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Tissue Specific Stem Cells
Version of Record online: 24 APR 2013
Copyright © 2013 AlphaMed Press
Volume 31, Issue 5, pages 1010–1021, May 2013
How to Cite
Park, H. J., Hong, M., Bronson, R. T., Israel, M. A., Frankel, W. N. and Yun, K. (2013), Elevated Id2 Expression Results in Precocious Neural Stem Cell Depletion and Abnormal Brain Development. STEM CELLS, 31: 1010–1021. doi: 10.1002/stem.1351
Author contributions: M.H. and H.J.P.: collection and analysis of data, and interpretation; R.T.B.: data analysis and interpretation; M.A.I.: provision of study material and manuscript writing; W.N.F.: collection of data, data analysis and interpretation, and manuscript writing; K.Y.: conception and design, financial support, collection of study material, collection and assembly of data, data analysis and interpretation, manuscript writing, and final approval of manuscript. H.J.P. and M.H. contributed equally to this article.
Disclosure of potential conflicts of interest is found at the end of this article.
First published online in STEM CELLSEXPRESS February 6, 2013.
- Issue online: 24 APR 2013
- Version of Record online: 24 APR 2013
- Accepted manuscript online: 6 FEB 2013 11:28PM EST
- Manuscript Accepted: 15 JAN 2013
- Manuscript Received: 5 OCT 2012
- NIH. Grant Number: NS031348
- TJL Cancer Center Support. Grant Number: CA034196
- Department of Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY
Additional Supporting Information may be found in the online version of this article.
|sc-12-0933_sm_SupplFigure1.tif||136K||S Figure 1. Video-EEG recording of a control mouse. Age-matched control mouse showed no seizure activity. The traces shown are the differential signal between each electrode pair (RF - right front electrode; LF - left front; RB –right back; LB – left back; positions relative to Bregma and midline). Scale bar=1 second.|
|sc-12-0933_sm_SupplFigure2.tif||1636K||Supplementary Figure 2. Id2 is not sufficient to induce premature gliogenesis in FID2;Nestin-cre mice. Antibody staining against GFAP (green) and OLIG2 (red) show no ectopic expression in the transgenic cortex at E15.5.|
|sc-12-0933_sm_SupplFigure3.pdf||1263K||Supplementary Figure 3. Id2 expression in committed neural progenitors does not change proliferation or survival. (A) A schematic for generating FID2;Neurogenin1-cre embryos. (B) Robust transgene expression, detected by antibody staining against GFP, in intermediate progenitors and differentiating neurons in the transgenic cortex at E15.5. (c) FID2;Neuro1-cre brains are not microcephalic at p20. (D) H&E staining of E15.5 control and FiD2;Neurogenin1-cre littermate cortices shows no observable morphological phenotype. (E) SOX2, (F) TBR2, and (G) TBR1 antibody staining also shows no significant differences between control and littermate transgenic embryos at E15.5. (H) Cleaved Caspase3 staining shows no change in expression, indicating that ectopic ID2 expression in progenitor cells do not induce apoptosis.|
|sc-12-0933_sm_SupplFigure4.tif||83K||Supplementary Figure 4. Realtime RT-PCR analysis of FID2;GFAP-cre cortices at E13.5 Realtime RT-PCR validation of selected genes from the microarray analysis and other G1-S regulators and p53 targets (n=5).|
|sc-12-0933_sm_SupplFigure5.tif||1157K||Supplementary Figure 5. P53 is activated in FID2;GFAP-cre cortex at E15.5 Antibody staining against p53 shows stabilization of p53 the protein in the transgenic cortex|
|sc-12-0933_sm_SupplFigure6.tif||1978K||Supplementary Figure 6. Astrocytoma in FID2;GFAP-cre;p53−/− express markers of gliomas. GFAP and PCNA staining confirm glioma formation in FID2;GFAPcre; p53−/− brain shown in Figure 7B.|
|sc-12-0933_sm_SupplTable.pdf||80K||Supplementary Table 1|
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