Inhibition of a spliceosome turnover pathway suppresses splicing defects.

ABSTRACT: Defects in assembly are suggested to signal the dissociation of faulty splicing complexes. A yeast genetic screen was performed to identify components of the putative discard pathway. Weak mutant alleles of SPP382 (also called NTR1) were found to suppress defects in two proteins required for spliceosome activation, Prp38p and Prp8p. Spp382p is shown necessary for cellular splicing, with premRNA and, for some alleles, excised intron, accumulating after inactivation. Like spp382-1, a mutant allele of AAR2 was identified in this suppressor screen. Like Spp382p, Aar2p has a reported role in spliceosome recycling and is found with Spp382p in a complex recovered with a mutant version of the spliceosomal core protein Prp8p. Possible insight into to the spp382 suppressor phenotype is provided by t

SUBMITTER: Pandit S 

PROVIDER: S-EPMC1564266 | biostudies-literature | 2006 Sep

REPOSITORIES: biostudies-literature