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Lamin A/C and emerin are critical for skeletal muscle satellite cell differentiation

Lamin A/C and emerin are critical for skeletal muscle satellite cell differentiation Downloaded from genesdev.cshlp.org on November 1, 2021 - Published by Cold Spring Harbor Laboratory Press Lamin A/C and emerin are critical for skeletal muscle satellite cell differentiation 1 2 1 1 Richard L. Frock, Brian A. Kudlow, Angela M. Evans, Samantha A. Jameson, 1,3,4 1,3,5 Stephen D. Hauschka, and Brian K. Kennedy 1 2 Department of Biochemistry, Molecular and Cellular Biology Program, University of Washington, Seattle, Washington 98195, USA Mutations within LMNA, encoding A-type nuclear lamins, are associated with multiple tissue-specific diseases, including Emery-Dreifuss (EDMD2/3) and Limb-Girdle muscular dystrophy (LGMD1B). X-linked EDMD results from mutations in emerin, a lamin A-associated protein. The mechanisms through which these mutations cause muscular dystrophy are not understood. Here we show that most, but not all, cultured muscle cells from lamin A/C knockout mice exhibit impaired differentiation kinetics and reduced differentiation potential. Similarly, normal muscle cells that have been RNA interference (RNAi) down-regulated for either A-type lamins or emerin have impaired differentiation potentials. Replicative myoblasts lacking A-type lamins or emerin also have decreased levels of proteins important for muscle differentiation including pRB, MyoD, desmin, and M-cadherin; up-regulated Myf5; but no changes in Pax3, Pax7, MEF2C, MEF2D, c-met, and -catenin. To determine whether impaired myogenesis http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Genes & Development Unpaywall

Lamin A/C and emerin are critical for skeletal muscle satellite cell differentiation

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Unpaywall
ISSN
0890-9369
DOI
10.1101/gad.1364906
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Abstract

Downloaded from genesdev.cshlp.org on November 1, 2021 - Published by Cold Spring Harbor Laboratory Press Lamin A/C and emerin are critical for skeletal muscle satellite cell differentiation 1 2 1 1 Richard L. Frock, Brian A. Kudlow, Angela M. Evans, Samantha A. Jameson, 1,3,4 1,3,5 Stephen D. Hauschka, and Brian K. Kennedy 1 2 Department of Biochemistry, Molecular and Cellular Biology Program, University of Washington, Seattle, Washington 98195, USA Mutations within LMNA, encoding A-type nuclear lamins, are associated with multiple tissue-specific diseases, including Emery-Dreifuss (EDMD2/3) and Limb-Girdle muscular dystrophy (LGMD1B). X-linked EDMD results from mutations in emerin, a lamin A-associated protein. The mechanisms through which these mutations cause muscular dystrophy are not understood. Here we show that most, but not all, cultured muscle cells from lamin A/C knockout mice exhibit impaired differentiation kinetics and reduced differentiation potential. Similarly, normal muscle cells that have been RNA interference (RNAi) down-regulated for either A-type lamins or emerin have impaired differentiation potentials. Replicative myoblasts lacking A-type lamins or emerin also have decreased levels of proteins important for muscle differentiation including pRB, MyoD, desmin, and M-cadherin; up-regulated Myf5; but no changes in Pax3, Pax7, MEF2C, MEF2D, c-met, and -catenin. To determine whether impaired myogenesis

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Genes & Development – Unpaywall

Published: Feb 15, 2006

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