Laminopathies disrupt epigenomic developmental programs and cell fate

Author:

Perovanovic Jelena12,Dell’Orso Stefania3,Gnochi Viola F.1,Jaiswal Jyoti K.12,Sartorelli Vittorio3,Vigouroux Corinne4567,Mamchaoui Kamel8,Mouly Vincent8,Bonne Gisèle8,Hoffman Eric P.12

Affiliation:

1. Center for Genetic Medicine Research, Children’s National Medical Center, Washington, DC 20010, USA.

2. Department of Integrative Systems Biology, The George Washington University School of Medicine and Health Sciences, Washington, DC 20010, USA.

3. Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20852, USA.

4. Assistance Publique–Hôpitaux de Paris (AP-HP), Hôpital Saint-Antoine, Laboratoire Commun de Biologie et Génétique Moléculaires, F-75012 Paris, France.

5. INSERM UMR_S938, Centre de Recherche Saint-Antoine, F-75012 Paris, France.

6. Sorbonne Universités, UPMC (Université Pierre et Marie Curie) Univ Paris 06, UMR_S938, F-75005 Paris, France.

7. ICAN (Institute of Cardiometabolism and Nutrition), F-75013 Paris, France.

8. Sorbonne Universités, UPMC Univ Paris 06, INSERM UMRS974, CNRS FRE3617, Center for Research in Myology, F-75013 Paris, France.

Abstract

Mutations in lamin A/C and emerin change myogenic cell fate by disrupting heterochromatin tethering to the nuclear envelope.

Funder

U.S. NIH

Intramural Research Program of the National Institute of Arthritis and Musculoskeletal and Skin Diseases

Association Francaise contre les Myopathies

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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