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Evolution of cellular innate immune genes in response to viral threats represents a rich area of study for understanding complex events that shape mammalian genomes. One of these genes,  TRIM5 , is a retroviral restriction factor that mediates a post-entry block to infection. Previous studies on the genomic cluster that contains  TRIM5  identified different patterns of gene amplification and the independent birth of  CypA  gene fusions in various primate species. However, the evolution of  Trim5  in the largest order of mammals, Rodentia, remains poorly characterized. Here, we present an expansive phylogenetic and genomic analysis of the  Trim5  cluster in rodents. Our findings reveal substantial evolutionary changes including gene amplifications, rearrangements, loss and fusion. We describe the first independent evolution of  TrimCyp  fusion genes in rodents. We show that the  TrimCyp  gene found in some  Peromyscus  species was acquired about 2 million years ago. When ectopically expressed, the  P. maniculatus  TRIMCyp shows anti-retroviral activity that is reversed by cyclosporine, but it does not activate Nf-κB or AP-1 promoters, unlike the primate TRIMCyps. These results describe a complex pattern of differential gene amplification in the  Trim5  cluster of rodents and identify the first functional  TrimCyp  fusion gene outside of primates and tree shrews.

Evolution of the rodent Trim5 cluster is marked by divergent paralogous expansions and independent acquisitions of TrimCyp fusions