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

Heiko Lickert, Jun K. Takeuchi, Ingo von Both, Johnathon R. Walls, Fionnuala McAuliffe, S. Lee Adamson, R. Mark Henkelman, Jeffrey L. Wrana, Janet Rossant () and Benoit G. Bruneau ()
Additional contact information
Heiko Lickert: Mount Sinai Hospital
Jun K. Takeuchi: The Hospital for Sick Children
Ingo von Both: Mount Sinai Hospital
Johnathon R. Walls: The Hospital for Sick Children
Fionnuala McAuliffe: Mount Sinai Hospital
S. Lee Adamson: Mount Sinai Hospital
R. Mark Henkelman: The Hospital for Sick Children
Jeffrey L. Wrana: Mount Sinai Hospital
Janet Rossant: Mount Sinai Hospital
Benoit G. Bruneau: The Hospital for Sick Children

Nature, 2004, vol. 432, issue 7013, 107-112

Abstract: 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.

Date: 2004
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DOI: 10.1038/nature03071

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