| Literature DB >> 27166947 |
Pablo Gómez-Del Arco1, Eusebio Perdiguero2, Paula Sofia Yunes-Leites3, Rebeca Acín-Pérez4, Miriam Zeini3, Antonio Garcia-Gomez5, Krishnamoorthy Sreenivasan6, Miguel Jiménez-Alcázar3, Jessica Segalés2, Dolores López-Maderuelo3, Beatriz Ornés3, Luis Jesús Jiménez-Borreguero7, Gaetano D'Amato8, David Enshell-Seijffers9, Bruce Morgan10, Katia Georgopoulos10, Abul B M M K Islam11, Thomas Braun6, José Luis de la Pompa8, Johnny Kim6, José A Enriquez4, Esteban Ballestar5, Pura Muñoz-Cánoves12, Juan Miguel Redondo13.
Abstract
Heart muscle maintains blood circulation, while skeletal muscle powers skeletal movement. Despite having similar myofibrilar sarcomeric structures, these striated muscles differentially express specific sarcomere components to meet their distinct contractile requirements. The mechanism responsible is still unclear. We show here that preservation of the identity of the two striated muscle types depends on epigenetic repression of the alternate lineage gene program by the chromatin remodeling complex Chd4/NuRD. Loss of Chd4 in the heart triggers aberrant expression of the skeletal muscle program, causing severe cardiomyopathy and sudden death. Conversely, genetic depletion of Chd4 in skeletal muscle causes inappropriate expression of cardiac genes and myopathy. In both striated tissues, mitochondrial function was also dependent on the Chd4/NuRD complex. We conclude that an epigenetic mechanism controls cardiac and skeletal muscle structural and metabolic identities and that loss of this regulation leads to hybrid striated muscle tissues incompatible with life.Entities:
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Year: 2016 PMID: 27166947 DOI: 10.1016/j.cmet.2016.04.008
Source DB: PubMed Journal: Cell Metab ISSN: 1550-4131 Impact factor: 27.287