The evolutionary forces responsible for intron loss are unresolved. Whereas research has focused on protein-coding genes, here we analyze noncoding small nucleolar RNA (snoRNA) genes in which introns, rather than exons, are typically the functional elements. Within the yeast lineage exemplified by the human pathogen Candida albicans, we find-through deep RNA sequencing and genome-wide annotation of splice junctions-extreme compaction and loss of associated exons, but retention of snoRNAs within introns. In the Saccharomyces yeast lineage, however, we find it is the introns that have been lost through widespread degeneration of splicing signals. This intron loss, perhaps facilitated by innovations in snoRNA processing, is distinct from that observed in protein-coding genes with respect to both mechanism and evolutionary timing.
|Evidence ID||Analyze ID||Interactor||Interactor Systematic Name||Interactor||Interactor Systematic Name||Type||Assay||Annotation||Action||Modification||Phenotype||Source||Reference||Note|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Gene Ontology Term||Gene Ontology Term ID||Qualifier||Aspect||Method||Evidence||Source||Assigned On||Annotation Extension||Reference|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Phenotype||Experiment Type||Experiment Type Category||Mutant Information||Strain Background||Chemical||Details||Reference|
|Evidence ID||Analyze ID||Regulator||Regulator Systematic Name||Target||Target Systematic Name||Experiment||Assay||Construct||Conditions||Strain Background||Reference|