Changes in Ca2+ handling in adult MG29-deficient skeletal muscle.
It was reported that a lack of Mitsugumin29 (MG29), a protein expressed at the triad junction, caused morphological changes in sarcoplasmic reticulum and T-tubules, reduced twitch/tetanus ratio, and increased susceptibility to fatigue in adult skeletal muscle and dysfunction of store-operated Ca2+ entry (SOC) in embryonic and neonatal muscles. To deepen our understanding of the role of MG29 in the Ca2+ handling in adult skeletal muscle,Ca2+ stores of wild-type and mutant muscle fibers were depleted by repetitive high-K+ treatments in a Ca2+-free medium. Although wild-type muscle showed only minor caffeine contracture after high-K+ response had disappeared, the mutant muscle showed remarkable caffeine contracture under the conditions used, suggesting functional compartmentalization of the Ca2+-store in the mutant. Activation of SOC in adult mutant muscle was observed upon the voltage-sensitive store depletion as is true with the wild-type muscle. Thus MG29 is not involved in the SOC activation at variance with the previous conclusion with immature muscles.
Kurebayashi
Nagomi
N
Department of Pharmacology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
Takeshima
Hiroshi
H
Nishi
Miyuki
M
Murayama
Takashi
T
Suzuki
Erika
E
Ogawa
Yasuo
Y
D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D007150:Immunohistochemistry; D051379:Mice; D018345:Mice, Knockout; D009124:Muscle Proteins; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism*; D013050:Spectrometry, Fluorescence; D016708:Synaptophysin / Q000031:analogs & derivatives* / Q000235:genetics / Q000502:physiology*
C111842:Mg29 protein, mouse; D009124:Muscle Proteins; D016708:Synaptophysin; D002110:Caffeine; D002118:Calcium