Fig 2. Wnt1^Cre-mediated neural crest-specific deletion of BAF155/170 leads to severe craniofacial defects and embryonic lethality.

(A-H) Phenotypic defects in control, BAF170-deficient (Wnt1^Cre/+;BAF170^fl/fl;BAF155^fl/+), BAF155-deficient (Wnt1^Cre/+;BAF155^fl/fl;BAF170^fl/+) and BAF155/170-deficient (Wnt1^Cre/+;BAF155^fl/fl;BAF170^fl/fl) embryos. Sagittal view of E9.5 (A-D), E10.5 (E-H), and E11.5 (I-L) embryos. No obvious developmental defects were observed at E9.5 between different genotypes (A-D). Developmental defects in neural-crest derived tissues, including craniofacial defects in BAF155/170-deficient embryos (H and L) when compared with their littermate controls (E and I). Among BAF155/170-deficient embryos, 7/10 showed severe craniofacial defects. Hemorrhage in the forebrain (telencephalon) of E11.5 BAF155/170-deficient embryos (3/10 embryos) (L). Craniofacial defects are also present in BAF155-deficient embryos (6/10 showed craniofacial deformities, enlarged blood vessels) but less severe than the BAF155/170-deficient embryos (K). No obvious morphological defects were observed in BAF170-deficient embryos (10/10) at the embryonic stages analyzed (F and J). n = 4–10 embryos were analyzed for each genotype at each given embryonic stage. Scale bars 200μM (A-H) and 500μM (E-H). fl, forelimb; hl, hindlimb; ht, heart; mc, metencephalon; tc, telencephalon.