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. 2020 Jan 9;21(3):e48512. doi: 10.15252/embr.201948512

Figure 2. CRMP2 regulates postnatal development of corpus callosum.

Figure 2

  1. CRMP2 deficiency leads to callosal hypoplasia. Shortening of corpus callosum (arrowheads) is apparent in both sagittal (first row) and coronal sections (second row) of adult brains. Scale bars: 1 mm.
  2. Quantification of callosal length in 30‐day‐old mice (P30, n = 3, crmp2 −/− is 80.8 ± 5% of WT, P = 0.003) and adult mice (n = 3, crmp2 −/− is 80.5 ± 3% of WT, P = 0.002), mean ± SD, *P < 0.05, t‐test.
  3. Labeling of adult corpus callosum with anti‐neurofilaments antibody in sagittal sections. Outline depicts missing posterior part of the tract in crmp2 −/− mice. Caudal part of the corpus callosum in WTs is located dorsally above the habenular commissure (hbc), while in crmp2 −/− mice, callosum terminates rostrally before reaching the hbc (arrows). PC indicates posterior commissure. Scale bars: 500 μm.
  4. The growth of GFP‐labeled callosal axons in the contralateral cortex at P6 (embryos were electroporated at E15.5). Note the disorganized paths of crmp2 −/− axons. Scale bars: 200 μm.
  5. Schematic drawing of the callosal axon path and axonal tortuosity calculation. Pyramidal neurons in layer II/III project their axons into the contralateral cortex [rectangle depicts the area displayed in (D)]. Axonal tortuosity quantification as shown in (F), tortuosity = 1 if a = b.
  6. Quantification of tortuosity of axons (WT n = 6 pups, crmp2 −/− n = 3 pups) upon their exit from the callosal tract (WT 1.016 ± 0.003 vs. crmp2 −/− 1.044 ± 0.012, P < 0.001), mean ± SD, ***P < 0.001, t‐test.
  7. DiI‐labeled callosal axons from P9 oblique brain sections (see the Appendix Fig S1) and their reconstruction in Neurolucida 360 (WT n = 6, crmp2 −/− n = 9). Scale bars: 200 μm.
  8. Polar histograms of callosal axons reconstructed in (G). Note the broader range of axon growth angles in crmp2 −/− mice.
  9. Left: schematic representation of polar histogram analysis by clustering the traced axons (WT n = 6 pups, crmp2 −/− n = 9 pups) into three groups based on the growth angles. Right: proportion of axons growing in selected clusters (WT, 0° to ±20°: 67.3 ± 10.3%; ±20° to ±40°: 21.2 ± 5.3%; ±40° to ±60°: 6.22 ± 3.2%; crmp2 −/−, 58.5 ± 5%, P = 0.047, 27.7 ± 4.3%, P = 0.022, 8.64 ± 2.25%, P = 0.11), mean ± SD, *P < 0.05, t‐test.