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The removal of introns from eukaryotic RNA transcripts requires the activities of five multi-component ribonucleoprotein complexes and numerous associated proteins. The lack of mutations affecting splicing factors essential for animal survival has limited the study of the  in vivo  regulation of splicing. From a screen for suppressors of the  Caenorhabditis elegans unc-93(e1500)  rubberband Unc phenotype, we identified mutations in genes that encode the  C. elegans  orthologs of two splicing factors, the U2AF large subunit (UAF-1) and SF1/BBP (SFA-1). The  uaf-1(n4588)  mutation resulted in temperature-sensitive lethality and caused the  unc-93  RNA transcript to be spliced using a cryptic 3′ splice site generated by the  unc-93(e1500)  missense mutation. The  sfa-1(n4562)  mutation did not cause the utilization of this cryptic 3′ splice site. We isolated four  uaf-1(n4588)  intragenic suppressors that restored the viability of  uaf-1  mutants at 25°C. These suppressors differentially affected the recognition of the cryptic 3′ splice site and implicated a small region of UAF-1 between the U2AF small subunit-interaction domain and the first RNA recognition motif in affecting the choice of 3′ splice site. We constructed a reporter for  unc-93  splicing and using site-directed mutagenesis found that the position of the cryptic splice site affects its recognition. We also identified nucleotides of the endogenous 3′ splice site important for recognition by wild-type UAF-1. Our genetic and molecular analyses suggested that the phenotypic suppression of the  unc-93(e1500)  Unc phenotype by  uaf-1(n4588)  and  sfa-1(n4562)  was likely caused by altered splicing of an unknown gene. Our observations provide  in vivo  evidence that UAF-1 can act in regulating 3′ splice-site choice and establish a system that can be used to investigate the  in vivo  regulation of RNA splicing in  C. elegans .

Mutations in the Caenorhabditis elegans U2AF Large Subunit UAF-1 Alter the Choice of a 3′ Splice Site In Vivo