Alu exonization, which is an evolutionary pathway that creates primate-specific 
transcriptomic diversity, is a powerful tool for studying alternative-splicing 
regulation. Through bioinformatic analyses combined with experimental 
methodology, we identified the mutational changes needed to create functional 5' 
splice sites in Alu. We revealed a complex mechanism by which the sequence 
composition of the 5' splice site and its base pairing with the small nuclear 
RNA U1 govern alternative splicing. We show that in Alu-derived GC introns the 
strength of the base pairing between U1 snRNA and the 5' splice site controls 
the skipping/inclusion ratio of alternative splicing. Based on these findings, 
we identified 7810 Alus within the human genome that are prone to exonization. 
Mutations in these Alus may cause genetic disorders or contribute to 
human-specific protein diversity.