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. 2018 Apr 6;6:12. doi: 10.1038/s41413-018-0013-z

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — SHP2 deficiency compromises osteogenic differentiation of OCPs and skeletal ossification, and can be rescued by haploinsufficiency of Sox9. a–c Frozen sections from 1.5-day-old mouse tibiae, hybridized to probes for murine Ctnnb1 (a), Col1α1 (b), and Ibsp (c). Enlarged views of the corresponding color-boxed areas are presented on the right. Note the reduced abundance of Ctnnb1, Col1α1, and Ibsp in cells within the periosteum and spongy bone in SHP2_Prrx1KO mice (middle row), compared with SHP2_Prrx1CTR mice (top row). These defects and defective ossification were partially rescued by Sox9 haploinsufficiency in SHP2_Prrx1KO;Sox9^fl/+;R26^mTmG mice (bottom row). d Images of femurs from 7-day-old SHP2_Prrx1CTR and SHP2_Prrx1KO mice, immunostained with antibodies against β-CATENIN and bone sialoprotein (BSP). Note the reduction of β-CATENIN and BSP abundance in periosteal areas (_*) of SHP2_Prrx1KO mice, compared with SHP2_Prrx1CTR controls (arrows). Arrowheads indicate calcified cortical bone in SHP2_Prrx1CTR mice (a–d, n = 3). e Bar graphs demonstrate the heights of epiphyseal cartilage (dark gray) and endochondral bone (light gray) of tibia from P0.5 neonates. Note that removal of one allele of Sox9 significantly increased the length of endochondral bone in SHP2_OCPKO^Res mice, compared to controls (n = 3, *^#P < 0.05, 2-way ANOVA).