Research article summary (published 11 Sep 2009):

AP2gamma regulates basal progenitor fate in a region- and layer-specific manner in the developing cortex.

Full Abstract

An important feature of the cerebral cortex is its layered organization, which is modulated in an area-specific manner. We found that the transcription factor AP2gamma regulates laminar fate in a region-specific manner. Deletion of AP2gamma (also known as Tcfap2c) during development resulted in a specific reduction of upper layer neurons in the occipital cortex, leading to impaired function and enhanced plasticity of the adult visual cortex. AP2gamma functions in apical progenitors, and its absence resulted in mis-specification of basal progenitors in the occipital cortex at the time at which upper layer neurons were generated. AP2gamma directly regulated the basal progenitor fate determinants Math3 (also known as Neurod4) and Tbr2, and its overexpression promoted the generation of layer II/III neurons in a time- and region-specific manner. Thus, AP2gamma acts as a regulator of basal progenitor fate, linking regional and laminar specification in the mouse developing cerebral cortex.

Author information

Author/s: Pinto, Luisa (L); Drechsel, Daniela (D); Schmid, Marie-Theres (MT); Ninkovic, Jovica (J); Irmler, Martin (M); Brill, Monika S (MS); Restani, Laura (L); Gianfranceschi, Laura (L); Cerri, Chiara (C); Weber, Susanne N (SN); Tarabykin, Victor (V); Baer, Kristin (K); Guillemot, François (F); Beckers, Johannes (J); Zecevic, Nada (N); Dehay, Colette (C); Caleo, Matteo (M); Schorle, Hubert (H); Götz, Magdalena (M);

Affiliation: Helmholtz Center Munich, German Research Center for Environmental Health, Institute for Stem Cell Research, Neuherberg/Munich, Germany. luisapinto(-atsign-)ecsaude.uminho.pt [corrected]

Journal and publication information

Publication Type: Journal Article

Journal: Nature neuroscience (Nat Neurosci), published in United States. (Language: eng)

Reference: 2009-Oct; vol 12 (issue 10) : pp 1229-37

Dates: Created 2009/09/28; Completed 2009/10/13;

PMID: 19749747, status: MEDLINE (last retrieved date: 10/13/2009)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

Comments and Corrections

CommentIn: Nat Neurosci. 2009 Oct;12(10):1211-2. (PMID: 19783976)

ErratumIn: Nat Neurosci. 2009 Oct;12(10):1237.

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MeSH headings (categories)

This article was linked to the MeSH Headings (categories) shown below.

Adult Animals Bromodeoxyuridine - metabolism Cell Count - methods Cell Differentiation - physiology Cell Line, Transformed Cerebral Cortex - cytology; embryology; growth & development Embryo, Mammalian Embryonic Stem Cells - physiology Evoked Potentials, Visual - genetics; physiology Eye Proteins - genetics; metabolism Fetus Gene Deletion Gene Expression Regulation, Developmental - genetics; physiology Green Fluorescent Proteins - genetics Homeodomain Proteins - genetics; metabolism Humans

Humans Immediate-Early Proteins - genetics Ki-67 Antigen - metabolism Macaca fascicularis Mice Mice, Inbred C57BL Mice, Transgenic Neurogenesis - physiology Paired Box Transcription Factors - genetics; metabolism Photic Stimulation - methods RNA, Messenger - metabolism Repressor Proteins - genetics; metabolism T-Box Domain Proteins - metabolism Transcription Factor AP-2 - genetics; physiology Transcription Factors - genetics Transfection - methods Tumor Suppressor Proteins - genetics

Note: Bold headings indicate primary MeSH headings or qualifiers.

Associated Chemicals: Btg2 protein, mouse (0) ; Eomes protein, mouse (0) ; Eye Proteins (0) ; Homeodomain Proteins (0) ; Immediate-Early Proteins (0) ; Ki-67 Antigen (0) ; PAX6 protein (0) ; Paired Box Transcription Factors (0) ; RNA, Messenger (0) ; Repressor Proteins (0) ; T-Box Domain Proteins (0) ; Transcription Factor AP-2 (0) ; Transcription Factors (0) ; Tumor Suppressor Proteins (0) ; empty spiracles homeobox proteins (0) ; Green Fluorescent Proteins (147336-22-9) ; Bromodeoxyuridine (59-14-3)

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