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Baf60c is essential for function of BAF chromatin remodelling complexes in heart development

Author

Listed:
  • Heiko Lickert

    (Mount Sinai Hospital)

  • Jun K. Takeuchi

    (The Hospital for Sick Children
    University of Toronto)

  • Ingo von Both

    (Mount Sinai Hospital)

  • Johnathon R. Walls

    (The Hospital for Sick Children
    University of Toronto)

  • Fionnuala McAuliffe

    (Mount Sinai Hospital
    University College Dublin)

  • S. Lee Adamson

    (Mount Sinai Hospital
    University of Toronto
    University of Toronto)

  • R. Mark Henkelman

    (The Hospital for Sick Children
    University of Toronto)

  • Jeffrey L. Wrana

    (Mount Sinai Hospital
    University of Toronto)

  • Janet Rossant

    (Mount Sinai Hospital
    University of Toronto)

  • Benoit G. Bruneau

    (The Hospital for Sick Children
    University of Toronto
    University of Toronto)

Abstract

Tissue-specific transcription factors regulate several important aspects of embryonic development. They must function in the context of DNA assembled into the higher-order structure of chromatin. Enzymatic complexes such as the Swi/Snf-like BAF complexes remodel chromatin to allow the transcriptional machinery access to gene regulatory elements1,2. Here we show that Smarcd3, encoding Baf60c, a subunit of the BAF complexes, is expressed specifically in the heart and somites in the early mouse embryo. Smarcd3 silencing by RNA interference in mouse embryos derived from embryonic stem cells causes defects in heart morphogenesis that reflect impaired expansion of the anterior/secondary heart field, and also results in abnormal cardiac and skeletal muscle differentiation. An intermediate reduction in Smarcd3 expression leads to defects in outflow tract remodelling reminiscent of human congenital heart defects. Baf60c overexpressed in cell culture can mediate interactions between cardiac transcription factors and the BAF complex ATPase Brg1, thereby potentiating the activation of target genes. These results reveal tissue-specific and dose-dependent roles for Baf60c in recruiting BAF chromatin remodelling complexes to heart-specific enhancers, providing a novel mechanism to ensure transcriptional regulation during organogenesis.

Suggested Citation

  • Heiko Lickert & Jun K. Takeuchi & Ingo von Both & Johnathon R. Walls & Fionnuala McAuliffe & S. Lee Adamson & R. Mark Henkelman & Jeffrey L. Wrana & Janet Rossant & Benoit G. Bruneau, 2004. "Baf60c is essential for function of BAF chromatin remodelling complexes in heart development," Nature, Nature, vol. 432(7013), pages 107-112, November.
    • Handle: RePEc:nat:nature:v:432:y:2004:i:7013:d:10.1038_nature03071
    DOI: 10.1038/nature03071
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    Cited by:

    1. Muran Xiao & Shinji Kondo & Masaki Nomura & Shinichiro Kato & Koutarou Nishimura & Weijia Zang & Yifan Zhang & Tomohiro Akashi & Aaron Viny & Tsukasa Shigehiro & Tomokatsu Ikawa & Hiromi Yamazaki & Mi, 2023. "BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state," Nature Communications, Nature, vol. 14(1), pages 1-22, December.
    2. Jiahui Du & Yili Liu & Jinrui Sun & Enhui Yao & Jingyi Xu & Xiaolin Wu & Ling Xu & Mingliang Zhou & Guangzheng Yang & Xinquan Jiang, 2024. "ARID1A safeguards the canalization of the cell fate decision during osteoclastogenesis," Nature Communications, Nature, vol. 15(1), pages 1-20, December.
    3. Debashish U. Menon & Oleksandr Kirsanov & Christopher B. Geyer & Terry Magnuson, 2021. "Mammalian SWI/SNF chromatin remodeler is essential for reductional meiosis in males," Nature Communications, Nature, vol. 12(1), pages 1-19, December.
    4. Cornelis J. Boogerd & Ilaria Perini & Eirini Kyriakopoulou & Su Ji Han & Phit La & Britt Swaan & Jari B. Berkhout & Danielle Versteeg & Jantine Monshouwer-Kloots & Eva Rooij, 2023. "Cardiomyocyte proliferation is suppressed by ARID1A-mediated YAP inhibition during cardiac maturation," Nature Communications, Nature, vol. 14(1), pages 1-17, December.

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