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<p>COUP-TFII<b>,</b> encoded by the <i>NR2F2</i> gene, is an orphan nuclear receptor highly expressed during embryonic development in several tissues. In erythropoiesis, COUP-TFII is active in yolk sac-derived cells prior to the switch to adult globin expression. Its broad expression pattern suggests a complex transcriptional regulation involving multiple, yet poorly defined, regulatory elements. Using integrative <i>in silico</i> and chromatin accessibility analyses, here we identified an erythroid-specific enhancer located 52Kb upstream of the <i>NR2F2</i> transcription start site. This element shows epigenetic features of an active enhancer in K562 erythroid cells. Notably, in subclones derived from adult HUDEP2 erythroid progenitor cells that spontaneously re-express fetal gamma globin, <i>NR2F2</i> is reactivated, concomitantly with the opening of the -52Kb enhancer. We also identify the transcription factor ZBTB7A as a repressor of <i>NR2F2</i>, as knock-out of <i>ZBTB7A</i> in HUDEP2 cells restores <i>NR2F2</i> expression and active chromatin marks at the -52Kb region<i>.</i> Our findings uncover a novel distal enhancer controlling <i>NR2F2</i> expression in erythroid cells.</p>

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A long-range enhancer at -52Kb drives expression of the COUP-TFII transcription factor in erythroid cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月1日

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  • Valentina Pastori,
  • Agata Labedz,
  • Maria A. Simanovich,
  • Martina Fabiano,
  • Carlotta Frigo,
  • Thijs Verheul,
  • Ludovica Proietti,
  • Florian Grebien,
  • Elisabetta Citterio,
  • Sjaak Philipsen,
  • Antonella Ellena Ronchi

摘要

COUP-TFII, encoded by the NR2F2 gene, is an orphan nuclear receptor highly expressed during embryonic development in several tissues. In erythropoiesis, COUP-TFII is active in yolk sac-derived cells prior to the switch to adult globin expression. Its broad expression pattern suggests a complex transcriptional regulation involving multiple, yet poorly defined, regulatory elements. Using integrative in silico and chromatin accessibility analyses, here we identified an erythroid-specific enhancer located 52Kb upstream of the NR2F2 transcription start site. This element shows epigenetic features of an active enhancer in K562 erythroid cells. Notably, in subclones derived from adult HUDEP2 erythroid progenitor cells that spontaneously re-express fetal gamma globin, NR2F2 is reactivated, concomitantly with the opening of the -52Kb enhancer. We also identify the transcription factor ZBTB7A as a repressor of NR2F2, as knock-out of ZBTB7A in HUDEP2 cells restores NR2F2 expression and active chromatin marks at the -52Kb region. Our findings uncover a novel distal enhancer controlling NR2F2 expression in erythroid cells.