Unlocking the genomic basis of speciation is a research priority in biology fuelled by the ongoing debate on species concepts and facilitated by the availability of an unprecedented large number of genomic resources. Through comparative genomics of both closely and distantly related mammalian species our research group, along with others, has contributed to models that explain genome structure and evolution. Such reconstructions have revealed that the genomic regions implicated in structural evolutionary changes, disrupt genomic synteny, and are clustered in regions more prone to break and reorganize. In searching for the origin (and consequences) of this evolutionary instability, we provided insights on the genomic features that characterize evolutionary regions. In addition, we have also observed that changes in gene expression that are caused by genome reshuffling may have a selective advantage through the development of new adaptive characters specific to mammalian lineages. Consequently, given the diversity of factors associated with genome reshuffling it is most unlikely that the sequence composition of genomes is solely responsible for genomic instability during evolution. This view represents a new interpretative evolutionary hypothesis that has recently been unified by our research group as the ‘Integrative Breakage Model’, which postulates that the permissiveness of some genomic regions to undergo chromosomal breakage and genomic rearrangements could be influenced by chromatin conformation. Here we will provide evidence that suggest that certain properties of local DNA sequences, together with the epigenetic state of the chromatin, are effecting gene expression and are key elements in determining the genomic distribution of evolutionary breakpoints during the cell cycle in mammals.
Unlocking the genomic basis of speciation is a research priority in biology fuelled by the ongoing debate on species concepts and facilitated by the availability of an unprecedented large number of genomic resources. Through comparative genomics of both closely and distantly related mammalian species our research group, along with others, has contributed to models that explain genome structure and evolution. Such reconstructions have revealed that the genomic regions implicated in structural evolutionary changes, disrupt genomic synteny, and are clustered in regions more prone to break and reorganize. In searching for the origin (and consequences) of this evolutionary instability, we provided insights on the genomic features that characterize evolutionary regions. In addition, we have also observed that changes in gene expression that are caused by genome reshuffling may have a selective advantage through the development of new adaptive characters specific to mammalian lineages. Consequently, given the diversity of factors associated with genome reshuffling it is most unlikely that the sequence composition of genomes is solely responsible for genomic instability during evolution. This view represents a new interpretative evolutionary hypothesis that has recently been unified by our research group as the ‘Integrative Breakage Model’, which postulates that the permissiveness of some genomic regions to undergo chromosomal breakage and genomic rearrangements could be influenced by chromatin conformation. Here we will provide evidence that suggest that certain properties of local DNA sequences, together with the epigenetic state of the chromatin, are effecting gene expression and are key elements in determining the genomic distribution of evolutionary breakpoints duri ...
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