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Purine-rich enhancers function in the AT-AC pre-mRNA splicing pathway and do so independently of intact U1 snRNP

Published online by Cambridge University Press:  01 December 1998

QIANG WU  and
ADRIAN R. KRAINER
QIANG WU
Affiliation:
Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA, and Program in Molecular and Cellular Biology, State University of New York at Stony Brook, Stony Brook, New York 11794, USA Present address: Department of Molecular and Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, Massachusetts 02138, USA.
ADRIAN R. KRAINER
Affiliation:
Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA, and Program in Molecular and Cellular Biology, State University of New York at Stony Brook, Stony Brook, New York 11794, USA
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Abstract

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.

Keywords

AT-AC intronexon definitionexonic splicing enhancer (ESE)pre-mRNA splicingU1 snRNP
Type
Research Article
Information
RNA , Volume 4 , Issue 12 , December 1998 , pp. 1664 - 1673
Copyright
© 1998 RNA Society

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