Article
Inhibition of a spliceosome turnover pathway suppresses splicing defects.
Proceedings of the National Academy of Sciences of the United States of America - 12 Sept 2006
Pandit Shatakshi, Lynn Bert, Rymond Brian C
Abstract excerpt
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...
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