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. Author manuscript; available in PMC: 2010 Jul 26.
Published in final edited form as: Nat Genet. 2007 Dec 16;40(1):61–68. doi: 10.1038/ng.2007.28

Figure 8.

Figure 8

Nkx2-5 haploinsufficiency protects against cardiac conduction defects induced by DMPK 3′ UTR mRNA. (a) PR intervals in Nkx2-5+/+ 5-313 heterozygotes increase much more than in Nkx2-5LacZ/+ 5-313 heterozygotes after induction of DMPK 3′ UTR mRNA toxicity (mean ± s.d.). * indicates that PR intervals are not significantly different before doxycycline induction (P = 0.08). ** indicates that PR intervals are significantly different after doxycycline induction (P = 0.00003). (b) RT-PCR confirms that Nkx2-5 mRNA expression is much lower in Nkx2-5LacZ/+ 5-313 heterozygote hearts than in Nkx2-5+/+ 5-313 heterozygote hearts (mean ± s.d.). (c) Representative protein blot demonstrating that NKX2-5 expression is lower in Nkx2-5LacZ/+ 5-313 heterozygote hearts than in Nkx2-5+/+ 5-313 heterozygote hearts (+/− indicates Nkx2-5LacZ/+ mice). Numbers below blot show relative NKX2-5 expression compared to uninduced Nkx2-5+/+ 5-313 heterozygotes. Uninduced skeletal muscle (sk.m.) extract was used as a negative control for NKX2-5. At least five mice were analyzed for each group for RT-PCR and protein blotting. Dox, doxycycline.