秀丽隐杆线虫中突变的剪接前导RNA的体内功能。
In vivo function of mutated spliced leader RNAs in Caenorhabditis elegans.
作者信息
Xie H, Hirsh D
机构信息
Department of Biochemistry and Molecular Biophysics, Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032, USA.
出版信息
Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4235-40. doi: 10.1073/pnas.95.8.4235.
The role of spliced leader RNA (SL RNA) in trans-splicing in Caenorhabditis elegans has been studied through a combination of in vitro mutagenesis and in vivo complementation of rrs-1 mutant nematodes, which lack endogenous SL1 RNA. Three classes of mutant SL1 RNAs have been found-those that rescue the lethal phenotype at low concentration of transforming DNA, those that rescue at high but not low concentration, and those that do not rescue at all. These studies showed that some mutations in the otherwise highly conserved 22-nt spliced leader are tolerated for splicing and post-splicing events. A longer spliced leader also can be tolerated but only when present in high copy number. Changes in the first 16 nucleotides result in the appearance of no SL RNA, consistent with the in vitro studies by others showing that the SL1 RNA promoter partly resides within the spliced leader sequence.
通过体外诱变和对缺乏内源性SL1 RNA的rrs-1突变线虫进行体内互补相结合的方法，研究了剪接前导RNA（SL RNA）在秀丽隐杆线虫反式剪接中的作用。已发现三类突变的SL1 RNA：一类在低浓度转化DNA时能挽救致死表型；一类在高浓度而非低浓度时能挽救；还有一类根本无法挽救。这些研究表明，原本高度保守的22个核苷酸的剪接前导序列中的一些突变在剪接和剪接后事件中是可以容忍的。较长的剪接前导序列也可以被容忍，但只有在高拷贝数时才行。前16个核苷酸的变化导致没有SL RNA出现，这与其他人的体外研究结果一致，即SL1 RNA启动子部分位于剪接前导序列内。
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