Distribution of T-Haplotypes in Natural Populations of Wild House Mice

Lenington, Sarah; Franks, Patricia C.; Williams, Jonathan K.

doi:10.2307/1381340

Cited by 42 publications

(46 citation statements)

References 25 publications

(22 reference statements)

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“…Thus t haplotypes are maintained as a polymorphism in natural populations (Petras, 1967;Figueroa et al 1988;Lenington, Franks & Williams, 1988). t haplotypes express no obvious phenotype in wild mice, and only with the recent availability of molecular probes that identify restriction fragment length polymorphisms (RFLPs) between t and wild-type DNA, has it become possible to definitively characterize the genotypes of large numbers of wild mice.…”

Section: Introductionmentioning

confidence: 99%

Recent evolution of mousethaplotypes at polymorphic microsatellites associated with thetcomplex responder (Tcr) locus

Ardlie

Silver

1996

Genet. Res.

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Microsatellites closely associated with each member of the TcplO 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 TcplO cluster on the t haplotype. Thus the amplified set of microsatellite loci (referred to collectively as TcplOms) provides a direct marker for this central component of the meiotic drive system associated with all naturally occurring t haplotypes. A unique TcplOms 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 t w5 group showed similarly-sized but non-identical TcplOms 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 TcplOms pattern was also shown to be useful in field studies for distinguishing among independent t haplotypes, when more than one is present within a single population.

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Section: Introductionmentioning

confidence: 99%

Recent evolution of mousethaplotypes at polymorphic microsatellites associated with thetcomplex responder (Tcr) locus

Ardlie

Silver

1996

Genet. Res.

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“…In particular, there is a striking difference between the equilibrium frequencies predicted by our deterministic model ( Fig. 1 and 3), and the much lower frequencies of t haplotypes in the field (Lenington et al 1988;Ruvinsky et al 1991). This is a general problem shared by most deterministic models of segregation distortion.…”

Section: Empirical Relevancementioning

confidence: 56%

“…Although empiricists mainly consider the allele frequencies in adults (e.g., Lenington et al 1988), the selection dynamics is more easily formulated in terms of the genotype frequencies at the zygote stage (Nagylaki 1992) or in terms of allele frequencies in male and female gametes (Lessard 1989). We focus on the allele frequencies in zygotes, because at that stage the frequencies do not differ between the sexes.…”

Section: Segregation Distortion In a Large Unstructured Populationmentioning

confidence: 99%

“…Variants of this gene complex, the so-called t haplotypes, lead to reduced viability and complete male sterility in homozygous condition. Nevertheless, t haplotypes reach appreciable frequencies (10%-25%) in most feral house-mouse populations (Lenington et al 1988). This polymorphism results from the fact that the negative fitness effects of t haplotypes at the individual level are counterbalanced by a fitness advantage at the gamete level.…”

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confidence: 99%

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COMPETITION BETWEEN SEGREGATION DISTORTERS: COEXISTENCE OF “SUPERIOR” AND “INFERIOR” HAPLOTYPES AT THEtCOMPLEX

et al. 1996

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Abstract.-By means of population genetical models, we investigate the competition between sex-specific segregation distorters. Although the models are quite general, they are motivated by a specific example, the t complex of the house mouse. Some variants at this gene complex, the t haplotypes, distort Mendelian segregation in heterozygous males in their favor. The selective advantage at the gamete level is counterbalanced by strong negative fitness effects at the individual level (male sterility or even lethality in both sexes). A plethora of different t haplotypes has been found, both in the field and in the lab. Up to now, however, models have focused on the equilibrium frequency of a single t haplotype. In contrast, we explicitly model the competition between several t haplotypes. A deterministic model for a large, well-mixed population predicts a surprisingly high degree of polymorphism. Haplotypes with seemingly inferior fitness characteristics may easily coexist with "superior" haplotypes. For instance, a lethal haplotype with a low segregation ratio may stably coexist with a sterile haplotype with a high segregation ratio. Stable coexistence is even possible for haplotypes with a segregation disadvantage. A simple stochastic model shows that the same principles apply in the context of a structured metapopulation. Although counterintuitive at first sight, all our results can be explained by the fact that segregation distorters have an inherent advantage when they are rare. We conclude that fitness comparisons are not sufficient to predict the outcome of competition when selective forces are acting at different levels. The t complex of the house mouse is a large complex of closely linked genes on chromosome 17. Variants of this gene complex, the so-called t haplotypes, lead to reduced viability and complete male sterility in homozygous condition. Nevertheless, t haplotypes reach appreciable frequencies (10%-25%) in most feral house-mouse populations (Lenington et al. 1988). This polymorphism results from the fact that the negative fitness effects of t haplotypes at the individual level are counterbalanced by a fitness advantage at the gamete level. In heterozygous males, Mendelian segregation is strongly distorted in favor of t haplotypes. In fact, segregation ratios greater than 0.95 are not uncommon.By now, a large number or different t haplotypes has been found. All t haplotypes lead to male sterility in homozygous condition, but they vary in their effects on viability. Some haplotypes are completely viable, some have a reduced viability, whereas still others induce complete lethality in homozygous condition (Klein et al. 1984). Although a large variety of fitness effects has been described, most t haplotypes in feral house-mouse populations lead to embryonic lethality both in males and in females (Silver 1993).The segregation ratio is also subject to considerable variation: segregation ratios vary from as low as 0.20 to as high as 1.00 (Bennett et al. 1983;Gummere et al. 1986;Lenington and Heisler 1991...

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“…In each bottle of experimental populations, 300-400 individuals were present, and females may avoid distorting males. This is known in M. mus.culus, where females from populations where t-haplotyp: IS present learn to avoid males bearing t-haplotype (Lenington et al 1988). Some D. melanogaster females from Zimbabwe refuse to mate with males from other populations (Wu et al 1995), indicating that females do have mate preferences.…”

Section: Driving X Chromosomesmentioning

confidence: 99%

EVOLUTION OF DRIVING X CHROMOSOMES AND RESISTANCE FACTORS IN EXPERIMENTAL POPULATIONS OFDROSOPHILA SIMULANS

Capillon

Atlan

1999

Evolution

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Abstract.-Sex-ratio drive is a particular case of meiotic drive, described in several Drosophila species, that causes males bearing driving X chromosome to produce a large excess of females in their progeny. In Drosophila simulans, driving X chromosomes and resistance factors located on the Y chromosome and on the autosomes have been previously reported. In this paper, we report the study of the dynamics of sex-ratio factors in experimental populations. We followed the evolution in frequency of driving X chromosomes in the absence of resistance factors and the evolution of resistance factors in the presence of driving X chromosomes. The driving X chromosome was lost, contrarily to theoretical expectations that predict its rapid invasion. Autosomal resistances increased in frequency, and resistant Y chromosomes invaded the population very quickly, as predicted by theoretical models. Fitness measurements showed that the loss of the driving X chromosome was due to a strong deleterious effect that was expressed only when distorting males were in competition with standard males. However, the spread of autosomal resistances reduced this deleterious effect. Implications for the maintenance of polymorphism in natural populations are discussed.

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Distribution of T-Haplotypes in Natural Populations of Wild House Mice

Cited by 42 publications

References 25 publications

Recent evolution of mousethaplotypes at polymorphic microsatellites associated with thetcomplex responder (Tcr) locus

Recent evolution of mousethaplotypes at polymorphic microsatellites associated with thetcomplex responder (Tcr) locus

COMPETITION BETWEEN SEGREGATION DISTORTERS: COEXISTENCE OF “SUPERIOR” AND “INFERIOR” HAPLOTYPES AT THEtCOMPLEX

EVOLUTION OF DRIVING X CHROMOSOMES AND RESISTANCE FACTORS IN EXPERIMENTAL POPULATIONS OFDROSOPHILA SIMULANS

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