Biomathematics Seminar: Evolution of gene duplicates in a regulatory context
17 November 2015 14:00 in CM105
Gene duplication is believed to play a major role in the evolution of genomic complexity. While there are several hypothesised consequences of duplication that allow such genes to show up in the genomic record, and several population genetic models that demonstrate such evolutionary outcomes, there is a paucity of mechanistic network models of phenotype that mediate the gene to evolution narrative. I will talk about a model in which duplicate genes are studied in the context of its regulatory interactions, showing how the emergent dynamical phenotypes enable duplicate genes to spread in a population. I will discuss how mutations in regulatory (cis) and protein-coding (trans) regions result in qualitatively different phenotypes. When cis-regulatory changes are introduced that partition multiple regulatory triggers among the duplicates, it is shown that mutually exclusive expression states of the duplicates that emerge are accompanied by a back-up facility: when a highly expressed gene is deleted, the previously unexpressed duplicate copy compensates for it. When the activating region of the protein is altered, both stable and stochastic oscillations occus at the single cell level. The diploid version of the regulatory network model can account for allele-specific expression variants, and a model of inheritance of the haplotype network enables us to trace the evolutionary consequence of heterozygous oscillatory phenotypes.
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