Meiotic drive at the Om locus in wild-derived inbred mouse strains

Kim, Kuikwon; Thomas, Sanlare; Howard, I. Brian; Bell, Timothy A.; Doherty, Heather E.; Ideraabdullah, Folami Y.; Detwiler, David A.; Villena, Fernando Pardo Manuel de

doi:10.1111/j.1095-8312.2005.00449.x

Cited by 9 publications

(15 citation statements)

References 23 publications

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“…Tissues were infused with RNAlater (Qiagen) and frozen at −80°C to preserve RNA integrity until extraction. Whole brain was isolated from mouse pups derived from crosses (DDKxC57BL/6J)F1 X PANCEVO/EiJ, (C57BL/6J X DDK)F1 X TIRANO/Ei and (C57BL/6J X DDK)F1 X ZALENDE/Ei [63] and (C57BL/6J X PERA)F1 X C57BL/6J [64]. These mouse crosses were generated for previous studies and reported elsewhere.…”

Section: Methodsmentioning

confidence: 99%

Genetic Architecture of Skewed X Inactivation in the Laboratory Mouse

et al. 2013

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X chromosome inactivation (XCI) is the mammalian mechanism of dosage compensation that balances X-linked gene expression between the sexes. Early during female development, each cell of the embryo proper independently inactivates one of its two parental X-chromosomes. In mice, the choice of which X chromosome is inactivated is affected by the genotype of a cis-acting locus, the X-chromosome controlling element (Xce). Xce has been localized to a 1.9 Mb interval within the X-inactivation center (Xic), yet its molecular identity and mechanism of action remain unknown. We combined genotype and sequence data for mouse stocks with detailed phenotyping of ten inbred strains and with the development of a statistical model that incorporates phenotyping data from multiple sources to disentangle sources of XCI phenotypic variance in natural female populations on X inactivation. We have reduced the Xce candidate 10-fold to a 176 kb region located approximately 500 kb proximal to Xist. We propose that structural variation in this interval explains the presence of multiple functional Xce alleles in the genus Mus. We have identified a new allele, Xcee present in Mus musculus and a possible sixth functional allele in Mus spicilegus. We have also confirmed a parent-of-origin effect on X inactivation choice and provide evidence that maternal inheritance magnifies the skewing associated with strong Xce alleles. Based on the phylogenetic analysis of 155 laboratory strains and wild mice we conclude that Xcea is either a derived allele that arose concurrently with the domestication of fancy mice but prior the derivation of most classical inbred strains or a rare allele in the wild. Furthermore, we have found that despite the presence of multiple haplotypes in the wild Mus musculus domesticus has only one functional Xce allele, Xceb. Lastly, we conclude that each mouse taxa examined has a different functional Xce allele.

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Section: Methodsmentioning

confidence: 99%

Genetic Architecture of Skewed X Inactivation in the Laboratory Mouse

et al. 2013

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“…The three crosses used as controls in this study, (C57BL/6 3 DDK)F 1 3 C57BL/6, (C57BL/6 3 DDK)F 1 3 DDK, and (C57BL/6 3 DDK)F 1 3 (C57BL/6 3 DDK)F 1 (in all crosses described in this study the dam is always listed first and the sire second unless otherwise indicated) have been described previously (Sapienza et al 1992;Pardo-Manuel de Villena et al 1996, 1997, 1999, 2000a. Some of the crosses involving inbred males have been previously described in our efforts to characterize a meiotic drive phenotype (Kim et al 2005;Wu et al 2005). Briefly, each male was mated to identical (C57BL/6 3 DDK)F 1 females and monitored daily for newborn pups.…”

Section: Methodsmentioning

confidence: 99%

The Paternal Gene of the DDK Syndrome Maps to the Schlafen Gene Cluster on Mouse Chromosome 11

Bell¹,

Casa-Esperón²,

Doherty³

et al. 2006

Genetics

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The DDK syndrome is an early embryonic lethal phenotype observed in crosses between females of the DDK inbred mouse strain and many non-DDK males. Lethality results from an incompatibility between a maternal DDK factor and a non-DDK paternal gene, both of which have been mapped to the Ovum mutant (Om) locus on mouse chromosome 11. Here we define a 465-kb candidate interval for the paternal gene by recombinant progeny testing. To further refine the candidate interval we determined whether males from 17 classical and wild-derived inbred strains are interfertile with DDK females. We conclude that the incompatible paternal allele arose in the Mus musculus domesticus lineage and that incompatible strains should share a common haplotype spanning the paternal gene. We tested for association between paternal allele compatibility/incompatibility and 167 genetic variants located in the candidate interval. Two diallelic SNPs, located in the Schlafen gene cluster, are completely predictive of the polar-lethal phenotype. These SNPs also predict the compatible or incompatible status of males of five additional strains.

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“…Stated another way, there is no reason to expect selective forces that influence the evolution of chromosome morphology and number—for example, meiotic drive, changes in cellular processes that affect meiosis and mitosis, and processes that underlie karyotypic orthoselection—will optimize organismal fitness (Sandler and Novitski 1957; Terzi 1972; Pardo‐Manuel de Villena and Sapienza 2001; Kim et al 2005). To the contrary, these processes are capable of driving chromosomal variants to fixation even if those variants are neutral, underdominant, or weakly maladaptive (Pardo‐Manuel de Villena and Sapienza 2001; Kim et al 2005). Consequently, I interpret θ i in the current study as karyotypic equilibria rather than adaptive optima, on the grounds that if chromosome number evolution proceeds according to an Ornstein–Uhlenbeck process, chromosome number in each lineage will equilibrate at a stationary distribution with mean θ and variance determined by the relationship between α and σ, irrespective of the causes of chromosome evolution.…”

Section: Modeling the Evolution Of Holocentric Chromosomesmentioning

confidence: 99%

Nonuniform Processes of Chromosome Evolution in Sedges (Carex: Cyperaceae)

Hipp

2007

Evolution

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Holocentric chromosomes-chromosomes that lack localized centromeres-occur in numerous unrelated clades of insects, flatworms, and angiosperms. Chromosome number changes in such organisms often result from fission and fusion events rather than polyploidy. In this study, I test the hypothesis that chromosome number evolves according to a uniform process in Carex section Ovales (Cyperaceae), the largest New World section of an angiosperm genus renowned for its chromosomal variability and species richness. I evaluate alternative models of chromosome evolution that allow for shifts in both stochastic and deterministic evolutionary processes and that quantify the rate of evolution and heritability/phylogenetic dependence of chromosome number. Estimates of Ornstein-Uhlenbeck model parameters and tree-scaling parameters in a generalized least squares framework demonstrate that (1) chromosome numbers evolve rapidly toward clade-specific stationary distributions that cannot be explained by constant variance (Brownian motion) evolutionary models, (2) chromosome evolution in the section is rapid and exhibits little phylogenetic inertia, and (3) explaining the phylogenetic pattern of chromosome numbers in the section entails inferring a shift in evolutionary dynamics at the root of a derived clade. The finding that chromosome evolution is not a uniform process in sedges provides a novel example of karyotypic orthoselection in an organism with holocentric chromosomes.

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Meiotic drive at the Om locus in wild-derived inbred mouse strains

Cited by 9 publications

References 23 publications

Genetic Architecture of Skewed X Inactivation in the Laboratory Mouse

Genetic Architecture of Skewed X Inactivation in the Laboratory Mouse

The Paternal Gene of the DDK Syndrome Maps to the Schlafen Gene Cluster on Mouse Chromosome 11

Nonuniform Processes of Chromosome Evolution in Sedges (Carex: Cyperaceae)

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