Regulation of tau exon 10 splicing by a double stem–loop structure in mouse intron 10

Abstract Tau exon 10 (E10) splicing is a crucial event in its developmental change of tau isoform and tauopathy. To investigate the splicing mechanism, we isolated and compared mouse tau genomic sequence with human sequence. We identified a new element in mouse intron 10 (I10) to suppress E10 splicing, which was located just after the stem–loop region previously proposed in human sequence and found to potentially form another stem–loop. Human I10 with a mutation (+29G to A) causing a decreased E10 splicing was also predicted to form similar double stem–loop, suggesting that this element is universally involved in regulation of E10 splicing.