Purine-rich enhancers function in the AT-AC pre-mRNA splicing pathway and do so independently of intact U1 snRNP.
A rare class of introns in higher eukaryotes is processed by the recently discovered AT-AC spliceosome. AT-AC introns are processed inefficiently in vitro, but the reaction is stimulated by exon-definition interactions involving binding of U1 snRNP to the 5' splice site of the downstream conventional intron. We report that purine-rich exonic splicing enhancers also strongly stimulate sodium channel AT-AC splicing. Intact U2, U4, or U6 snRNAs are not required for enhancer function or for exon definition. Enhancer function is independent of U1 snRNP, showing that splicing stimulation by a downstream 5' splice site and by an exonic enhancer differ mechanistically.
Wu
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Q
Cold Spring Harbor Laboratory, New York 11724, USA.
Krainer
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AR
D001483:Base Sequence; D004742:Enhancer Elements, Genetic; D005091:Exons; D011687:Purines / Q000378:metabolism*; D012322:RNA Precursors / Q000235:genetics*; D012326:RNA Splicing; D012333:RNA, Messenger / Q000235:genetics*; D012342:RNA, Small Nuclear / Q000378:metabolism; D017412:Ribonucleoprotein, U1 Small Nuclear / Q000378:metabolism*
D011687:Purines; D012322:RNA Precursors; D012333:RNA, Messenger; D012342:RNA, Small Nuclear; D017412:Ribonucleoprotein, U1 Small Nuclear