Neural tube defects and impaired neural progenitor cell proliferation in Gβ1-deficient mice
Version of Record online: 23 FEB 2010
Copyright © 2010 Wiley-Liss, Inc.
Volume 239, Issue 4, pages 1089–1101, April 2010
How to Cite
Okae, H. and Iwakura, Y. (2010), Neural tube defects and impaired neural progenitor cell proliferation in Gβ1-deficient mice. Dev. Dyn., 239: 1089–1101. doi: 10.1002/dvdy.22256
- Issue online: 16 MAR 2010
- Version of Record online: 23 FEB 2010
- Manuscript Accepted: 25 JAN 2010
- Core Research for Evolutional Science and Technology of the Japan Science and Technology Corporation
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Global COE Program (Integrative Life Science Based on the Study of Biosignaling Mechanisms), MEXT, Japan
Additional Supporting Information may be found in the online version of this article.
|DVDY_22256_sm_suppfig1.tif||3687K||Supp. Fig. S1. A: Gβ1−/− mice that did not have NTDs. Gβ1−/− mice did not ingest milk (arrows) and died within 2 days after birth. B,C: H&E stained lung sections from P0 mice. The alveolar space of Gβ1−/− mice is reduced, suggesting that these mice have respiratory defects. D,E: H&E stained lung sections from E17.5 embryos. Gross morphology of the lung is normal in Gβ1−/− embryos. F: X-gal staining of the diaphragm of a P0 Gβ1+/− mouse. G: X-gal staining of the rib of a P0 Gβ1+/− mouse. Strong signals are detected in the peripheral nervous system (arrows in F, G). H: Ventral views of the upper jaw at E18.5. Cleft palate is not observed in Gβ1−/− embryos. Bars = 100 μm in C, E; 200 μm in F, G.|
|DVDY_22256_sm_suppfig2.tif||1883K||Supp. Fig. S2. H&E staining of coronal sections of the telencephalon at E18.5. Brain malformations are observed in Gβ1−/− embryos with NTDs. Th, thalamus; Cx, cortex; Hc, hippocampus. Bar = 1 mm.|
|DVDY_22256_sm_suppfig3.tif||1543K||Supp. Fig. S3. Effects of LPA on morphology of neural progenitor cells. While 0.1 μM LPA weakly induces contraction of WT neural progenitor cells (A), 1 μM LPA strongly induces it (B). Both 0.1 and 1 μM LPA strongly induce contraction of Gβ1−/− cells (C, D). Bar = 100 μm in D.|
|DVDY_22256_sm_suppfig4.tif||81K||Supp. Fig. S4. Effects of Gallein on EGF-induced cell proliferation. Gallein (10 μM) was added 2 hr before stimulation. Neural progenitor cells were stimulated with 20 ng/ml EGF for two days. Cell proliferation was measured as described in the Experimental Procedures section and is expressed as fold increase compared with untreated WT cells. Gallein is not toxic to neural progenitor cells. Data are means ± SD.|
|DVDY_22256_sm_suppfig5.tif||600K||Supp. Fig. S5. Normal mitotic orientation of cortical progenitors in Gβ1−/− embryos. A: Visualization and classification of mitotic orientation of cortical progenitors at the ventricular surface (VS) of the telencephalon. Cortical VZ was stained with hematoxylin. Cortical progenitors were classified into three groups according to the angle of mitotic cleavage plane to the VS. B–D: Quantification of cleavage plane orientation. Mitotic orientation of Gβ1−/− cortical progenitors is not affected. P = 0.17 at E10.5, 0.76 at E14.5, and 0.07 at E15.5; χ2 test.|
|DVDY_22256_sm_suppfig6.tif||684K||Supp. Fig. S6. H&E stained retinal sections from P60–P90 mice. Retinal degeneration is not observed in Gβ1+/− mice. GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; OPL, outer plexiform layer; ONL, outer nuclear layer; Ph, photoreceptors. Bar = 100 μm in B.|
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