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. Author manuscript; available in PMC: 2011 Mar 22.
Published in final edited form as: Nat Med. 2009 Dec 6;16(1):106–110. doi: 10.1038/nm.2068

Figure 3.

Figure 3

Effect of proliferation on HNF-1β target gene expression and chromatin modifications. (a) Renal expression of Umod, Pkhd1, Pkd2, Kif12, Crb3, Tcfap2b, Tmem27 and Bicc1 mRNA transcripts in wild-type or in mutant adult kidneys 3–4 weeks after the inactivation that was induced in proliferative P0 pups or in quiescent kidneys at P30, respectively. Data are means ± s.e.m.; n = 4–8 for each experimental group. *P < 0.05; **P < 0.01. Ribosomal protein L13 (Rpl13) was used to normalize values. (b) BrdU and Pkd2 (top) or Kif12 (bottom) staining in kidneys of wild-type and mutant mice 2 weeks after ischemia. Colocalization analysis shows that, in wild-type tubules after ischemia, Pkd2 and Kif12 expression (brown cytoplasm) is maintained in cells that have proliferated (blue nuclei). In contrast, in Hnf1b-deficient tubules, Pkd2 and Kif12 expression is selectively turned off in cells that have proliferated. Scale bars, 100 μm. (c) Chromatin modifications in the mIMCD3 cell line expressing a HNF-1β dominant-negative mutant. Chromatin immunoprecipitation of activating (H3K9ac) or inhibiting (H3K9me3 or H3K27me3) histone H3 modifications of the Pkhd1 gene at various locations with respect to the transcriptional start site (indicated on the x axis) in control cells or in cells expressing a dominant-negative mutant of HNF-1β. The results are representative of a set of three independent experiments. Error bars represent s.e.m. *P < 0.05. (d) Chromatin immunoprecipitation of activating modifications (H3K9ac or H3K4me3) of histone H3 on the Pkhd1 gene at various locations with respect to the transcriptional start site (indicated on the x axis) in kidneys from wild-type or Hnf1b-deleted mice inactivated shortly after birth. Immunoprecipitation of total histone H3 is used as a control. Enrichments are calculated with respect to the Rpl13 gene for activating modifications and for the Acta2 gene (encoding smooth muscle α-actin) for repressive modifications. The results are representative of a set of three independent experiments. *P < 0.05.