Fig. 6: HNF1A binding to HASTER mediates negative regulation of HNF1A.
From: The HASTER lncRNA promoter is a cis-acting transcriptional stabilizer of HNF1A
a, Doxycycline (Dox)-induced HNF1A overexpression in EndoC-βH3 cells activated HASTER and blocked endogenous HNF1A (n = 3 independent experiments). b, HNF1A overexpression in clonal EndoC-βH3 cell lines with homozygous deletions of both HASTER promoters (n = 4 independent experiments). c, HNF1A transactivation of HASTER is separable from repression of its promoter. Wild-type HNF1A or HNF1A containing a deletion of an endogenous IDR, HNF1B or HNF1B fused to an unrelated IDR were expressed in EndoC-βH3 cells. Green fluorescent protein (GFP) and GFP fused to the unrelated IDR are shown as controls (n = 4 independent experiments). NS, not significant. d, Expression of HNF1A containing a deletion of an IDR and of HNF1B fused to an unrelated IDR in EndoC-βH3 cells, essentially as represented in b with the addition of experiments with HASTER promoter deletions to show that the effects are dependent on HASTER (n = 4 independent experiments). In a–d, the data are presented as TBP-normalized relative expression (means ± s.d.) and statistical significance was determined by two-tailed Student‘s t-test.
