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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Splice-site Pairing Is An Intrinsically High Fidelity Process
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Splice-site Pairing Is An Intrinsically High Fidelity Process

机译：拼接位点配对是一个固有的高保真过程

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摘要

The extensive alternative splicing in higher eukaryotes has initiated a debate whether alternative mRNA isoforms are generated by an inaccurate spliceosome or are the consequence of highly degenerate splice sites within the human genome. Here, we established a quantitative assay to evaluate the accuracy of splice-site pairing by determining the number of incorrect exon-skipping events made from constitutively spliced pre-mRNA transcripts. We demonstrate that the spliceosome pairs exons with an astonishingly high degree of accuracy that may be limited by the quality of pre-mRNAs generated by RNA pol Ⅱ. The error rate of exon pairing is increased by the effects of the neurodegenerative disorder spinal muscular atrophy because of reduced levels of Survival of Motor Neuron, a master assembler of spliceosomal components. We conclude that all multi-intron-containing genes are alternatively spliced and that the reduction of SMN results in a general splicing defect that is mediated through alterations in the fidelity of splice-site pairing.
机译：高等真核生物中广泛的替代剪接引发了争论，即替代的mRNA亚型是由不正确的剪接体产生的还是人类基因组中高度简并的剪接位点的结果。在这里，我们建立了定量分析方法，通过确定由组成性剪接前mRNA转录本产生的不正确的外显子跳跃事件的数量来评估剪接位点配对的准确性。我们证明，剪接体对具有极高的准确性，可能受到RNA polⅡ产生的前mRNA的质量的限制。外显子配对的错误率由于神经退行性疾病脊柱肌肉萎缩的影响而增加，这是因为运动神经元（剪接体组件的主要组装者）的存活水平降低。我们得出的结论是，所有包含多内含子的基因都被选择性剪接，SMN的减少导致一般剪接缺陷，该缺陷是通过剪接位点配对保真度的改变而介导的。

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