IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v432y2004i7013d10.1038_nature03071.html
   My bibliography  Save this article

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
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature03071
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.
    File URL: https://libkey.io/10.1038/nature03071?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    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. 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.
    3. 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.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:nature:v:432:y:2004:i:7013:d:10.1038_nature03071. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.