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The SWI/SNF BAF-A complex is essential for neural crest development.

Ronald L Chandler1, Terry Magnuson1

  • 1Department of Genetics, University of North Carolina at Chapel Hill, United States.

Developmental Biology
|January 26, 2016
PubMed
Summary

Mutations in ARID1A, a component of SWI/SNF chromatin remodeling complexes, cause severe heart and craniofacial defects in neural crest cells (NCCs), impacting embryonic development and potentially leading to Coffin-Siris Syndrome.

Keywords:
ARID1ABAF-ACoffin-Siris syndromeNeural crestSWI/SNF

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Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • Mutations in chromatin remodelers are linked to neurocristopathies, disorders affecting neural crest cells (NCCs).
  • The precise role of specific chromatin remodeler subunits in NCC development is not fully understood.

Purpose of the Study:

  • To investigate the function of ARID1A-containing SWI/SNF complexes in NCC development.
  • To elucidate the causal relationship between ARID1A mutations and NCC defects.

Main Methods:

  • Generation of mouse models with homozygous and monoallelic loss of ARID1A in NCCs.
  • Analysis of embryonic lethality, craniofacial morphology, cardiac development, and NCC apoptosis.

Main Results:

  • Homozygous ARID1A loss in NCCs leads to embryonic lethality due to heart defects.
  • Monoallelic ARID1A loss causes craniofacial abnormalities, with homozygous loss exacerbating ventral bone reduction.
  • Mutant embryos exhibit cardiac outflow tract septation defects and apoptosis of migrating cardiac NCCs.

Conclusions:

  • Distinct chromatin remodeling complexes regulate separate events in NCC development.
  • ARID1A is crucial for cardiac NCC survival and development, and its dysfunction may contribute to Coffin-Siris Syndrome.