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

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© 2015. Published by The Company of Biologists Ltd

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Fig. 5. — Shox2 antagonizes Nkx2-5 transcriptional output on the pacemaker program. (A-C′) A comparison of Hcn4 and Cx40 expression in the transition region of the Nkx2-5⁻ SAN head and the Nkx2-5⁺ SA junction reveals a clear boundary (dotted lines) between the SAN cells and atrial cells in controls (A,A′), the conversion of Hcn4⁺/Cx40⁻ cells to Hcn4⁻/Cx40⁺ cells in the Nkx2-5^IRESCre/+;Shox2^F/F (Shox2^Nkx2-5Cre) SA junction (B,B′), and the rescue of this phenotype in Nkx2.5^Cre/IRESCre;Shox2^F/F (Nkx2-5^hypo;Shox2^F/F) mice (C,C′). (D-I) Expression of SAN markers, including Hcn4, Isl1 and Tbx3, is restored in the SA junction of Nkx2-5^hypo;Shox2^F/F mice. Dotted lines delineate the border between the SAN and atrial tissue that can be otherwise clearly observed in controls. (J-L′) Comparison of Hcn4 and Cx40 expression in the PV myocardium of control (J,J′), Nkx2-5^hypo (K,K′) and Nkx2-5^hypo;Shox2^F/F (L,L′) mice. Arrowheads point to PV myocardium.