Figures
Inactivation of FAM20C leads to hypophosphatemic rickets.
The Sox2-Cre—mediated conditional knockout (cKO) of Fam20c leads to significant skeletal defects. X-ray imaging of 5-month-old cKO mice (right) shows smaller stature, distorted spine, and hypomineralized skeleton when compared with their wild type littermates (left). The skeletal defects along with lower phosphorus and higher FGF23 levels in the serum of cKO mice are consistent with a diagnosis of hypophosphatemic rickets, indicating that FAM20C plays an essential role in biomineralization and maintenance of total body phosphorus homeostasis. See Wang et al.
Image Credit: Xiaofang Wang (Texas A&M Health Science Center, Baylor College of Dentistry).
Citation: (2012) PLoS Genetics Issue Image | Vol. 8(5) May 2012. PLoS Genet 8(5): ev08.i05. https://doi.org/10.1371/image.pgen.v08.i05
Published: May 31, 2012
Copyright: © 2012 Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The Sox2-Cre—mediated conditional knockout (cKO) of Fam20c leads to significant skeletal defects. X-ray imaging of 5-month-old cKO mice (right) shows smaller stature, distorted spine, and hypomineralized skeleton when compared with their wild type littermates (left). The skeletal defects along with lower phosphorus and higher FGF23 levels in the serum of cKO mice are consistent with a diagnosis of hypophosphatemic rickets, indicating that FAM20C plays an essential role in biomineralization and maintenance of total body phosphorus homeostasis. See Wang et al.
Image Credit: Xiaofang Wang (Texas A&M Health Science Center, Baylor College of Dentistry).