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1.
Figure 6

Figure 6. From: Nuclear Receptor HNF4? Binding Sequences are Widespread in Alu Repeats.

Gene-specific HNF4α-Alu sequences in primate genomes. Presence (+) and absence (-) of the HNF4α-Alu element in the indicated HNF4α target genes as determined by ChIP analysis (Figure 3) in all the sequenced primate genomes. Age in millions of years ago (MYA) of the divergence from the primate lineage is given on the right.

Eugene Bolotin, et al. BMC Genomics. 2011;12:560-560.
2.
Figure 5

Figure 5. From: Nuclear Receptor HNF4? Binding Sequences are Widespread in Alu Repeats.

Distribution of HNF4α binding sites in Alu repeats. Frequency histogram showing the position of HNF4α binding sites in AluY, AluS, and AluJ families of SINEs as well as the precursors FLAM and FRAM. The approximate age of the repeats is indicated. The slight variation in peaks at positions 31, 62 and 200 are due to small differences in the length of the Alu repeats.

Eugene Bolotin, et al. BMC Genomics. 2011;12:560-560.
3.
Figure 2

Figure 2. From: Nuclear Receptor HNF4? Binding Sequences are Widespread in Alu Repeats.

The vast majority of HNF4α binding sites in the human genome are found in Alu repeats. A. Numerical results from PBM3 described in Fig. 1 and in the text. B. Position weight matrices (PWMs) generated with Weblogo [76] of sequences bound by human HNF4α2 in the PBM, categorized by the type of sequence. The DR1-derived PWM was from 994 sequences bound by HNF4α2, the DR2-derived PWM from 50 sequences and the Alu-derived sequences from 66 sequences. The non canonical PWM is from Bolotin et al. [42].

Eugene Bolotin, et al. BMC Genomics. 2011;12:560-560.
4.
Figure 1

Figure 1. From: Nuclear Receptor HNF4? Binding Sequences are Widespread in Alu Repeats.

Schematic diagram of the protein binding microarray (PBM) designed to test the ability of HNF4α to bind Alu-derived DNA sequences. Top, schematic structure of a generic Alu element (~300 nt long) comprised of two related, but non identical monomers, the right and left arms (adapted from [75]). Box A and B are RNA Pol III internal promoters. Relative positions of the 200 Alu-derived 13-mers incorporated into PBM3 are also shown. Bottom, remaining DNA probes on PBM3 and workflow.

Eugene Bolotin, et al. BMC Genomics. 2011;12:560-560.
5.
Figure 7

Figure 7. From: Nuclear Receptor HNF4? Binding Sequences are Widespread in Alu Repeats.

Alu insertions in the promoters of IL32, APOM and PRODH2 genes. Screen shots from UCSC Genome Browser of human and other indicated primate genomes in the region of the HNF4α-Alu element ChIP'd by HNF4α in the IL32 (A), APOM (B) and PRODH2 (C) genes. Shown from top to bottom in each figure are non Alu HNF4α binding sites from Bolotin et al. [42] (Non Alu PBM); Alu sites from this study (Alu PBM); mRNA from RefSeq track (RNA); HNF4α ChIP signal in HepG2 from the Custom Track by UC Davis (http://genome.ucsc.edu/ENCODE/) (ChIP-Seq); DNA sequence conservation in four primate genomes (Rhesus, Marmoset, Orangutan, Chimp); PCR product amplified after ChIP in Fig. 3 (ChIP product); repeats from Repeat Masker 3.2.7 with the relevant Alu sequence indicated (Repeats).

Eugene Bolotin, et al. BMC Genomics. 2011;12:560-560.
6.
Figure 3

Figure 3. From: Nuclear Receptor HNF4? Binding Sequences are Widespread in Alu Repeats.

HNF4α binds Alu elements in vivo. A. HNF4α chromatin immunoprecipitation (ChIP) of HepG2 cells using 16 sets of PCR primers as indicated. Shown is an ethidium-bromide-stained agarose gel of the qPCR products after ~40 cycles for graphical representation only. In, input control of genomic DNA. IgG, control IP with normal rabbit IgG. H4, IP with HNF4α antibody raised in rabbit. Fold change, ratio of the H4 to IgG signal determined by quantitative real time PCR (qPCR). Pos and neg control, regions of the CDKN1A promoter in which HNF4α was shown previously to bind or not, respectively [71]; Alu generic, amplification with generic primers that recognize all Alu elements. Shown are the results from one of two or more independent ChIP experiments performed in duplicate, except for APOM, GSTM4, PRLR and SOCS2 which are from one ChIP experiment. The largest fold change values obtained for a given gene are indicated. B. Schematic diagram of promoters of HNF4α target genes. Diamonds, position of HNF4α binding sites in Alu elements identified in this study; triangles, other HNF4α binding sites predicted by PBM from Bolotin et al. [42]; vertical lines, position of the PCR primers used in the ChIP; arrows, start sites of transcription. See additional file 2: Table S2 for sequences of all the PCR primers.

Eugene Bolotin, et al. BMC Genomics. 2011;12:560-560.
7.
Figure 4

Figure 4. From: Nuclear Receptor HNF4? Binding Sequences are Widespread in Alu Repeats.

HNF4α activates transcription from Alu elements. A. Reporter gene assay with the HNF4α-Alu elements from the indicated human gene promoters fused to a minimal core promoter driving luciferase (pGL4.23). Shown is luciferase activity (relative light units, RLU) normalized to β-gal activity (normalized RLU) from HEK 293T cells transiently transfected with 1 μg of reporter and different amounts of either empty vector or human HNF4α2 expression vector (100, 200, 300 and 500 ng). Reporter constructs contain only the HNF4α-Alu element and immediately adjacent sequence; they do not contain any additional known HNF4α binding sites. Data are the mean normalized RLU of triplicate samples from one representative experiment from two or more that were performed. P-values of the HNF4α2 signal compared to the empty vector are indicated. Fold induction by HNF4α2 compared to the empty vector is indicated. B. As in (A) but with two different reporter constructs containing classical HNF4α response elements (RE-1 and RE-2). Shown is fold induction by 500 ng HNF4α2 compared to the parent construct (pGL4.23). C. As in (A) but of the native human APOA4 promoter (-1343 to +247) fused to luciferase (pGL4.10) without (WT) or with mutations (MUT) in either the HNF4α-Alu element (Alu) or a classical HNF4α site identified by a previous PBM analysis (HNF4α-PBM) (see Figure 3). Shown is the fold induction by 500 ng HNF4α2 compared to the empty expression vector from one experiment performed in six replicates. A second independent experiment performed in triplicate gave similar results. (B) and (C), sequence of the relevant HNF4α binding sites are given with the spacer nucleotide in lower case and mutations in red.

Eugene Bolotin, et al. BMC Genomics. 2011;12:560-560.

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