C-Terminal Region Truncation of RELN Disrupts an Interaction with VLDLR, Causing Abnormal Development of the Cerebral Cortex and Hippocampus

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Figure 3.
Figure 3.

Differential genetic interaction with Apoer2null and Vldlrnull mice in the cerebral cortex and hippocampus. A, RelnCTRdel/Apoer2null double-homozygote mice, but not RelnCTRdel/Vldlrnull double-homozygote mice, display reeler-like cortical layer inversion. RelnCTRdel/Vldlrnull mice appear similar to RelnCTRdel and Vldlrnull mice without inversion. Sagittal sections of P21 brains were immunostained with anti-CUX1 and anti-CTIP2 antibodies. White dotted lines indicate the pial surface. Scale bar, 250 μm. B, RelnCTRdel/Apoer2null double-homozygote mice display the marginal zone invasion. RelnCTRdel/Vldlrnull, RelnCTRdel, and Vldlrnull mice appear similar to each other with the marginal zone invasion. Scale bar, 100 μm. C, RelnCTRdel/Apoer2null double-homozygote mice, but not RelnCTRdel/Vldlrnull double-homozygote mice, display reeler-like hippocampus. Nissl staining images of P21 brain coronal sections are shown. Scale bar, 500 μm.

  1. The Journal of Neuroscience vol. 37 no. 4 960-971
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