The Genetic Basis of Transmission-Ratio Distortion and Male Sterility Due to the t Complex

1991 ◽  
Vol 137 (3) ◽  
pp. 349-358 ◽  
Author(s):  
Mary F. Lyon
Keyword(s):  
Male Sterility ◽  
Genetic Basis ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
T Complex ◽  
Ratio Distortion

scholarly journals A structural gene (Tcp-1) within the mouse t complex is separable from effects on tail length and lethality but may be associated with effects on spermatogenesis

1981 ◽  
Vol 38 (2) ◽  
pp. 115-123 ◽  
Author(s):  
Lee M. Silver
Keyword(s):  
Genetic Basis ◽  
Genetic Factors ◽  
Tail Length ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Cell Protein ◽  
Wild Type ◽  
T Complex ◽  
Interaction Factor ◽  
Ratio Distortion

SUMMARYThe Tcp-1 gene is located within the t complex and codes for a major testicular cell protein called p63/6.9. All wild-type chromosomes carry the Tcp-1b allele which codes for a basic form of this protein, while all complete t haplotypes carry the Tcp-1a allele which codes for an acidic form of this protein. It is not clear whether the Tcp-1 gene is associated with phenotypic effects of t haplotypes on embryogenesis and/or spermatogenesis, since the genetic basis for these effects is extremely complex. The elegant analysis of Lyon & Mason (1977) has allowed the identification and separation of a family of genetic factors which interact to produce the observed phenotypes associated with various combinations of t haplotypes. The data summarized in this report indicate that the Tcp-1a locus is separable from all of the identified t haplotype factors except for one; a complete correlation has been obtained between Tcp-1a and a proximal t haplotype factor which is involved in effects on transmission ratio distortion. Two other novel points emerge from this analysis. First, it appears that the tail interaction factor and the proximal sperm factors represent distinct genetic loci. Second, the accumulated data lead to the proposal that the TOrl chromosome carries a short segment of t haplotype chromatin containing Tcp-1a and proximal sperm factors involved in transmission ratio distortion and sterility.

scholarly journals Deletion of mouse t-complex distorter-1 produces an effect like that of the t-form of the distorter

1992 ◽  
Vol 59 (1) ◽  
pp. 27-33 ◽  
Author(s):  
Mary F. Lyon
Keyword(s):  
Male Sterility ◽  
Differential Susceptibility ◽  
Proximal Part ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Transmission Ratio ◽  
T Complex ◽  
Severe Impairment ◽  
Ratio Distortion ◽  
Distorter Gene

SummaryAn allele of the mouse brachyury locus, T22H, had been shown previously to involve a deletion of several markers in the proximal part of chromosome 17, and almost certainly includes deletion of the t-complex distorter gene Tcd-1. The effects of T22H on transmission ratio distortion and male sterility caused by the t-complex were compared with those of a partial t-haplotype th51, which carries the t-form of the distorter Tcd-1t. In combination with the complete haplotypetf32, T22H caused severe impairment of male fertility, but males of genotype T22H/t6 or T22H/thSl were normally fertile. These results were very similar to those obtained when th51 was in combination with the same haplotypes. In effect on transmission ratio T22H was again similar to thSI, in that it produced a marked increase in the transmission of the haplotype t6. To test whether the effects of T22H were due to deletion of elements other than Tcd-1, the effect of T22H on transmission of the partial haplotype th2 was compared with that of the deletion Thv. Again T22H markedly increased transmission of the t-haplotype and the effect was significantly greater than the small effect produced by Thp.It is concluded that deletion of the distorter Tcd-1 has an effect like that of the t-form of this distorter, Tcd-1t, and hence that Ted-11 must be an amorph or hypomorph. It is speculated that other t-complex distorters, Tcd-2t and Tcd-3t may also be amorphs or hypomorphs. Thus, the phenomena of transmission ratio distortion and male sterility due to the t-complex appear to be brought about by differential susceptibility of wild-type and t-responder alleles, Tcr+ and Tcrt, to a shortage of distorter gene product.

scholarly journals Gene dosage effects on transmission ratio distortion and fertility in mice that carry t haplotypes

1989 ◽  
Vol 54 (3) ◽  
pp. 221-225 ◽  
Author(s):  
Lee M. Silver
Keyword(s):  
Gene Dosage ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Double Dose ◽  
Absolute Level ◽  
T Complex ◽  
Gene Dosage Effects ◽  
Ratio Distortion ◽  
The Individual ◽  
Very High

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.

scholarly journals Deletion analysis of male sterility effects of t–haplotypes in the mouse

1990 ◽  
Vol 56 (2-3) ◽  
pp. 179-183 ◽  
Author(s):  
Dorothea Bennett ◽  
Karen Artzt
Keyword(s):  
Male Sterility ◽  
Deletion Analysis ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Transmission Ratio ◽  
Wild Type ◽  
Ratio Distortion ◽  
Very High

SummaryWe present data on the effects of three chromosome 17 deletions on transmission ratio distortion (TRD) and sterility of several t-haplotypes. All three deletions have similar effects on male TRD: that is, Tdel/tcomplete genotypes all transmit their t–haplotype in very high proportion. However, each deletion has different effects on sterility of heterozygous males, with Tor/t being fertile, Thp/t less fertile, and Torl/t still less fertile. These data suggest that wild-type genes on chromosomes homologous to f-haplotypes can be important regulators of both TRD and fertility in males, and that the wild-type genes concerned with TRD and fertility are at least to some extent different. The data also provide a rough map of the positions of these genes.

scholarly journals Targeted Mutagenesis of a Candidate t Complex Responder Gene in Mouse t Haplotypes Does Not Eliminate Transmission Ratio Distortion

Genetics ◽  
1996 ◽  
Vol 144 (2) ◽  
pp. 785-792
Author(s):  
U Kevin Ewulonu ◽  
Kerry Schimenti ◽  
Barbara Kuemerle ◽  
Terry Magnuson ◽  
John Schimenti
Keyword(s):  
Es Cells ◽  
Targeted Mutagenesis ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Functional Assay ◽  
T Complex ◽  
Actual Nature ◽  
Splicing Pattern ◽  
Ratio Distortion ◽  
T Haplotype

Abstract Transmission ratio distortion (TRD) associated with mouse t haplotypes causes +/t males to transmit the t-bearing chromosome to nearly all their offspring. Of the several genes involved in this phenomenon, the t complex responder (Tcrt) locus is absolutely essential for TRD to occur. A candidate Tcrt gene called Tcpl0bt was previously cloned from the genetically defined Tcrt region. Its location, restricted expression in testis, and a unique postmeiotic alternative splicing pattern supported the idea that Tcp10bt was Tcrt. To test this hypothesis in a functional assay, ES cells were derived from a viable partial t haplotype, and the Tcp10bt gene was mutated by homologous recombination. Mutant mice were mated to appropriate partial t haplotypes to determine whether the targeted chromosome exhibited transmission ratios characteristic of the responder. The results demonstrated that the targeted chromosome retained full responder activity. Hence, Tcp10bt does not appear to be Tcrt. These and other observations necessitate a reevaluation of genetic mapping data and the actual nature of the responder.

scholarly journals The mouse t complex distorter-3 (Tcd-3) locus and transmission ratio distortion

1993 ◽  
Vol 62 (2) ◽  
pp. 133-137 ◽  
Author(s):  
Lee M. Silver ◽  
Christine Buck
Keyword(s):  
Recombination Event ◽  
The Self ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Low Transmission ◽  
T Complex ◽  
Single Well ◽  
Ratio Distortion ◽  
Distorter Locus

SummaryA novel central partial t haplotype was generated by screening for a recombination event between overlapping distal and proximal partial haplotypes. This haplotype contains just two elements Tcrt and Tcd-3t —involved in the t-specific transmission ratio distortion phenotype. Breeding analysis of males that carry this chromosome provides evidence that Tcd-3 is, indeed, a distorter locus and not a second responder. Furthermore, the data indicate that a single well-defined distorter locus is insufficient to overcome completely the self-destructive, low transmission ratio distortion phenotype expressed by the t allele at the t complex responder locus, although a small, but highly significant, effect was observed.

scholarly journals Mechanisms of transmission ratio distortion at hybrid sterility loci within and between Mimulus species

2017 ◽  
Author(s):  
Rachel E. Kerwin ◽  
Andrea L. Sweigart
Keyword(s):  
Male Sterility ◽  
Native Species ◽  
Hybrid Sterility ◽  
Transmission Ratio Distortion ◽  
Transmission Ratio ◽  
Hybrid Male ◽  
Hybrid Male Sterility ◽  
Hybrid Incompatibility ◽  
Hybrid Transmission ◽  
Ratio Distortion

ABSTRACTHybrid incompatibilities are a common correlate of genomic divergence and a potentially important contributor to reproductive isolation. However, we do not yet have a detailed understanding of how hybrid incompatibility loci function and evolve within their native species, or why they are dysfunctional in hybrids. Here, we explore these issues for a well-studied, two-locus hybrid incompatibility between hybrid male sterility 1 (hms1) and hybrid male sterility 2 (hms2) in the closely related yellow monkeyflower species Mimulus guttatus and M. nasutus. By performing reciprocal backcrosses with introgression lines, we find evidence for gametic expression of the hms1-hms2 incompatibility. Surprisingly, however, hybrid transmission ratios at hms1 do not reflect this incompatibility, suggesting additional mechanisms counteract the effects of gametic sterility. Indeed, our backcross experiment shows hybrid transmission bias toward M. guttatus through both pollen and ovules, an effect that is particularly strong when hms2 is homozygous for M. nasutus alleles. In contrast, we find little evidence for hms1 transmission bias in crosses within M. guttatus, providing no indication of selfish evolution at this locus. Although we do not yet have sufficient genetic resolution to determine if hybrid sterility and transmission ratio distortion map to the same loci, our preliminary fine-mapping uncovers a genetically independent hybrid lethality system involving at least two loci linked to hms1. This fine-scale dissection of transmission ratio distortion at hms1 and hms2 provides insight into genomic differentiation between closely related Mimulus species and reveals multiple mechanisms of hybrid dysfunction.

Quantitation of two-dimensional gel proteins reveals unequal amounts of Tcp-1 gene products during mouse spermatogenesis but no correlation with transmission ratio distortion

Development ◽  
1985 ◽  
Vol 89 (1) ◽  
pp. 123-131
Author(s):  
Edwin R. Sánchez ◽  
Craig Hammerberg ◽  
Robert P. Erickson
Keyword(s):  
Protein A ◽  
Intrinsic Property ◽  
Transmission Ratio Distortion ◽  
Molecular Probe ◽  
Transmission Ratio ◽  
T Complex ◽  
In Vivo Labelling ◽  
Ratio Distortion

The discovery of a protein, p63/6·9, that is synthesized by both somatic and germ cells and coded for by a gene, Tcp-1, within the t complex provides a molecular probe for examining transmission ratio distortion in t mice. Two electromorphs of this protein exist. The acidic protein (a) is encoded by t-haplotype chromosomes, while the basic protein (b) is encoded by wild-type 17th chromosomes. We have measured the relative amounts of p63/6·9a and p63/6·9b for various t-complex bearing males and for several stages of spermatogenesis. There was no correlation between the ratio of p63/6·9a to b and the magnitude of transmission ratio distortion but the relative amounts of these proteins present in testicular cells can vary depending on the method of labelling. In vivo labelling results in the detection of two-fold greater amounts of p63/6·9a while in vitro labelling produces equimolar amounts of these two proteins. These data suggest that unequal synthesis or degradation of the p63/6·9 proteins occurs during spermatogenesis. It is proposed that increased synthesis of p63/6·9a in vivo is an intrinsic property of t-haplotypes.

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