Meiotic drive of noncentromeric loci in mammalian meiosis II eggs

Silva, Duílio Mazzoni Zerbinato de Andrade

doi:10.1016/j.gde.2023.102082

Cited by 3 publications

(2 citation statements)

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“…Female meiotic drive can occur in either of the two meiotic divisions, depending on when the driving locus segregates from its homolog. 26 Homologous centromeres segregate in meiosis I, and therefore selfish centromeres cheat exclusively in meiosis I. 34 In contrast, a non-centromeric locus like R2d2 can cheat either in meiosis I or II depending on the crossover position (Figure 1B).…”

Section: Resultsmentioning

confidence: 99%

“…21,23–25 Other loci usually do not control chromosome-spindle interactions, and therefore, it is unknown how non-centromeric meiotic drivers manipulate their segregation patterns, except for maize knob that exploit an asymmetry specific to plant female meiosis. 3,26–28 We chose the selfish R2d2 ( Responder to drive 2 ) locus as a model system to tackle this question. R2d2 is a repetitive DNA of a 127 kb-long monomer found on mouse chromosome 2 and experiences transmission rates above 95% from heterozygous female mice.…”

Section: Introductionmentioning

confidence: 99%

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An egg sabotaging mechanism drives non-Mendelian transmission in mice

Clark,

Greenberg,

Silva

et al. 2024

Preprint

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SummaryDuring meiosis, homologous chromosomes segregate so that alleles are transmitted equally to haploid gametes, following Mendel’s Law of Segregation. However, some selfish genetic elements drive in meiosis to distort the transmission ratio and increase their representation in gametes. The established paradigms for drive are fundamentally different for female vs male meiosis. In male meiosis, selfish elements typically kill gametes that do not contain them. In female meiosis, killing is predetermined, and selfish elements bias their segregation to the single surviving gamete (i.e., the egg in animal meiosis). Here we show that a selfish element on mouse chromosome 2,R2d2, drives using a hybrid mechanism in female meiosis, incorporating elements of both male and female drivers. IfR2d2is destined for the polar body, it manipulates segregation to sabotage the egg by causing aneuploidy that is subsequently lethal in the embryo, so that surviving progeny preferentially containR2d2. In heterozygous females,R2d2orients randomly on the metaphase spindle but lags during anaphase and preferentially remains in the egg, regardless of its initial orientation. Thus, the egg genotype is either euploid withR2d2or aneuploid with both homologs of chromosome 2, with only the former generating viable embryos. Consistent with this model,R2d2heterozygous females produce eggs with increased aneuploidy for chromosome 2, increased embryonic lethality, and increased transmission ofR2d2. In contrast to a male meiotic driver, which kills its sister gametes produced as daughter cells in the same meiosis,R2d2eliminates “cousins” produced from meioses in which it should have been excluded from the egg.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

An egg sabotaging mechanism drives non-Mendelian transmission in mice

Clark,

Greenberg,

Silva

et al. 2024

Preprint

Self Cite

View full text Add to dashboard Cite

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An egg-sabotaging mechanism drives non-Mendelian transmission in mice

Clark,

Greenberg,

Silva

et al. 2024

Current Biology

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Female meiotic drive shapes the distribution of rare inversion polymorphisms in Drosophila melanogaster

Koury

2023

Genetics

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In all species, new chromosomal inversions are constantly being formed by spontaneous rearrangement and then stochastically eliminated from natural populations. In Drosophila, when new chromosomal inversions overlap with a pre-existing inversion in the population, their rate of elimination becomes a function of the relative size, position, and linkage phase of the gene rearrangements. These altered dynamics result from complex meiotic behavior wherein overlapping inversions generate asymmetric dyads that cause both meiotic drive/drag and segmental aneuploidy. In this context, patterns in rare inversion polymorphisms of a natural population can be modeled from the fundamental genetic processes of forming asymmetric dyads via crossing-over in meiosis I and preferential segregation from asymmetric dyads in meiosis II. Here, a mathematical model of crossover-dependent female meiotic drive is developed and parameterized with published experimental data from Drosophila melanogaster laboratory constructs. This mechanism is demonstrated to favor smaller, distal inversions and accelerate the elimination of larger, proximal inversions. Simulated sampling experiments indicate that the paracentric inversions directly observed in natural population surveys of Drosophila melanogaster are a biased subset that both maximizes meiotic drive and minimizes the frequency of lethal zygotes caused by this cytogenetic mechanism. Incorporating this form of selection into a population genetic model accurately predicts the shift in relative size, position, and linkage phase for rare inversions found in this species. The model and analysis presented here suggest that this weak form of female meiotic drive is an important process influencing the genomic distribution of rare inversion polymorphisms.

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Meiotic drive of noncentromeric loci in mammalian meiosis II eggs

Cited by 3 publications

References 46 publications

An egg sabotaging mechanism drives non-Mendelian transmission in mice

An egg sabotaging mechanism drives non-Mendelian transmission in mice

An egg-sabotaging mechanism drives non-Mendelian transmission in mice

Female meiotic drive shapes the distribution of rare inversion polymorphisms in Drosophila melanogaster

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