scholarly journals Recent evolution of mouse t haplotypes at polymorphic microsatellites associated with the t complex responder (Tcr) locus

1996 ◽  
Vol 67 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Kristin G. Ardlie ◽  
Lee M. Silver
Keyword(s):  
Field Studies ◽  
Complementation Group ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Recent Common Ancestor ◽  
Central Component ◽  
Wild Mice ◽  
T Complex ◽  
Founding Population ◽  
Ratio Distortion

SummaryMicrosatellites closely associated with each member of the Tcp1O gene family were amplified simultaneously from t haplotype and wild-type forms of mouse chromosome 17, by PCR. The t complex responder (Tcr) locus, which plays a central role in transmission ratio distortion, maps within the Tcp10 cluster on the t haplotype. Thus the amplified set of microsatellite loci (referred to collectively as Tcp10ms) provides a direct marker for this central component of the meiotic drive system associated with all naturally occurring t haplotypes. A unique Tcp10ms pattern of microsatellite alleles was obtained for a number of independent, laboratory-maintained complete and partial t haplotypes. Independent t chromosomes found in wild mice from US populations also had unique patterns, even when they were classified within the same lethal complementation group. Wild and laboratory chromosomes in the tw5 group showed similarly-sized but non-identical Tcp10ms patterns, suggesting they share a recent common ancestor. These chromosomes are likely to have derived from an ancestral chromosome within the founding population of North American house mice. The Tcp10ms pattern was also shown to be useful in field studies for distinguishing among independentt haplotypes, when more than one is present within a single population.

scholarly journals Distorter genes of the mouse t-complex impair male fertility when heterozygous

1987 ◽  
Vol 49 (1) ◽  
pp. 57-60 ◽  
Author(s):  
Mary F. Lyon
Keyword(s):  
Male Fertility ◽  
Genetic Background ◽  
Inbred Strains ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Male Mice ◽  
Wild Type ◽  
T Complex ◽  
Ratio Distortion ◽  
Harmful Effects

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.

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 Narrowing the Critical Regions for Mouse t Complex Transmission Ratio Distortion Factors by Use of Deletions

Genetics ◽  
2000 ◽  
Vol 155 (2) ◽  
pp. 793-801 ◽  
Author(s):  
Mary F Lyon ◽  
John C Schimenti ◽  
Edward P Evans
Keyword(s):  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Transmission Ratio ◽  
Critical Interval ◽  
Enhanced Transmission ◽  
T Complex ◽  
Ratio Distortion ◽  
Critical Regions ◽  
Complex Transmission ◽  
T Haplotype

Abstract Previously a deletion in mouse chromosome 17, T22H, was shown to behave like a t allele of the t complex distorter gene Tcd1, and this was attributed to deletion of this locus. Seven further deletions are studied here, with the aim of narrowing the critical region in which Tcd1 must lie. One deletion, T30H, together with three others, T31H, T33H, and T36H, which extended more proximally, caused male sterility when heterozygous with a complete t haplotype and also enhanced transmission ratio of the partial t haplotype t 6, and this was attributed to deletion of the Tcd1 locus. The deletions T29H, T32H, and T34H that extended less proximally than T30H permitted male fertility when opposite a complete t haplotype. These results enabled narrowing of the critical interval for Tcd1 to between the markers D17Mit164 and D17Leh48. In addition, T29H and T32H enhanced the transmission ratio of t6, but significantly less so than T30H. T34H had no effect on transmission ratio. These results could be explained by a new distorter located between the breakpoints of T29H and T34H (between T and D17Leh66E). It is suggested that the original distorter Tcd1 in fact consists of two loci: Tcd1a, lying between D17Mit164 and D17Leh48, and Tcd1b, lying between T and D17Leh66E.

scholarly journals Physical Mapping of Male Fertility and Meiotic Drive Quantitative Trait Loci in the MousetComplex Using Chromosome Deficiencies

Genetics ◽  
2000 ◽  
Vol 155 (2) ◽  
pp. 803-812 ◽  
Author(s):  
Antonio Planchart ◽  
Yun You ◽  
John C Schimenti
Keyword(s):  
Wild Mouse ◽  
Complex Trait ◽  
Proximal Region ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Variant Form ◽  
Recombination Suppression ◽  
T Complex ◽  
Ratio Distortion ◽  
In Trans

AbstractThe t complex spans 20 cM of the proximal region of mouse chromosome 17. A variant form, the t haplotype (t), exists at significant frequencies in wild mouse populations and is characterized by the presence of inversions that suppress recombination with wild-type (+) chromosomes. Transmission ratio distortion and sterility are associated with t and affect males only. It is hypothesized that these phenomena are caused by trans-acting distorter/sterility factors that interact with a responder locus (Tcrt) and that the distorter and sterility factors are the same because homozygosity of the distorters causes male sterility. One factor, Tcd1, was previously shown to be amorphic using a chromosome deletion. To overcome limitations imposed by recombination suppression, we used a series of deletions within the t complex in trans to t chromosomes to characterize the Tcd1 region. We find that the distorter activity of Tcd1 is distinct from a linked sterility factor, originally called tcs1. YACs mapped with respect to deletion breakpoints localize tcs1 to a 1.1-Mb interval flanked by D17Aus9 and Tctex1. We present evidence for the existence of multiple proximal t complex regions that exhibit distorter activity. These studies demonstrate the utility of chromosome deletions for complex trait analysis.

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 t-Specific DNA polymorphisms among wild mice from Israel and Spain.

Genetics ◽  
1988 ◽  
Vol 119 (1) ◽  
pp. 157-160
Author(s):  
F Figueroa ◽  
E Neufeld ◽  
U Ritte ◽  
J Klein
Keyword(s):  
Laboratory Mouse ◽  
The Other ◽  
Dna Polymorphisms ◽  
Chromosome 17 ◽  
Mouse Strains ◽  
Laboratory Mice ◽  
Wild Type ◽  
Wild Mice ◽  
T Complex ◽  
Length Polymorphisms

Abstract Lehrach and his coworkers have isolated a series of DNA probes that specifically hybridize with different regions of mouse chromosome 17 within the t complex. The probes display restriction fragment length polymorphisms, RFLPs, which are specific for the t haplotypes in all laboratory mouse strains tested thus far. Some of these probes have been used to test wild mice populations for these t-associated DNA forms. It is demonstrated that populations from Germany, Switzerland, Italy, Greece, Yugoslavia, Australia, Costa Rica, and Venezuela contain chromosomes in which all the tested DNA loci display the t-specific polymorphisms. The frequency of mice carrying these chromosomes is as high as 31%. Wild mice from Israel and Spain, on the other hand, carry chromosomes displaying t-specific DNA forms only at one or two of the probed loci, while the other loci carry the wild-type (+) forms. These chromosomes thus resemble the partial t haplotypes known from the study of laboratory mice. One possible interpretation of these findings is that these DNA polymorphisms contributed to the assembly of the complete t haplotypes and that these haplotypes may have originated in the Middle East.

A premature acrosome reaction is programmed by mouse t haplotypes during sperm differentiation and could play a role in transmission ratio distortion

Development ◽  
1989 ◽  
Vol 106 (4) ◽  
pp. 769-773 ◽  
Author(s):  
J. Brown ◽  
J.A. Cebra-Thomas ◽  
J.D. Bleil ◽  
P.M. Wassarman ◽  
L.M. Silver
Keyword(s):  
Acrosome Reaction ◽  
Genetic Data ◽  
Transmission Ratio Distortion ◽  
Chromosome 17 ◽  
Relative Advantage ◽  
Transmission Ratio ◽  
Ratio Distortion ◽  
Sperm Dysfunction

Mouse t haplotypes are variant forms of chromosome 17 that can be transmitted at non-Mendelian ratios by heterozygous +/t males. The accumulated genetic data indicate that ‘+-sperm’ and ‘t-sperm’ are produced in equal numbers but that most ‘+-sperm’ are rendered dysfunctional, so that ‘t-sperm’ have a relative advantage at fertilization. To date, the basis for this t-induced sperm dysfunction has remained unknown. Here we demonstrate that a high proportion of sperm obtained from certain strains of +/t mice undergo a premature acrosome reaction under in vitro capacitation conditions. The simplest interpretation of these data, in conjunction with previous results, is that developing ‘+-spermatids’ are preprogrammed by ‘t-spermatids’ to undergo this premature reaction. Since acrosome-reacted sperm are unable to participate in the process of fertilization, this defect could account for the extreme distortion of transmission ratio observed from mice heterozygous for a class of complete t haplotypes.

scholarly journals Identification of the t Complex–encoded Cytoplasmic Dynein Light Chain Tctex1 in Inner Arm I1 Supports the Involvement of Flagellar Dyneins in Meiotic Drive

1998 ◽  
Vol 140 (5) ◽  
pp. 1137-1147 ◽  
Author(s):  
Alistair Harrison ◽  
Patricia Olds-Clarke ◽  
Stephen M. King
Keyword(s):  
Light Chain ◽  
Meiotic Drive ◽  
Cytoplasmic Dynein ◽  
Transmission Ratio Distortion ◽  
Dynein Light Chain ◽  
Mouse Sperm ◽  
T Complex ◽  
Ratio Distortion ◽  
Dynein Arms ◽  
Mendelian Transmission

The cytoplasmic dynein light chain Tctex1 is a candidate for one of the distorter products involved in the non-Mendelian transmission of mouse t haplotypes. It has been unclear, however, how the t-specific mutations in this protein, which is found associated with cytoplasmic dynein in many tissues, could result in a male germ cell–specific phenotype. Here, we demonstrate that Tctex1 is not only a cytoplasmic dynein component, but is also present both in mouse sperm and Chlamydomonas flagella. Genetic and biochemical dissection of the Chlamydomonas flagellum reveal that Tctex1 is a previously undescribed component of inner dynein arm I1. Combined with the recent identification of another putative t complex distorter, Tctex2, within the outer dynein arm, these results support the hypothesis that transmission ratio distortion (meiotic drive) of mouse t haplotypes involves dysfunction of both flagellar inner and outer dynein arms but does not require the cytoplasmic isozyme.

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.

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