PMID:11715025

Citation	Babu, GJ, Loukianov, E, Loukianova, T, Pyne, GJ, Huke, S, Osol, G, Low, RB, Paul, RJ and Periasamy, M (2001) Loss of SM-B myosin affects muscle shortening velocity and maximal force development. Nat. Cell Biol. 3:1025-9
Abstract	We used an exon-specific gene-targeting strategy to generate a mouse model deficient only in the SM-B myosin isoform. Here we show that deletion of exon-5B (specific for SM-B) in the gene for the heavy chain of smooth muscle myosin results in a complete loss of SM-B myosin and switching of splicing to the SM-A isoform, without affecting SM1 and SM2 myosin content. Loss of SM-B myosin does not affect survival or cause any overt smooth muscle pathology. Physiological analysis reveals that absence of SM-B myosin results in a significant decrease in maximal force generation and velocity of shortening in smooth muscle tissues. This is the first in vivo study to demonstrate a functional role for the SM-B myosin isoform. We conclude that the extra seven-residue insert in the surface loop 1 of SM-B myosin is a critical determinant of crossbridge cycling and velocity of shortening.
Links	PubMed Online version:10.1038/ncb1101-1025
Keywords	Animals; Female; Gene Expression; Heart/physiology; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Muscle, Smooth/metabolism; Muscle, Smooth/physiology; Protein Isoforms/genetics; Protein Isoforms/physiology; RNA Splicing; Smooth Muscle Myosins/genetics; Smooth Muscle Myosins/physiology; Urinary Bladder/metabolism
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