Mystery of intron gain: new data and new models.
Despite their ubiquity, the mechanisms and evolutionary forces responsible for the origins of spliceosomal introns remain mysterious. Recent molecular evidence supports the idea that intronic RNAs can reverse splice into RNA transcripts, a crucial step for an influential model of intron gain. However, a paradox attends this model because the rate of intron gain is expected to be orders of magnitude lower than the rate of intron loss in general, in contrast to findings from several lineages. We suggest two possible resolutions to this paradox, based on steric considerations and on the possibility of co-option by specific introns of retroelement transposition pathways, respectively. In addition, we introduce two potential mechanisms for intron creation, based on hybrid RNA-DNA reverse splicing and on template switching errors by reverse transcriptase.
Roy
Scott William
SW
National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20892, USA. royscott@ncbi.nlm.nih.gov
Irimia
Manuel
M
D000818:Animals; D004247:DNA / Q000378:metabolism; D019143:Evolution, Molecular; D006801:Humans; D007438:Introns / Q000235:genetics*; D008957:Models, Genetic; D012326:RNA Splicing; D012194:RNA-Directed DNA Polymerase
D004247:DNA; D012194:RNA-Directed DNA Polymerase