Abstract
The t-haplotype of mice is a classical model for autosomal transmission distortion. A largely non-recombining variant of the proximal region of chromosome 17, it is transmitted to more than 90% of the progeny of heterozygous males through the disabling of sperm carrying a standard chromosome. While extensive genetic and functional work has shed light on individual genes involved in drive, much less is known about the evolution and function of the rest of its hundreds of genes. Here, we characterize the sequence and expression of dozens of t-specific transcripts and of their chromosome 17 homologues. Many genes showed reduced expression of the t-allele, but an equal number of genes showed increased expression of their t-copy, consistent with increased activity or a newly evolved function. Genes on the t-haplotype had a significantly higher non-synonymous substitution rate than their homologues on the standard chromosome, with several genes harbouring dN/dS ratios above 1. Finally, the t-haplotype has acquired at least two genes from other chromosomes, which show high and tissue-specific expression. These results provide a first overview of the gene content of this selfish element, and support a more dynamic evolutionary scenario than expected of a large genomic region with almost no recombination.
Highlights
Genetic variants that increase their own transmission rate during gametogenesis will spread in the population even if neutral or detrimental with respect to the fitness of the organism [1]
The t-haplotype has acquired at least two genes from other chromosomes, which show high and tissue-specific expression. These results provide a first overview of the gene content of this selfish element, and support a more dynamic evolutionary scenario than expected of a large genomic region with almost no recombination
There has been considerable progress in identifying specific genes underlying the driving mechanisms of different distorters [5,6,7,8,9,10,11,12,13], but much less is known about how the rest of the gene content of these selfish haplotypes differs from that of their homologous genomic region, and what evolutionary pressures contributed to these changes [7,11,14]
Summary
Genetic variants that increase their own transmission rate during gametogenesis will spread in the population even if neutral or detrimental with respect to the fitness of the organism [1]. Reduced recombination between the driving region and its homologous chromosome is often achieved by large inversions, which may trap hundreds of other genes on the driving haplotype [19,20,21,22] These genes are expected to be subject to less efficient purifying selection, which may be compounded if deleterious mutations hitch-hike when new driver mutations sweep to fixation. We describe two highly expressed t-specific genes, which were gained from other chromosomes These results highlight the dynamic evolution of this nonrecombining selfish chromosome, at odds with a simple scenario of reduced purifying selection that is expected for a large low recombination region, and potentially suggesting that significant sections of the genome may be co-opted for 2 transmission distortion
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call