Transmission-ratio distortion through F-1 females at chromosome 11 loci linked to Om in the mouse DDK syndrome

被引:0
作者
deVillena, FPM
Slamka, C
Fonseca, M
Naumova, AK
Paquette, J
Pannunzio, P
Smith, M
Verner, A
Morgan, K
Sapienza, C
机构
[1] TEMPLE UNIV,SCH MED,DEPT PATHOL & LAB MED,CANC RES INST,PHILADELPHIA,PA 19140
[2] IMMUNE RESPONSE CORP,CARLSBAD,CA 92008
[3] EL CAJON HIGH SCH,EL CAJOU,CA 92021
[4] HOP ST JUSTINE,DEPT ENDOCRINOL,MONTREAL,PQ H3T 1C5,CANADA
[5] WAGAR HIGH SCH,COTE ST LUC,PQ H4W 1X8,CANADA
[6] MCGILL UNIV,DEPT HUMAN GENET,MONTREAL,PQ H3A 1A2,CANADA
[7] MCGILL UNIV,DEPT MED,MONTREAL,PQ H3A 1A2,CANADA
关键词
D O I
暂无
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
We determined the genotypes of >200 off spring that are survivors of matings between female reciprocal F-1 hybrids (between the DDK and C57BL/6J inbred mouse strains) and C57BL/6J males at markers linked to the Ovum mutant (Om) locus on chromosome II. In contrast to the expectations of our previous genetic model to explain the ''DDK syndrome,'' the genotypes of these offspring do not reflect preferential survival of individuals that receive C57BL/6J alleies from the F-1 females in the legion of chromosome II to which the Om locus has been mapped. In fact, we observe significant transmission-ratio distortion in favor of DDK alleles in this region. These results are also in contrast to the expectations of Wakasugi's genetic model for the inheritance of Om, in which he proposed equal transmission of DDK and non-DDK alleles from F-1 females. We propose that the results of these experiments may be explained by reduced expression of the maternal DDK Om allele or expression of the maternal DDE( Om allele in only a portion of the ova of F-1 females.
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页码:1299 / 1304
页数:6
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