Limited complementarity between U1 snRNA and a retroviral 5' splice site permits its attenuation via RNA secondary structure.

ABSTRACT: Multiple types of regulation are used by cells and viruses to control alternative splicing. In murine leukemia virus, accessibility of the 5' splice site (ss) is regulated by an upstream region, which can fold into a complex RNA stem-loop structure. The underlying sequence of the structure itself is negligible, since most of it could be functionally replaced by a simple heterologous RNA stem-loop preserving the wild-type splicing pattern. Increasing the RNA duplex formation between U1 snRNA and the 5'ss by a compensatory mutation in position +6 led to enhanced splicing. Interestingly, this mutation affects splicing only in the context of the secondary structure, arguing for a dynamic interplay between structure and primary 5'ss sequence. The reduced 5'ss accessibility could also be counter

SUBMITTER: Zychlinski D 

PROVIDER: S-EPMC2794156 | biostudies-literature | 2009 Dec

REPOSITORIES: biostudies-literature