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. Author manuscript; available in PMC: 2018 Sep 1.
Published in final edited form as: Dev Biol. 2017 Jun 19;429(1):260–270. doi: 10.1016/j.ydbio.2017.06.020

Fig. 1.

Fig. 1

Skull deformities developed in caBmpr1a;P0-Cre mice were rescued by a heterozygosity of Bmpr1a. (A) (a–e) ca-Bmpr1a;P0-Cre;Bmpr1b+/− (ca1A;1bH) and ca-Bmpr1a;P0-Cre;Acvr1+/− (ca1A;AcH) displayed short, broad snouts and hypertelorism same as ca-Bmpr1a;P0-Cre (ca1A) while ca-Bmpr1a;P0-Cre;Bmpr1a+/− (ca1A;1aH) showed phenotypes similar to Control (Cont) at P17. (f–j) Skeletal staining at P17 revealed premature fusion at the anterior frontal (AF) suture in ca1A, ca1A;1bH and ca1A;AcH whereas the AF suture in Cont and ca1A;1aH was still patent. (k–o) MicroCT image showed more skull cavities in ca1A, ca1A;1bH and ca1A;AcH compared with ca1A;1aH. (B) Bone volume (BV/TV) in nasal and frontal bones were quantified by microCT. Data presented were means ± SD of five different skulls and three independent experiments. AF, anterior frontal suture; N, nasal bone; PF, posterior frontal suture. n=5 per group, * p<1 ×10−6, ** p<0.01.