4.8 Article

NuRD and CAF-1-mediated silencing of the D4Z4 array is modulated by DUX4-induced MBD3L proteins

Journal

ELIFE
Volume 7, Issue -, Pages -

Publisher

ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.31023

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Funding

  1. National Cancer Institute [T32CA009657]
  2. National Human Genome Research Institute [T32HG00035, T32HG000035]
  3. National Institute of General Medical Sciences [T32GM007270]
  4. FSH Society [FSHS-22014-01]
  5. Eunice Kennedy Shriver National Institute of Child Health and Human Development [T32HD007183]
  6. National Institute of Neurological Disorders and Stroke [P01NS069539]
  7. Prinses Beatrix Spierfonds [W.OP14-01]
  8. Spieren voor Spieren
  9. National Institute of Arthritis and Musculoskeletal and Skin Diseases [R01AR066248, R01AR045203]
  10. Friends of FSH Research

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The DUX4 transcription factor is encoded by a retrogene embedded in each unit of the D4Z4 macrosatellite repeat. DUX4 is normally expressed in the cleavage-stage embryo, whereas chromatin repression prevents DUX4 expression in most somatic tissues. Failure of this repression causes facioscapulohumeral muscular dystrophy (FSHD) due to mis-expression of DUX4 in skeletal muscle. In this study, we used CRISPR/Cas9 engineered chromatin immunoprecipitation (enChIP) locus-specific proteomics to characterize D4Z4-associated proteins. These and other approaches identified the Nucleosome Remodeling Deacetylase (NuRD) and Chromatin Assembly Factor 1 (CAF-1) complexes as necessary for DUX4 repression in human skeletal muscle cells and induced pluripotent stem (iPS) cells. Furthermore, DUX4-induced expression of MBD3L proteins partly relieved this repression in FSHD muscle cells. Together, these findings identify NuRD and CAF-1 as mediators of DUX4 chromatin repression and suggest a mechanism for the amplification of DUX4 expression in FSHD muscle cells.

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