scholarly journals Analysis of Case-Parent Trios Using a Loglinear Model with Adjustment for Transmission Ratio Distortion

2016 ◽  
Vol 7 ◽  
Author(s):  
Lam O. Huang ◽  
Claire Infante-Rivard ◽  
Aurélie Labbe
2006 ◽  
Vol 14 (3) ◽  
pp. 299-306 ◽  
Author(s):  
Nicola L Dean ◽  
J Concepción Loredo-Osti ◽  
T Mary Fujiwara ◽  
Kenneth Morgan ◽  
Seang Lin Tan ◽  
...  

Genetics ◽  
1996 ◽  
Vol 142 (4) ◽  
pp. 1299-1304
Author(s):  
F Pardo-Manuel de Villena ◽  
C Slamka ◽  
M Fonseca ◽  
A K Naumova ◽  
J Paquette ◽  
...  

Abstract We determined the genotypes of >200 offspring that are survivors of matings between female reciprocal F1 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 11. 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 alleles from the F1 females in the region of chromosome 11 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 F1 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 DDK Om allele in only a portion of the ova of F1 females


2006 ◽  
Vol 17 (3) ◽  
pp. 239-247 ◽  
Author(s):  
Reiner Schulz ◽  
Lara A. Underkoffler ◽  
Joelle N. Collins ◽  
Rebecca J. Oakey

Genomics ◽  
1992 ◽  
Vol 12 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Stephen H. Pilder ◽  
Cindy L. Decker ◽  
Salim Islam ◽  
Christine Buck ◽  
Judith A. Cebra-Thomas ◽  
...  

1991 ◽  
Vol 57 (2) ◽  
pp. 153-157 ◽  
Author(s):  
William Garside ◽  
Christine Ruangvoravat ◽  
Patricia Dolan ◽  
Nina Hillman

SummaryThe effects of different types of insemination (normal and delayed matings and in vitro fertilization) on the transmission ratio distortion (TRD) of three t haplotypes were determined. The tw73 haplotype which contains all of the loci known to affect TRD is transmitted at equivalent frequencies in normal matings and in in vitro fertilizations (0·84 and 0·85, respectively) but at a significantly lower frequency (0·62) in delayed matings. The distal partial th18 haplotype is transmitted at equivalent frequencies in all types of insemination (0·66 to 0·70) while the proximal partial tw18 haplotype is transmitted in Mendelian frequencies in normal matings and in in vitro inseminations but at a significantly lower frequency in delayed matings. The results are discussed with reference to the current genetic model for transmission ratio distortion.


1989 ◽  
Vol 54 (3) ◽  
pp. 221-225 ◽  
Author(s):  
Lee M. Silver

SummaryComplete t haplotypes can be transmitted at distorted ratios from heterozygous +/t male mice as a consequence of t-specific alleles at a series of t complex distorter loci (Tcd-1t through Tcd-4t) and a t complex responder locus. Partial t haplotypes that lack the Tcd-2t allele cannot be transmitted at the very high ratios characteristic of complete t haplotypes. The breeding studies reported here tested the possibility that the absence of Tcd-2t could be compensated for by the presence of double doses of other Tcdt alleles. The results indicate that a double dose of Tcd-4t alone will not work, but that a double dose of both Tcd-1t and Tcd-4t can promote a very high transmission ratio in the absence of Tcd-2t. These results suggest that the extent to which transmission ratios are distorted is dependent upon the absolute level of expression of the individual Tcd genes. Further studies of genotypic effects on transmission ratio distortion, as well as fertility, lead to the suggestion of a fifth t complex distorter (Tcd-5) locus within t haplotypes.


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