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Interlocus gene conversion (IGC) homogenizes paralogs. Little is known regarding the mutation events that cause IGC and even less is known about the IGC mutations that experience fixation. To disentangle the rates of fixed IGC mutations from the tract lengths of these fixed mutations, we employ a composite likelihood procedure. We characterize the procedure with simulations. We apply the procedure to duplicated primate introns and to protein-coding paralogs from both yeast and primates. Our estimates from protein-coding data concerning the mean length of fixed IGC tracts were unexpectedly low and are associated with high degrees of uncertainty. In contrast, our estimates from the primate intron data had lengths in the general range expected from IGC mutation studies. While it is challenging to separate the rate at which fixed IGC mutations initiate from the average number of nucleotide positions that these IGC events affect, all of our analyses indicate that IGC is responsible for a substantial proportion of evolutionary change in duplicated regions. Our results suggest that IGC should be considered whenever the evolution of multigene families is examined.
RNA-Seq and gene expression microarrays provide comprehensive profiles of gene activity, but lack of reproducibility has hindered their application. A key challenge in the data analysis is the normalization of gene expression levels, which is current
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