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. Author manuscript; available in PMC: 2018 May 22.
Published in final edited form as: Dev Cell. 2017 May 22;41(4):366–381.e4. doi: 10.1016/j.devcel.2017.04.014

Figure 2. Ric8a mutation results in primary vascular defects in the embryonic LGE.

Figure 2

See also Figure S2.

(A–B) IB4 labeling shows LGE vascular defects in ric8a; nestin-cre mutants (B) in comparison to wildtype (A) at E14.5.

(C–D) Anti-laminin staining shows glomeruloid structures (arrows) in mutant LGE (D) at E16.5.

(E–F) Anti-PDGFRβ staining (red) shows similar pericyte (arrows) coverage along vessel (IB4, green) in wildtype (E) and mutant LGE (F).

(G–H) Anti-collagen IV staining shows defective basement membrane maturation in mutants (H) in comparison to wildtype (G).

(I–J) Anti-Nestin staining shows comparable radial glial scaffold between wildtype (I) and mutant (J) LGE at E14.5.

(K–L) Anti-Tubulin βIII (Tuj) staining shows comparable neuronal development between wildtype (K) and mutant (L) LGE at E14.5.

(M) Quantification of vessel density in wildtype and mutant LGE during embryogenesis. **, p < 0.01; n = 3.

(N) Quantification of perciyte density along vessels in wildtype and mutants (p = 0.59, n = 5).

(O) Quantification of collagen IV staining intensity shows significant reductions in mutants. *, p < 0.05; n = 4. AU, arbitrary units.

Scale bar: 200 μm for A, B, K, L, N and O, 100 μm for D, E, J and I, and 50μm in F and G.