A compensatory base change in human U2 snRNA can suppress a branch site mutation.
Open Access
- 1 October 1989
- journal article
- research article
- Published by Cold Spring Harbor Laboratory in Genes & Development
- Vol. 3 (10) , 1545-1552
- https://doi.org/10.1101/gad.3.10.1545
Abstract
We have developed an assay to test whether U2 snRNA can base-pair with the branch site during mammalian mRNA splicing. The beta 110 point mutation (GG----AG) within the first intron of human beta-globin generates a new 3' splice site that is preferentially used. We show here that use of the normal 3' splice site can be restored either by improving the match of a cryptic branch site to the branch site consensus or by introducing mutant U2 snRNAs with greater complementarity to the cryptic branch site. These data indicate that human U2 snRNA can form base pairs with the mRNA precursor; however, base pairing appears to be optional because some mammalian branch sites do not match the consensus.This publication has 47 references indexed in Scilit:
- Genetic analysis of the role of human U1 snRNA in mRNA splicing: I. Effect of mutations in the highly conserved stem-loop I of U1.Genes & Development, 1989
- Alternative splicing of SV40 early pre-mRNA is determined by branch site selection.Genes & Development, 1988
- Two conserved domains of yeast U2 snRNA are separated by 945 nonessential nucleotidesCell, 1988
- The role of the mammalian branchpoint sequence in pre-mRNA splicing.Genes & Development, 1988
- Internal sequences that distinguish yeast from metazoan U2 snRNA are unnecessary for pre-mRNA splicingNature, 1988
- Recognition of the TACTAAC box during mRNA splicing in yeast involves base pairing to the U2-like snRNACell, 1987
- A compensatory base change in U1 snRNA suppresses a 5′ splice site mutationCell, 1986
- Sequences required for 3′ end formation of human U2 small nuclear RNACell, 1985
- Cryptic branch point activation allows accurate in vitro splicing of human β-globin intron mutantsCell, 1985
- β+ Thalassemia: Aberrant splicing results from a single point mutation in an intronCell, 1981