Polymorphism of <i>t</i>-complex genes in European wild mice

Klein, Jan; Sípos, Péter; Figueroa, Felipe

doi:10.1017/s0016672300026239

Cited by 139 publications

(91 citation statements)

References 12 publications

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“…The reason for so many abnormal embryos developed in early pregnancy has been explained in mice (Bennett, 1975;Kline, 1975;Lyon, 1981;Klein et al, 1984). More than 16 complementation groups of recessive genes which affect early embryo development have been found in mice.…”

Section: Discussionmentioning

confidence: 99%

Heterogenous Macromolecular Contributions to Early Mouse Embryo Development

Hsu¹

1990

Dev Growth Differ

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Mouse embryos have been cultured for more than one half of its gestation period by providing sera from definite species of animals as the inducer at the proper stage of development. The processes of normal development at four different but discrete phases have been described.( of these growth factors in serum has been described (Hsu, 1980). It indicates that the differential biological activity which induces the early mouse embryogenesis among the sera from different animal species is due to the various degree of sequence homology between the growth factor family among the different species of animals.

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Section: Discussionmentioning

confidence: 99%

Heterogenous Macromolecular Contributions to Early Mouse Embryo Development

Hsu¹

1990

Dev Growth Differ

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“…In this case, complementation meant that two tailless mice carrying the same mutation (T/t x ) bred true for taillessness because both homozygotes (T/T and t x /t x ) died, producing a balanced lethal system whereas, in contrast, two different ones (t x and t y ) made one class of normal tailed progeny (Figure 2). In total, 16 different t complementation groups were identified (Klein et al 1984). Dorothea Bennett studied many of the lethals extensively (Bennett 1964), finding that they affected different stages of development from morula to nearly completed fetus.…”

Section: Brachyurymentioning

confidence: 99%

Mammalian Developmental Genetics in the Twentieth Century

Artzt

2012

Genetics

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This Perspectives is a review of the breathtaking history of mammalian genetics in the past century and, in particular, of the ways in which genetic thinking has illuminated aspects of mouse development. To illustrate the power of that thinking, selected hypothesis-driven experiments and technical advances are discussed. Also included in this account are the beginnings of mouse genetics at the Bussey Institute, Columbia University, and The Jackson Laboratory and a retrospective discussion of one of the classic problems in developmental genetics, the T/t complex and its genetic enigmas.

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“…Here we focus on two extreme types of distorters, "sterile" distorters, which are fully viable (Vii = 1), and "lethal" distorters (Vii = 0). At the t complex, lethality of homozygous individuals is caused by closely linked recessive lethals, which are often different for different t haplotypes (Klein et al 1984). Hence, t lt2 heterozygotes for two lethal haplotypes may be fully viable (V12 = 1) if t l and t2 belong to different "complementation groups."…”

Section: Segregation Distortion In a Large Unstructured Populationmentioning

confidence: 99%

“…As a matter of fact, until recently t haplotypes could be classified only as being different if they belonged to different complementation groups. No fewer than 16 complementation groups for 'viability have been described (Klein et al 1984). Complementation with respect to male fertility is also amply documented (e.g., Lyon 1991; Johnson et al 1995).…”

Section: Empirical Relevancementioning

confidence: 99%

“…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).…”

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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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Polymorphism of t-complex genes in European wild mice

Cited by 139 publications

References 12 publications

Heterogenous Macromolecular Contributions to Early Mouse Embryo Development

Heterogenous Macromolecular Contributions to Early Mouse Embryo Development

Mammalian Developmental Genetics in the Twentieth Century

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

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