Document Detail

Increased susceptibility to fatigue of slow- and fast-twitch muscles from mice lacking the MG29 gene.
MedLine Citation:
PMID:  11074012     Owner:  NLM     Status:  MEDLINE    
Mitsugumin 29 (MG29), a major protein component of the triad junction in skeletal muscle, has been identified to play roles in the formation of precise junctional membrane structures important for efficient signal conversion in excitation-contraction (E-C) coupling. We carried out several experiments to not only study the role of MG29 in normal muscle contraction but also to determine its role in muscle fatigue. We compared the in vitro contractile properties of three muscles types, extensor digitorum longus (EDL) (fast-twitch muscle), soleus (SOL) (slow-twitch muscle), and diaphragm (DPH) (mixed-fiber muscle), isolated from mice lacking the MG29 gene and wild-type mice prior to and after fatigue. Our results indicate that the mutant EDL and SOL muscles, but not DPH, are more susceptible to fatigue than the wild-type muscles. The mutant muscles not only fatigued to a greater extent but also recovered significantly less than the wild-type muscles. Following fatigue, the mutant EDL and SOL muscles produced lower twitch forces than the wild-type muscles; in addition, fatiguing produced a downward shift in the force-frequency relationship in the mutant mice compared with the wild-type controls. Our results indicate that fatiguing affects the E-C components of the mutant EDL and SOL muscles, and the effect of fatigue in these mutant muscles could be primarily due to an alteration in the intracellular Ca homeostasis.
R Y Nagaraj; C M Nosek; M A Brotto; M Nishi; H Takeshima; T M Nosek; J Ma
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2000-11-09
Journal Detail:
Title:  Physiological genomics     Volume:  4     ISSN:  1531-2267     ISO Abbreviation:  Physiol. Genomics     Publication Date:  2000 Nov 
Date Detail:
Created Date:  2000-11-21     Completed Date:  2001-02-15     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9815683     Medline TA:  Physiol Genomics     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  43-9     Citation Subset:  IM    
Department of Physiology and Biophysics, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106-4963, USA.
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MeSH Terms
Electric Stimulation
Genetic Predisposition to Disease / genetics*
Mice, Inbred C57BL
Mice, Knockout
Muscle Contraction / genetics
Muscle Fatigue / genetics*
Muscle Fibers, Fast-Twitch / metabolism*,  physiology
Muscle Fibers, Slow-Twitch / metabolism*,  physiology
Muscle Proteins / deficiency*,  genetics*,  physiology
Signal Transduction / genetics
Synaptophysin / analogs & derivatives*,  deficiency*,  genetics*
Grant Support
Reg. No./Substance:
0/Mg29 protein, mouse; 0/Muscle Proteins; 0/Synaptophysin

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