Loss of SM-B myosin affects muscle shortening velocity and maximal force development.

Babu GJ, Loukianov E, Loukianova T, Pyne GJ, Huke S, Osol G, Low RB, Paul RJ, Periasamy M
Nat Cell Biol. 2001 3 (11): 1025-9

PMID: 11715025 · DOI:10.1038/ncb1101-1025

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.

MeSH Terms (13)

Animals Female Gene Expression Heart Male Mice Mice, Inbred C57BL Mice, Knockout Muscle, Smooth Protein Isoforms RNA Splicing Smooth Muscle Myosins Urinary Bladder

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