Open AccessPhysical interaction of junctophilin and the Ca V 1.1 C terminus is crucial for skeletal muscle contraction
Author(s) -
Tsutomu Nakada,
Toshihide Kashihara,
Masatoshi Komatsu,
Katsuhiko Kojima,
Toshikazu Takeshita,
Mitsuhiko Yamada
Publication year - 2018
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.1716649115
Subject(s) - endoplasmic reticulum , skeletal muscle , calcium , biophysics , membrane , contraction (grammar) , muscle contraction , microbiology and biotechnology , membrane channel , plasma membrane ca2+ atpase , chemistry , voltage dependent calcium channel , depolarization , calcium in biology , intracellular , biology , biochemistry , anatomy , atpase , endocrinology , organic chemistry , enzyme
Significance For robust contraction of skeletal muscles, the L-type calcium channel acts as a key molecule by transducing membrane depolarization to calcium release from the sarcoplasmic reticulum. Proper intracellular localization of L-type calcium channels at the junctional membrane complex where the plasma membranes are closely apposed to the membranes of the sarcoplasmic reticulum is necessary for this process. Junctophilins are known to stabilize the structure of the junctional membrane complex by bridging the plasma membrane and the sarcoplasmic membrane. We report that junctophilins recruit L-type calcium channels to the junctional membrane through physical interaction with the CaV 1.1 subunits of the channels. This protein–protein interaction at triads ensures efficient contraction in differentiated adult skeletal muscle.
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