Autosomes 22 pairs are homologous in humans, whereas male sex chromosomes XY are non-homologouswhile female sex chromosomes XX are homologous. With recurrent mutation to the differences between autosomes and sex chromosomes in Bedford allele, the substitution will eventually become fixed, with the waiting time determined by the mutation rate and strength of selection in favor of the mutation.
J Struct Funct Genomics 3: 35— Related to this, we do not know if Y chromosome incorporations are selection-driven events, as proposed by Carvalho and Clark [ 21 ] or, alternatively, mutations fixed by genetic drift; it is also possible that some were selection-driven events perhaps D.
Alternative hypothesis for the re-appearance of Y-linkage in the montium and pseudoobscura lineages The duplicated Y hypothesis Fig 5 is bold, but as far as we can see it is the best explanation for the data.
In sex chromosomes the centromere position os non-identical.
PLoS Biol 7 : e doi To accommodate the potential impact of both linkage and epistasis, we first developed two-locus, bi-allelic population genetic models with arbitrary fitnesses assigned to each genotype and sex Table 1. This being true, the montium Y should had acquired other male genes besides the nine mentioned above.
Choi, J. One or more loci on these chromosomes then segregate for alleles under sexually antagonistic selection. Andrews, S. After alignment, the flagstat tool in SAMtools 21 was used to calculate the percent reads correctly mapped to the reference genome. Samanthi Udayangani holds a B.
The genome analysis toolkit: a MapReduce framework for analyzing next-generation DNA sequencing data.
Vibranovski, B. Sex-dependent gene expression and evolution of the Drosophila transcriptome. Cambridge University Press; Boston: SLY1 protein colocalized with Speer gene cluster in These results are in agreement with a recent analysis by Fry , which focused on opportunities for stable polymorphism on the X and autosomes, and runs counter to the intuition that sexual antagonism will generally lead to an enrichment of sex-linked, sex-biased genes.