scholarly journals Search for differences among t haplotypes in distorter and responder genes

1990 ◽  
Vol 55 (1) ◽  
pp. 13-19 ◽  
Author(s):  
Mary F. Lyon

SummaryTransmission ratio distortion due to the mouse t complex is thought to be due to harmful effects of trans-acting distorter genes acting on a responder, with the t complex form of the responder being relatively resistant to this harmful action of the distorters. Previous work had indicated that naturally occurring t haplotypes differed in their responders or in distorters lying near the responder, with the result that animals doubly heterozygous for two responder-carrying haplotypes transmitted these haplotypes unequally. In the present work t haplotypes could be divided into three types on the basis of their transmission when doubly heterozygous with the responder-carrying partial haplotype tlowH. The majority, t0, t6, tw1, tw2 and tw73, were transmitted equally with tlowH, a second group, including tw5 and two haplotypes derived from it, were transmitted less frequently than tlowH, and the single member of a third group, t32, was transmitted in excess of tlowH This last result suggests that the underlying differences are in the responder itself, rather than in the distorters. Search for differences among t haplotypes in distorters produced some equivocal results possibly resulting from effects of genetic background. In particular, results of others suggesting presence of a fourth distorter, Tcd-4, were not confirmed.

1987 ◽  
Vol 49 (1) ◽  
pp. 57-60 ◽  
Author(s):  
Mary F. Lyon

SummaryMale mice heterozygous for two distorter genes, Tcd-1 and Tcd-2, of the mouse t-complex but homozygous wild type for the responder, were generated by crossing animals carrying the partial t-haplotypes th51 and th18 to inbred strains. The fertility of these males was then compared with that of their brothers carrying normal chromosome 17s. On three of the inbred backgrounds used, C3H/HeH, C57BL/6J and TFH/H, the th51th18 + / + + + males were significantly less fertile than their normal sibs. With the fourth inbred strain used, SM/JH, both types of male were nonnally fertile. This confirmed earlier preliminary findings that when both homologues of chromosome 17 carry wild-type alleles of the responder, heterozygosity for the distorter genes is sufficient to impair fertility, but the effect varies with genetic background. These results are consistent with the concept that both the transmission ratio distortion and the male sterility caused by the t-complex are due to harmful effects of the distorter genes on wild-type alleles of the responder.


1987 ◽  
Vol 50 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Mary F. Lyon ◽  
Joanna Zenthon

SummaryThe transmission ratio distortion seen in males heterozygous for a mouse t-complex has been explained on the basis of trans-acting distorter genes, having a harmful effect on a responder gene. The t-complex form of the responder is relatively resistant to these harmful effects and hence is preferentially transmitted. Animals homozygous for the t-complex responder would be expected to show equal transmission of the two homologous chromosomes, but this is not always so. Studies described in this paper have shown differences among complete t's in their transmission when opposite a constant responder carrying partial t-haplotype. In addition, the proximal partial haplotypes th49 and tw18, both derived from tw5 but of different lengths, behave differently when opposite a responder. The three central partial haplotypes, tlowH, tlow2H and tlow3H, also differ, in that tlow3H shows lower transmission than tlowH or tloW2H when opposite either wild-type, or another responder, or distorter genes. These results can be explained either on the basis of differences in the responder region of various haplotypes, including the possibility of varying numbers of copies of the relevant sequences, or on the basis of differences in cis-acting (as opposed to trans-acting) distorter genes.


Genetics ◽  
1986 ◽  
Vol 114 (1) ◽  
pp. 235-245
Author(s):  
Gregory R Gummere ◽  
Paulette J McCormick ◽  
Dorothea Bennett

ABSTRACT Transmission ratio distortion is a characteristic of complete t-haplotypes, such that heterozygous males preferentially transmit the t-haplotype bearing chromosome 17 to the majority of their progeny. At least two genes contained within the t-haplotype have been identified as being required for such high transmission ratios. In this study we examine the effects of the genetic background and the chromosome homologous to the t-haplotype on transmission ratio distortion. We use two different congenic lines: (1) BTBRTF/Nev.Ttf/t12, in which the t12 haplotype has a transmission ratio of 52%, and (2) C3H/DiSn.Ttf/t12, in which the t12 haplotype has a transmission ratio of 99%. By intercrossing these two strains to produce reciprocal F1 and F2 generations, we have isolated the effects of the homologous chromosome 17 from the effects of the genetic background. We demonstrate that both the homologous chromosome and the genetic background have profound effects on t-haplotype transmission ratio distortion. Furthermore, it is evident that the t-haplotype transmission ratio behaves as a quantitative character rather than an intrinsic property of t-haplotypes.


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 ◽  
...  

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