condi- 

 tions his X chromosome so that sons re- 

 ceiving it cannot distort. When a distorting 

 male is mated to an unrelated SD + SD + 

 female having separate X's, all the SD-con- 

 taining sons can distort since each received 

 an unchanged maternal X. (Note that the 

 daughters carry one unchanged maternal and 



