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Snf2l regulates Foxg1-dependent progenitor cell expansion in the developing brain.
Darren J Yip1, Chelsea P Corcoran, Matías Alvarez-Saavedra
1Regenerative Medicine Program, Ottawa Hospital Research Institute, and Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada.
Developmental Cell
|April 21, 2012
Summary
Chromatin remodeler Snf2l and transcription factor Foxg1 antagonistically regulate brain size. Snf2l mutations increase Foxg1, causing progenitor expansion and delayed differentiation in developing mouse brains.
Area of Science:
- Neuroscience
- Developmental Biology
- Genetics
Background:
- Progenitor cell balance is crucial for brain development.
- Chromatin remodeling complexes regulate this balance.
- Specific pathways linking chromatin changes to cortical histogenesis are not well understood.
Purpose of the Study:
- To investigate the genetic interaction between the chromatin remodeler Snf2l and the neurogenesis regulator Foxg1.
- To elucidate the roles of Snf2l and Foxg1 in regulating cortical histogenesis and brain size.
Main Methods:
- Utilized Snf2l mutant mice to study forebrain development.
- Analyzed gene expression, progenitor cell proliferation, and differentiation.
- Performed chromatin immunoprecipitation to assess Snf2l binding to the Foxg1 locus.
Main Results:
- Snf2l mutant mice displayed forebrain hypercellularity.
- Increased Foxg1 expression was observed in Snf2l mutants.
- Progenitor cell expansion and delayed differentiation were evident.
- Snf2l was shown to bind the Foxg1 locus during midneurogenesis.
- Reducing Foxg1 dosage rescued the observed phenotype.
Conclusions:
- Snf2l and Foxg1 function antagonistically to control brain size.
- This interaction is critical for balancing progenitor cell self-renewal and differentiation during brain development.
