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. Author manuscript; available in PMC: 2015 Aug 5.
Published in final edited form as: Annu Rev Biochem. 2015 Mar 12;84:291–323. doi: 10.1146/annurev-biochem-060614-034316

Figure 6.

Figure 6

RNA–RNA and RNA–protein interactions that regulate mutually exclusive splicing of the Drosophila DSCAM exon 6 exon cluster. A model for the mechanism by which the heterogeneous nuclear ribonucleoprotein (hnRNP) hrp36 prevents the inclusion of multiple DSCAM exon 6 variants. hrp36 (yellow circles) binds to all the exon 6 variants (orange) and represses their inclusion. When the conserved cis-acting RNA selector sequence upstream of a specific exon interacts by RNA–RNA base pairing with the conserved exon 6 cis-acting RNA docking site located upstream of the exon 6 cluster of 48 exons, it results in the derepression of hrp36 on the exon immediately downstream, but not for the other 47 exon 6 variants. In this way, only a single exon 6 variant is included. hrp36 competes with serine–arginine repeat (SR) proteins (green circles) for binding to the exon 6 variants. In the absence of hrp36, these activators can bind to all the exon 6 variants and function to enhance their splicing to other exon 6 exons. Figure modeled on data from Reference 16.