Amino‐terminally truncated desmin rescues fusion of des −/− myoblasts but negatively affects cardiomyogenesis and smooth muscle development

FEBS Letters

Capetanaki, Yassemi¹  Höllrigl, Alexandra²  Kim, Jai Up¹  Puz, Sonja²  Al-Dubai, Haifa²  Weitzer, Georg² 

[1] Department of Molecular and Cell Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA;Institute of Medical Biochemistry, Vienna Bio Center, University of Vienna, Dr. Bohrgasse 9, A-1030 Vienna, Austria

关键词: Desmin;    Muscle development;    In vitro differentiation;    Cardiomyogenesis;    ES cells;    embryonic stem cells;    EB;    embryoid body;    IF;    intermediate filament;    HSV;    herpes simplex virus;    tk;    thymidine kinase;   

DOI  :  10.1016/S0014-5793(02)02995-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Desmin fulfils important functions in maintenance of muscle cells and mutations in the desmin gene have been linked to a variety of myopathies. To ascertain the role of desmin's amino-terminal domain in muscle cells we generated embryonic stem cells constitutively expressing desmin^Δ1–48 in a null background and investigated muscle cell development in vitro. Desmin^Δ1–48 lacking the first 48 amino acid residues promotes fusion of myoblasts, rescues myogenesis and down-regulates vimentin expression in embryoid bodies, but hampers cardiomyogenesis and blocks smooth muscle development. These results demonstrate that desmin's amino-terminus has different roles in skeletal, cardiac, and smooth muscle cell development and function.

【 授权许可】

Unknown