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. Author manuscript; available in PMC: 2017 Jun 1.
Published in final edited form as: Curr Genet. 2016 Sep 14;63(3):375–380. doi: 10.1007/s00294-016-0647-6

Fig. 2.

Fig. 2

Mammalian-like mechanisms of splice site definition in fission yeast. Exonic splicing enhancer (ESE) sequences recruit SR and SR-related proteins, which recruit or stabilize early spliceosome assembly. Failure of these components to assemble across the exon may result in exon-skipping. Mutations in Bpb1, U2AF-59, and U2AF-23 result in exon-skipping, which can be suppressed by overexpression of Srp2. Naturally skipped exons have particularly non-consensus downstream 5′ splice sites, suggesting cross-exon interactions may contribute to recognition of upstream 3′ splice sites. Phosphorylation of Bpb1 is necessary for efficient splicing of introns with non-consensus branch point sequences. Pwi1 is an SR-related protein which is required for splicing of introns with non-consensus 5′ splice sites in fission yeast. Though the PWI domain can bind RNA, it is not clear whether it directly binds the ESE during ESE-dependent splicing