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Dynamic regulation of sarcoplasmic reticulum Ca 2+ stores by stromal interaction molecule 1 and sarcolipin during muscle differentiation
Author(s) -
Seth Malini,
Li Tianyu,
Graham Victoria,
Burch Jarrett,
Finch Elizabeth,
Stiber Jonathan A.,
Rosenberg Paul B.
Publication year - 2012
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.23760
Subject(s) - stim1 , endoplasmic reticulum , myogenesis , microbiology and biotechnology , biology , myocyte , endocrinology , medicine
Abstract During muscle development, the sarco/endoplasmic reticulum (SR/ER) undergoes remodeling to establish a specialized internal Ca 2+ store for muscle contraction. We hypothesized that store operated Ca 2+ entry (SOCE) is required to fill Ca 2+ stores and is, therefore, critical to creating a mature SR/ER. Stromal interaction molecule 1 (STIM1) functions as a sensor of internal Ca 2+ store content and an activator of SOCE channels. Myocytes lacking STIM1 display reduced SR Ca 2+ content and altered expression of key SR proteins. Sarcolipin (SLN), an inhibitor of the SR calcium pump, was markedly increased in the muscle of mutant STIM1 mice. SLN opposes the actions of STIM1 by limiting SOCE, reducing SR Ca 2+ content and delaying muscle differentiation. During mouse muscle development SLN is highly expressed in embryonic muscle, while the expression of STIM1 is up‐regulated postnatally. These results suggest that SOCE regulates SR/ER specialization and that SLN and STIM1 act in opposing fashions to govern SOCE during myogenesis. Developmental Dynamics 241:639–647, 2012. © 2012 Wiley Periodicals, Inc.