Figure 6.

Model for putative Brr2-mediated enhancement of splicing fidelity and regulation of alternative splicing. Depending on the state of the NTR and the Sad1 protein in competing alternative splicing scenarios (left and right branches), Brr2 may be more or less prone to disrupt the tri-snRNP in a non-productive fashion, thus differentially channeling the different substrates along the splicing or discard pathways. Similarly, depending on the level of Brr2 inhibition in competing alternative splicing scenarios, the helicase may elicit spliceosome activation slowly or quickly, kinetically controlling the levels of protein isoforms produced.