Journal of Heredity Advance Access originally published online on July 27, 2009
Journal of Heredity 2009 100(5):591-596; doi:10.1093/jhered/esp062
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Genome Evolution Collection |
Endogenous Mechanisms for the Origins of Spliceosomal Introns
From the Department of Biology, Indiana University, 1001 East Third Street, Bloomington, IN 47405 (Catania and Gao); and the Department of Ecology and Evolutionary Biology, University of California, 621 Charles E. Young Drive South, Box 951606, Los Angeles, CA 90095-1606 (Scofield)
Address correspondence to Francesco Catania at the address above, or e-mail: fcatania{at}indiana.edu.
Over 30 years since their discovery, the origin of spliceosomal introns remains uncertain. One nearly universally accepted hypothesis maintains that spliceosomal introns originated from self-splicing group-II introns that invaded the uninterrupted genes of the last eukaryotic common ancestor (LECA) and proliferated by "insertion" events. Although this is a possible explanation for the original presence of introns and splicing machinery, the emphasis on a high number of insertion events in the genome of the LECA neglects a considerable body of empirical evidence showing that spliceosomal introns can simply arise from coding or, more generally, nonintronic sequences within genes. After presenting a concise overview of some of the most common hypotheses and mechanisms for intron origin, we propose two further hypotheses that are broadly based on central cellular processes: 1) internal gene duplication and 2) the response to aberrant and fortuitously spliced transcripts. These two nonmutually exclusive hypotheses provide a powerful way to explain the establishment of spliceosomal introns in eukaryotes without invoking an exogenous source.
Key Words: group-II introns • internal gene duplication • intronization • spliceosomal introns
Corresponding Editor: Michael Lynch