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Background Nitric oxide signaling through the cGMP kinase (cGK1a) activates Myosin Phosphatase (MP) leading to calcium de-sensitization of force production. Leucine zipper (LZ) motifs present in the C-terminus of MYPT1 and N-terminus of cGK1a are thought to be essential for the hetero-dimerization of cGK1 and MYPT1 and cGK1 activation of MP [1]. An isoform of MYPT1 that lacks the C-terminal LZ motif is generated by the alternative splicing of a 31 nt 3’ exon (E23). We have shown that the expression of these MYPT1 isoforms is tissuespecific, developmentally regulated and modulates in disease [2]. MYPT1 E23-/LZ+ isoform is expressed in tonic smooth muscle of the large arteries and veins while MYPT1 E23+/LZisoform is expressed in the phasic smooth muscle of the intestines, portal vein and small resistance arteries. There is a good though incompletely characterized correlation between the expression of MYPT1 isoforms and sensitivity to NO/cGMPmediated relaxation, making this alternative splicing event an excellent model for the study of smooth muscle phenotypic diversity in relation to vascular function.

Transformer (Tra2β): master regulator of myosin phosphatase alternative splicing and smooth muscle responses to NO/cGMP signaling