Roy Scott William, Irimia Manuel
National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20892, USA.
Trends Genet. 2009 Feb;25(2):67-73. doi: 10.1016/j.tig.2008.11.004. Epub 2008 Dec 11.
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.
尽管剪接体内含子普遍存在，但其起源所涉及的机制和进化力量仍然成谜。最近的分子证据支持这样一种观点，即内含子RNA可以反向剪接到RNA转录本中，这是一个有影响力的内含子获得模型的关键步骤。然而，该模型存在一个悖论，因为一般来说，内含子获得的速率预计比内含子丢失的速率低几个数量级，这与几个谱系的研究结果相反。我们分别基于空间位阻因素和特定内含子对逆转录元件转座途径的选择性利用可能性，提出了两种可能解决这一悖论的方法。此外，我们还介绍了两种潜在的内含子产生机制，分别基于RNA-DNA杂交反向剪接和逆转录酶的模板转换错误。
