Fig. 5: BMAL1 influences recruitment of HIF2α to a subset of target genes. | Nature Communications

Fig. 5: BMAL1 influences recruitment of HIF2α to a subset of target genes.

From: BMAL1 and ARNT enable circadian HIF2α responses in clear cell renal cell carcinoma

Fig. 5

A Venn diagram depicting the numbers of genomic sites (“peaks”) identified in chromatin fragments isolated by CUT&RUN procedure from 786O cells using antibodies recognizing BMAL1 (blue) or HIF2α (red). n = 3 samples per condition. B Chromatin binding profiles of BMAL1 and HIF2α in CUT&RUN samples (n = 3 per condition) prepared from 786O cells expressing the indicated shRNAs. Peaks are depicted in four clusters: BMAL1 peaks in 786O cells expressing shControl (top cluster: 1813 peaks), HIF2α peaks in 786 O cells expressing shControl (second cluster: 1207 peaks), peaks associated with both BMAL1 and HIF2α in 786 O cells expressing shControl (third cluster: 336 peaks), or HIF2α peaks identified only in 786 O cells expressing shBMAL1 (bottom cluster: 393 peaks). C Transcription factor binding motifs enriched in chromatin associated with BMAL1 (blue), HIF2α (red), or both (common, gray) in shControl cells. p-values were calculated in HOMER based on the hypergeometric distribution as described in ref. 40. D Representative genome browser tracks for BMAL1 and HIF2α CUT&RUN in 786 O cells expressing shControl or shBMAL1, showing peaks in VEGFA, SERPINE1, and NR1D1 loci. Data represent merged read counts for triplicate samples for each condition. Source data are provided as a Source Data file.

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