Adaptive diversification of vomeronasal receptor 1 genes in rodents

The vomeronasal receptor 1 (V1R) are believed to be pheromone receptors in rodents. Here we used computational methods to identify 95 and 62 new putative V1R genes from the draft rat and mouse genome sequence, respectively. The rat V1R repertoire consists of 11 subfamilies, 10 of which are shared with the mouse, while rat appears to lack the H and I subfamilies found in mouse and possesses one unique subfamily (M). The estimations of the relative divergence times suggest that many subfamilies originated after the split of rodents and primates. The analysis also reveals that these clusters underwent an expansion very close to the split of mouse and rat. In addition, maximum likelihood analysis showed that the nonsynonymous and synonymous rate ratio for most of these clusters was much higher than one, suggesting the role of positive selection in the diversification of these duplicated V1R genes. Because V1R are thought to mediate the process of signal transduction in response to pheromone detection, we speculate that the V1R genes have evolved under positive Darwinian selection to maintain the ability to discriminate between large and complex pheromonal mixtures.

Stepwise loss of motilin and its specific receptor genes in rodents

Specific interactions among biomolecules drive virtually all cellular functions and underlie phenotypic complexity and diversity. Biomolecules are not isolated particles, but are elements of integrated interaction networks, and play their roles through specific interactions. Simultaneous emergence or loss of multiple interacting partners is unlikely. If one of the interacting partners is lost, then what are the evolutionary consequences for the retained partner? Taking advantages of the availability of the large number of mammalian genome sequences and knowledge of phylogenetic relationships of the species, we examined the evolutionary fate of the motilin (MLN) hormone gene, after the pseudogenization of its specific receptor, MLN receptor (MLNR), on the rodent lineage. We speculate that the MLNR gene became a pseudogene before the divergence of the squirrel and other rodents about 75 mya. The evolutionary consequences for the MLN gene were diverse. While an intact open reading frame for the MLN gene, which appears functional, was preserved in the kangaroo rat, the MLN gene became inactivated independently on the lineages leading to the guinea pig and the common ancestor of the mouse and rat. Gain and loss of specific interactions among biomolecules through the birth and death of genes for biomolecules point to a general evolutionary dynamic: gene birth and death are widespread phenomena in genome evolution, at the genetic level; thus, once mutations arise, a stepwise process of elaboration and optimization ensues, which gradually integrates and orders mutations into a coherent pattern.

Origin and evolution of new exons in rodents

Gene number difference among organisms demonstrates that new gene origination is a fundamental biological process in evolution. Exon shuffling has been universally observed in the formation of new genes. Yet to be learned are the ways new exons originate and evolve, and how often new exons appear. To address these questions, we identified 2695 newly evolved exons in the mouse and rat by comparing the expressed sequences of 12,419 orthologous genes between human and mouse, using 743,856 pig ESTs as the outgroup. The new exon origination rate is about 2.71 x 10(-3) per gene per million years. These new exons have markedly accelerated rates both of nonsynonymous substitutions and of insertions/ deletions (indels). A much higher proportion of new exons have Kappa(a)/Kappa(s) ratios > 1 (where K-a is the nonsynonymous substitution rate and K-s is the synonymous substitution rate) than K do the old exons shared by human and mouse, implying a role of positive selection in the rapid evolution. The majority of these new exons have sequences unique in the genome, suggesting that most new exons might originate through "exonization" of intronic sequences. Most of the new exons appear to be alternative exons that are expressed at low levels.