Snf2l Regulates Foxg1-Dependent Progenitor Cell Expansion in the Developing Brain

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• 作者：Darren  ; J. Yip¹ ; ³ ; ⁶ ; Chelsea  ; P. Corcoran¹ ; ³ ; ⁶ ; Matí ; as Alvarez-Saavedra¹ ; ⁴ ; ⁶ ; Adriana DeMaria¹ ; Stephen Rennick¹ ; ³ ; Alan  ; J. Mears² ; ⁴ ; Michael  ; A. Rudnicki¹ ; ⁴ ; Claude Messier⁵ ; David  ; J. Picketts¹ ; ³ ; ^{dpicketts@ohri.ca}
• 刊名：Developmental Cell
• 出版年：2012
• 出版时间：17 April, 2012
• 年：2012
• 卷：22
• 期：4
• 页码：871-878
• 全文大小：1703 K

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Summary

Balancing progenitor cell self-renewal and differentiation is essential for brain development and is regulated by the activity of chromatin remodeling complexes. Nevertheless, linking chromatin changes to specific pathways that control cortical histogenesis remains a challenge. Here we identify a genetic interaction between the chromatin remodeler Snf2l and Foxg1, a key regulator of neurogenesis. m>Snf2lm> mutant mice exhibit forebrain hypercellularity arising from increased m>Foxg1m> expression, increased progenitor?cell expansion, and delayed differentiation. We demonstrate that Snf2l binds to the m>Foxg1m> locus at midneurogenesis and that the phenotype is rescued by reducing m>Foxg1m> dosage, thus revealing that Snf2l?and Foxg1 function antagonistically to regulate brain size.