Molecular coevolution among cryptically simple expansion segments of eukaryotic 26S/28S rRNAs

The set of "expansion segments" of any eukaryotic 26S/28S ribosomal RNA(rRNA) gene is responsible for the bulk of the difference in length betweenthe prokaryotic 23S rRNA gene and the eukaryotic 26S/28S rRNA gene. Theexpansion segments are also responsible for interspecific fluctuations inlength during eukaryotic evolution. They show a consistent bias in basecomposition in any species; for example, they are AT rich in Drosophilamelanogaster and GC rich in vertebrate species. Dot-matrix comparisons ofsets of expansion segments reveal high similarities between members of aset within any 28S rRNA gene of a species, in contrast to the little orspurious similarity that exists between sets of expansion segments fromdistantly related species. Similarities among members of a set of expansionsegments within any 28S rRNA gene cannot be accounted for by theirbase-compositional bias alone. In contrast, no significant similarityexists within a set of "core" segments (regions between expansion segments)of any 28S rRNA gene, although core segments are conserved between species.The set of expansion segments of a 26S/28S gene is coevolving as a unit ineach species, at the same time as the family of 28S rRNA genes, as a whole,is undergoing continual homogenization, making all sets of expansionsegments from all ribosomal DNA (rDNA) arrays in a species similar insequence. Analysis of DNA simplicity of 26S/28S rRNA genes shows a directcorrelation between significantly high relative simplicity factors (RSFs)and sequence similarity among a set of expansion segments. A similarcorrelation exists between RSF values, overall rDNA lengths, and thelengths of individual expansion segments. Such correlations suggest thatmost length fluctuations reflect the gain and loss of simple sequencemotifs by slippage-like mechanisms. We discuss the molecular coevolution ofexpansion segments, which takes place against a background of slippage-likeand unequal crossing-over mechanisms of turnover that are responsible forthe accumulation of interspecific differences in rDNA sequences.