Abstract
The t-haplotype, a mouse meiotic driver found on chromosome 17, has been a model for autosomal segregation distortion for close to a century, but several questions remain regarding its biology and evolutionary history. A recently published set of population genomics resources for wild mice includes several individuals heterozygous for the t-haplotype, which we use to characterize this selfish element at the genomic and transcriptomic level. Our results show that large sections of the t-haplotype have been replaced by standard homologous sequences, possibly due to occasional events of recombination, and that this complicates the inference of its history. As expected for a long genomic segment of very low recombination, the t-haplotype carries an excess of fixed nonsynonymous mutations compared to the standard chromosome. This excess is stronger for regions that have not undergone recent recombination, suggesting that occasional gene flow between the t and the standard chromosome may provide a mechanism to regenerate coding sequences that have accumulated deleterious mutations. Finally, we find that t-complex genes with altered expression largely overlap with deleted or amplified regions, and that carrying a t-haplotype alters the testis expression of genes outside of the t-complex, providing new leads into the pathways involved in the biology of this segregation distorter.
Highlights
The t-haplotype, a mouse meiotic driver found on chromosome 17, has been a model for autosomal segregation distortion for close to a century, but several questions remain regarding its biology and evolutionary history
We examined the extent of differentiation between the t-haplotype and the standard chromosome 17 of M. m. domesticus, for which there were four mice carrying the t-haplotype
Heterozygous SNPs were used; in t-carriers these SNPs correspond to differences between the t-haplotype and the standard chromosome, whereas in control individuals they correspond to general levels of heterozygosity
Summary
The t-haplotype, a mouse meiotic driver found on chromosome 17, has been a model for autosomal segregation distortion for close to a century, but several questions remain regarding its biology and evolutionary history. MEIOTIC drivers ( known as segregation distorters) are selfish alleles or chromosome variants that can transmit themselves to over 50% of the progeny of heterozygous individuals (Burt and Trivers 2009; Lindholm et al 2016), often by killing or inactivating gametes that carry the nondriver allele. This requires the combined action of at least one distorter gene, which attacks gametes, and a responder gene, which protects gametes carrying the driver [reviewed in Lindholm et al (2016)]. The extent to which the hundreds of genes on the t-haplotype have deteriorated, and whether occasional recombination with the standard chromosome is sufficient to maintain genetic integrity in meiotic drivers over millions of years (Dyer et al 2007; Pieper and Dyer 2016), remain open questions
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