Protooncogene Ski cooperates with the chromatin-remodeling factor Satb2 in specifying callosal neurons. / Baranek, Constanze; Dittrich, Manuela; Parthasarathy, Srinivas et al.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 109, No. 9, 28.02.2012, p. 3546-3551.Research output: Contribution to journal › Article › peer-review
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TY - JOUR
T1 - Protooncogene Ski cooperates with the chromatin-remodeling factor Satb2 in specifying callosal neurons
AU - Baranek, Constanze
AU - Dittrich, Manuela
AU - Parthasarathy, Srinivas
AU - Bonnon, Carine Gaiser
AU - Britanova, Olga
AU - Lanshakov, Dmitriy
AU - Boukhtouche, Fatiha
AU - Sommer, Julia E.
AU - Colmenares, Clemencia
AU - Tarabykin, Victor
AU - Atanasoski, Suzana
N1 - © Copyright 2012 Elsevier B.V., All rights reserved. © MEDLINE® is the source for the MeSH terms of this document.
PY - 2012/2/28
Y1 - 2012/2/28
N2 - First insights into the molecular programs orchestrating the progression from neural stem cells to cortical projection neurons are emerging. Loss of the transcriptional regulator Ski has been linked to the human 1p36 deletion syndrome, which includes central nervous system defects. Here, we report critical roles for Ski in the maintenance of the neural stem cell pool and the specification of callosal neurons. Ski-deficient callosal neurons lose their identity and ectopically express the transcription factor Ctip2. The misspecified callosal neurons largely fail to form the corpus callosum and instead redirect their axons toward subcortical targets. We identify the chromatin-remodeling factor Satb2 as a partner of Ski, and show that both proteins are required for transcriptional repression of Ctip2 in callosal neurons. We propose a model in which Satb2 recruits Ski to the Ctip2 locus, and Ski attracts histone deacetylases, thereby enabling the formation of a functional nucleosome remodeling and deacetylase repressor complex. Our findings establish a central role for Ski-Satb2 interactions in regulating transcriptional mechanisms of callosal neuron specification.
AB - First insights into the molecular programs orchestrating the progression from neural stem cells to cortical projection neurons are emerging. Loss of the transcriptional regulator Ski has been linked to the human 1p36 deletion syndrome, which includes central nervous system defects. Here, we report critical roles for Ski in the maintenance of the neural stem cell pool and the specification of callosal neurons. Ski-deficient callosal neurons lose their identity and ectopically express the transcription factor Ctip2. The misspecified callosal neurons largely fail to form the corpus callosum and instead redirect their axons toward subcortical targets. We identify the chromatin-remodeling factor Satb2 as a partner of Ski, and show that both proteins are required for transcriptional repression of Ctip2 in callosal neurons. We propose a model in which Satb2 recruits Ski to the Ctip2 locus, and Ski attracts histone deacetylases, thereby enabling the formation of a functional nucleosome remodeling and deacetylase repressor complex. Our findings establish a central role for Ski-Satb2 interactions in regulating transcriptional mechanisms of callosal neuron specification.
KW - Cell fate
KW - Cortical development
KW - Transcriptional regulation
UR - http://www.scopus.com/inward/record.url?scp=84857722718&partnerID=8YFLogxK
U2 - 10.1073/pnas.1108718109
DO - 10.1073/pnas.1108718109
M3 - Article
C2 - 22334647
AN - SCOPUS:84857722718
VL - 109
SP - 3546
EP - 3551
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 9
ER -
ID: 34442521