Skip to main content
. Author manuscript; available in PMC: 2020 Jul 22.
Published in final edited form as: Dev Cell. 2019 Jun 6;50(2):212–228.e6. doi: 10.1016/j.devcel.2019.05.015

Figure 3. Activation of p53 in the facial ectoderm and telencephalon induces craniofacial defects.

Figure 3

(A) P21 Foxg1-Cre;Trp53LSL−25,26,53,54/+ mice have slightly smaller eyes than controls (100%, n=5).

(B) Foxg1-Cre;Trp53LSL−25,26/+ embryos are viable at E18.5 (i) and display the following phenotypes at E9.5–18.5: small eyes (ii-v, 100%, n=15), retinal coloboma (arrow, ii-v, 93%, n=15), an absence of a lens (L, v, 100%, n=6), hypoplastic nasal passages (vi, 100%, n=6), a blocked nasal airway and nasopharynx (vii-viii, 100%, n=4), hypoplastic inner ears (dotted outline, ix, 100%, n=3), small otic vesicles (Ov, x, 100%, n=6), and small telencephalons (Te, xi-xii, 100%, n=6). NPh: nasopharynx, PS: palatal shelves, T: tongue.

(C) Foxg1-Cre;Mdm2flox/flox embryos have no eyes and lack the entire frontonasal region, including the nasal septum (NS), at E12.5–14.5 (i-iii, 100%, n=4), display exencephaly at E12.5–14.5 (Ex, ii, 25%, n=4), have no discernable otic vesicle (Ov) at E9.5 (iv, 100%, n=6), and have a telencephalon (Te) that is smaller than controls at E9.5 (*, iv, 100%, n=6) and largely absent at E10.5–12.5 (v-vi, 100%, n=4). T: tongue.

Scale bar: 5mm (A,Bi), 1mm (Bxi;Ci,ii,iv,v), 400µm (Biii-x,xii;Ciii,vi). Sectioning plane: coronal (Bv,vii,xii), transverse (Bvi,ix;Ciii,vi), sagittal (Bviii). See also Figure S1, Figure S2, Table S1.