Table of Contents
ISRN Structural Biology
Volume 2013 (2013), Article ID 634341, 6 pages
Research Article

Human Tonic and Phasic Smooth Muscle Myosin Isoforms Are Unresponsive to the Loop 1 Insert

1Department of Biochemistry and Molecular Biology, Mayo Clinic Rochester, 200 First Street SW, Rochester, MN 55905, USA
2Department of Physiology and Biomedical Engineering, Mayo Clinic Rochester, 200 First Street SW, Rochester, MN 55905, USA

Received 7 October 2013; Accepted 5 November 2013

Academic Editors: N. M. Kad, F. Polticelli, and K. L. Sale

Copyright © 2013 Katalin Ajtai et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Smooth muscle myosin gene products include two isoforms, SMA and SMB, differing by a 7-residue peptide in loop 1 (i7) at the myosin active site where ATP is hydrolyzed. Using chicken isoforms, previous work indicated that the i7 deletion in SMA prolongs strong actin binding by inhibiting active site ingress and egress of nucleotide when compared to i7 inserted SMB. Additionally, i7 deletion inhibits Pi release associated with the switch 2 closed→open transition in actin-activated ATPase. Switch 2 is far from loop 1 indicating i7 deletion has an allosteric effect on Pi release. Chicken SMA and SMB have unknown and robust nucleotide-sensitive tryptophan (NST) fluorescence increments, respectively. Human SMA and SMB both lack NST increments while Pi release in Ca2+ATPase is not impacted by i7 deletion. The NST reports relay helix movement following conformation change in switch 2 but in the open→closed transition. The NST is common to all known myosin isoforms except human smooth muscle. Other independent works on human SMA and SMB motility indicate no functional effect of i7 deletion. Smooth muscle myosin is a stunning example of species-specific myosin structure/function divergence underscoring the danger in extrapolating disease-linked mutant effects on myosin across species.