Molecular evolution of a small gene family of wound inducible Kunitz trypsin inhibitors in Populus.

Maximum likelihood models of codon substitutions were used to analyze the molecular evolution of a Kunitz trypsin inhibitor (KTI) gene family in Populus and Salix. The methods support previous assertions that the KTI genes comprise a rapidly evolving gene family. Models that allow for codon specific estimates of the ratio of nonsynonymous to synonymous substitutions (omega) among sites detect positive Darwinian selection at several sites in the KTI protein. In addition, branch-specific maximum likelihood models show that there is significant heterogeneity in omega among branches of the KTI phylogeny. In particular, omega is substantially higher following duplication than speciation. There is also evidence for significant rate heterogeneity following gene duplication, suggesting different evolutionary rates in newly arisen gene duplicates. The results indicate uneven evolutionary rates both between sites in the KTI protein and among different lineages in the KTI phylogeny, which is incompatible with a neutral model of sequence evolution.