Inactivation of aPKC results in the loss of adherens junctions in neuroepithelial cells without affecting neurogenesis in mouse neocortex

DEV02330 Supplementary Material

Files in this Data Supplement:

• Supplemental Figure 1 -

  Fig. S1. Loss of aPKCλ does not affect apoptosis. Active caspase 3-positive cell (A) and TUNEL positive cells (B) quantified and graphed in control and aPKCλ cKO embryo at E16.5.

• Supplemental Figure 2 -

  Fig. S2. Loss of aPKCλ does not impair the cortical plate and subplate. (A,B) Coronal sections of the neocortex from control (left panel) and aPKCλ cKO embryos (right panel) at E16.5 are stained with antibody against MAP2 (A) and chondroitin sulfate proteoglycan (CSPG) (B) to examine the structure of the cortical plate and the subplate, respectively. Scale bars: 100 μm.

• Supplemental Figure 3 -

  Fig. S3. Loss of aPKCλ disrupts tissue architecture of ganglionic eminence. Transverse sections of brains in control (A) and aPKCλ cKO embryos (B) at E13.5 are stained with Eosin and Hematoxylin. Fusion of the right and left medial ganglionic eminences (arrowhead) is observed in the aPKCλ cKO embryo. Scale bars: 100 μm.

• Supplemental Figure 4 -

  Fig. S4. Loss of aPKCλ results in the disappearance of proteins associated with neuroepithelial adherens junctions. Coronal sections of the neocortical region in control and aPKCλ cKO embryos at E15.5 are double-stained with antibodies against PAR3 and N-cadherin (A) or PAR6β and N-cadherin (B). LV, lateral ventricle. Scale bars: 10 μm.