Open AccessA compensatory base change in human U2 snRNA can suppress a branch site mutation.
Author(s) -
Yuan Zhuang,
Alan M. Weiner
Publication year - 1989
Publication title -
genes and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.136
H-Index - 438
eISSN - 1549-5477
pISSN - 0890-9369
DOI - 10.1101/gad.3.10.1545
Subject(s) - biology , snrnp , rna splicing , intron , splice site mutation , splice , small nuclear rna , genetics , mutant , binding site , point mutation , prp24 , mutation , microbiology and biotechnology , gene , rna , rna dependent rna polymerase
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.