Insights into relationships among rodent lineages based on mitochondrial genome sequence data
Frabotta, Laurence John
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This dissertation has two major sections. In Chapter II, complete mitochondrial (mt DNA) genome sequences were used to construct a hypothesis for affinities of most major lineages of rodents that arose quickly in the Eocene and were well established by the end of the Oligocene. Determining the relationships among extant members of such old lineages can be difficult. Two traditional schemes on subordinal classification of rodents have persisted for over a century, dividing rodents into either two or three suborders, with relationships among families or superfamilies remaining problematic. The mtDNA sequences for four new rodent taxa (Aplodontia, Cratogeomys, Erethizon, and Hystrix), along with previously published Euarchontoglires taxa, were analyzed under parsimony, likelihood, and Bayesian criteria. Likelihood and Bayesian analyses of the protein-coding genes converged on a single topology that weakly supported rodent monophyly and was significantly better than the parsimony trees. Analysis of the tRNAs failed to recover a monophyletic Rodentia and did not reach convergence on a stationary distribution after fifty million generations. Most relationships hypothesized in the likelihood topology have support from previous data. Mt tRNAs have been largely ignored with respect to molecular evolution or phylogenetic utility. In Chapter III, the mt tRNAs from 141 mammals were used to refine secondary structure models and examine their molecular evolution. Both H- and L-encoded tRNAs are AT-rich with different %G and GC-skew and a difference in skew between H- and L-strand stems. Proportion of W-C pairs is higher in the H-strand and GU/UG pairs are higher in the L-strand, suggesting increased mismatch compensation in L-strand tRNAs. Among rodents, the number of variable stem base-pairs was nearly 75% of that observed across all mammals combined. Compensatory base changes were present only at divergences of 4% or greater. Neither loop reduction nor an accumulation of deleterious mutations, both suggestive of mutational meltdown (Muller's ratchet), was observed. Mutations associated with human pathologies are correlated only with the coding strand, with H-strand tRNAs being linked to substantially more of these mutations.