Abstract
REMOVAL of introns from eukaryotic nuclear messenger RNA precursors is catalysed by a large ribonucleoprotein complex called the spliceosome, which consists of four small nuclear ribonu-cleoprotein particles (Ul, U2, U5, and U4/U6 snRNPs) and auxiliary protein factors1,2. We have begun a genetic analysis of mammalian U2 snRNA by making second-site mutations in a suppressor U2 snRNA3. Here we find that several mutations in the 5′ end of U2 (nucleotides 3–8) are deleterious and that one of these can be rescued by compensatory base changes in the 3′ end of U6 (nucleotides 92–95). The results demonstrate genetically that the base-pairing interaction between U2 (nucleotides 37–11) and U6 snRNA (nucleotides 87–95), originally proposed on the basis of psoralen photocrosslinking experiments4, can influence the efficiency of mRNA splicing in mammals. The U2/U6 interac-tion in yeast, however, is fairly tolerant to mutation5 (D. J. Field and J. D. Friesen, personal communication), emphasizing the potential for facultative RNA interactions within the spliceosome.
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Datta, B., Weiner, A. Genetic evidence for base pairing between U2 and U6 snRNA in mammalian mRNA splicing. Nature 352, 821–824 (1991). https://doi.org/10.1038/352821a0
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DOI: https://doi.org/10.1038/352821a0
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