GATA-2 transcription factor is predominantly expressed in hematopoietic stem and progenitor cells (HS/PCs), and counteracts erythroid specific transcription factor GATA-1 to modulate proliferation and differentiation of hematopoietic cells. During hematopoietic cell differentiation, GATA-2 exhibits dynamic expression patterns, regulated by collaborations between GATA-1 and epigenetic regulators. Here, we show that histone specific demethylase1 (LSD1) regulates the expression of GATA-2 gene during erythroid differentiation. Knockdown of LSD1 leads to increased GATA-2 expression and inhibits induced MEL and embryonic stem cell differentiation. Furthermore, we demonstrate that LSD1 binds at the 1S promoter of GATA-2 gene locus, and suppresses GATA-2 expression through histone demethylation. Thus, our data reveals that LSD1 mediates erythroid cell differentiation by epigenetic modification of GATA-2 gene locus.

Disclosures

No relevant conflicts of interest to declare.

Topics:
gata2 gene, histones, repression, gata1 protein, human, transcription factor, photon correlation spectroscopy, portacaval shunt, surgical, precordial catch syndrome, binding (molecular function), embryonic stem cells

Author notes

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Asterisk with author names denotes non-ASH members.

© 2014 by The American Society of Hematology
2014
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