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Fig. 5 | Stem Cell Research & Therapy

Fig. 5

From: Sin3a drives mesenchymal-to-epithelial transition through cooperating with Tet1 in somatic cell reprogramming

Fig. 5

The interaction of Sin3a and Tet1 is critical for Tet1 occupation and hydroxymethylation at the promoter of epithelial genes. A Co-IP analysis of the interaction of SIN3A and TET1 at Day 5 in shSin3a-1 cells overexpressing wild-type Sin3a or Sin3a mutants (Sin3aF147A and Sin3aF182A). Nonsense mutations were introduced into the wild-type Sin3a and Sin3a mutants to protect against shSin3a-1 targeting. B–E ChIP-qPCR results (n = 4 independent experiments) of Sin3a occupation at the promoter of epithelial markers (Cldn3 (B), Pkp1 (C), Krt8 (D), and E-cadherin (E)) at Day 5 of reprogramming. F–I ChIP-qPCR results of Tet1 occupation at the promoter of epithelial markers at Day 5 of reprogramming. J hMeDIP-qPCR results of 5hmC levels at the promoter of epithelial markers in shSin3a-1 cells overexpressing wild-type Sin3a or Sin3a mutants. Data in F–J were representative of three independent experiments. Significance was estimated by student’s unpaired t test. Error bars represent SD. *P < 0.05, **P < 0.01, and ***P < 0.001 versus pMKO.1-treated group with FUGW vector (the white column), #P < 0.05, ##P < 0.01, and ###P < 0.001 versus shSin3a-1-treated group with FUGW vector (the blue column), $P < 0.05, $$P < 0.01, and $$$P < 0.001 versus the wild-type Sin3a overexpression group (the red column)

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