Over-expression of EDAG in the myeloid cell line 32D: Induction of GATA-1 expression and erythroid/megakaryocytic phenotype

✍ Scribed by Ya-li Ding; Cheng-Wang Xu; Zhi-Dong Wang; Yi-Qun Zhan; Wei Li; Wang-Xiang Xu; Miao Yu; Chang-Hui Ge; Chang-Yan Li; Xiao-Ming Yang

• Publisher: John Wiley and Sons
• Year: 2010
• Tongue: English
• Weight: 562 KB
• Volume: 110
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.22597

✦ Synopsis

Abstract

Erythroid differentiation‐associated gene (EDAG), a hematopoietic tissue‐specific transcription regulator, plays a key role in maintaining the homeostasis of hematopoietic lineage commitment. However, the mechanism and genes regulated by EDAG remain unknown. In this study, we showed that overexpression of EDAG in a myeloid cell line 32D led to an erythroid phenotype with increased number of benzidine‐positive cells and up‐regulation of erythroid specific surface marker TER119. The megakaryocytic specific marker CD61 was also induced significantly. Using a genome‐wide microarray analysis and a twofold change cutoff, we identified 332 genes with reduced expression and 288 genes with increased expression. Among up‐regulation genes, transcription factor GATA‐1 and its target genes including EKLF, NF‐E2, Gfi‐1b, hemogen, SCL, hemoglobin alpha, beta and megakaryocytic gene GPIX were increased. Silencing of EDAG by RNA interference in K562 cells resulted in down‐regulation of these genes. Taken together, EDAG functions as a positive regulator of erythroid/megakaryocytic differentiation in 32D cells associated with the induction of GATA‐1 and its target genes. J. Cell. Biochem. 110: 866–874, 2010. © 2010 Wiley‐Liss, Inc.