Open AccessNicotinic acid adenine dinucleotide phosphate regulates skeletal muscle differentiation via action at two-pore channels
Author(s) -
Parvinder K. Aley,
Anna Mikołajczyk,
Barbara Munz,
Grant C. Churchill,
Antony Galione,
Felicitas Berger
Publication year - 2010
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.1007381107
Subject(s) - microbiology and biotechnology , ryanodine receptor , c2c12 , skeletal muscle , signal transduction , biochemistry , calcium signaling , chemistry , cellular differentiation , cell signaling , myocyte , biology , myogenesis , receptor , endocrinology , gene
Calcium signaling is essential for the differentiation of many cell types, including skeletal muscle cells, but its mechanisms remain elusive. Here we demonstrate a crucial role for nicotinic acid adenine dinucleotide phosphate (NAADP) signaling in skeletal muscle differentiation. Although the inositol trisphosphate pathway may have a partial role to play in this process, the ryanodine signaling cascade is not involved. In both skeletal muscle precursors and C2C12, cells interfering with NAADP signaling prevented differentiation, whereas promoting NAADP signaling potentiated differentiation. Moreover, siRNA knockdown of two-pore channels, the target of NAADP, attenuated differentiation. The data presented here strongly suggest that in myoblasts, NAADP acts at acidic organelles on the recently discovered two-pore channels to promote differentiation.