Splicing in Caenorhabditis elegans does not require an AG at the 3' splice acceptor site

R. V. Aroian, A. D. Levy, M. Koga, Y. Ohshima, J. M. Kramer, P. W. Sternberg

研究成果: ジャーナルへの寄稿学術誌査読

52 被引用数 (Scopus)

抄録

The dinucleotide AG, found at the 3' end of virtually all eukaryotic pre- mRNA introns, is thought to be essential for splicing. Reduction-of-function mutations in two Caenorhabditis elegans genes, the receptor tyrosine kinase gene let-23 and the collagen gene dpy-10, both alter the AG at the end of a short (ca. 50-nucleotide) intron to AA. The in vivo effects of these mutations were studied by sequencing polymerase chain reaction-amplified reverse-transcribed RNA isolated from the two mutants. As expected, we find transcripts that splice to a cryptic AG, skip an exon, and retain an unspliced intron. However, we also find significant levels of splicing at the mutated 3' splice site (AA) and at nearby non-AG dinucleotides. Our results indicate that for short C. elegans introns an AG is not required for splicing at either the correct 3' splice site or incorrect sites. Analysis of a splice site mutant involving a longer, 316-nucleotide C. elegans intron indicates that an AG is also not required there for splicing. We hypothesize that elements besides the invariant AG, e.g., an A-U-rich region, a UUUC motif, and/or a potential branch point sequence, are directing the selection of the 3' splice site and that in wild-type genes these elements cooperate so that proper splicing occurs.

本文言語英語
ページ(範囲)626-637
ページ数12
ジャーナルMolecular and cellular biology
13
1
DOI
出版ステータス出版済み - 1993
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 分子生物学
  • 細胞生物学

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