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. 2015 Jul 15;142(14):2521–2532. doi: 10.1242/dev.120220

Fig. 3.

Fig. 3.

Shox2 is required for maintaining the default SAN cell fate in the Nkx2-5+ domain. (A-H) Immunohistochemistry shows colocalization of Hcn4, Shox2, Tbx3 and Isl1, the absence of Cx40, as well as a relatively low level of cTnT in the Nkx2-5+ SA junction of the E14.5 wild-type embryo. (A′-H′) Immunohistochemistry reveals absence of Hcn4, Tbx3 and Isl1 expression but elevated Cx40 and cTnT levels in the Nkx2-5+ SA junction of E14.5 Nkx2-5IRESCre/+;Shox2F/F (Shox2Nkx2-5Cre) mice. The expression pattern of these genes remained unaltered in the Nkx2-5− SAN head region compared with controls. (I-J) 3D reconstruction and comparison of the SAN from E14.5 wild-type (I) and Nkx2-5IRESCre/+;Shox2F/F (I′) embryos based on the Hcn4+ domain revealed significantly reduced size of the SAN in the mutant (J) (n=3 each). White arrowheads point to the Nkx2-5+ SA junction and open arrowheads point to the Nkx2-5− SAN head. **P<0.01.