GATA factor switching during erythroid differentiation

被引:86
作者
Kaneko, Hiroshi [1 ]
Shimizu, Ritsuko [2 ]
Yamamoto, Masayuki [1 ]
机构
[1] Tohoku Univ, Grad Sch Med, Dept Med Biochem, Aoba Ku, Sendai, Miyagi 9808575, Japan
[2] Tohoku Univ, Grad Sch Med, Dept Expt Hematol, Aoba Ku, Sendai, Miyagi 9808575, Japan
关键词
erythropoiesis; GATA factor switching; gene regulation; hematopoietic GATA factors; ERYTHROPOIESIS IN-VIVO; DEFINITIVE ERYTHROPOIESIS; CHROMATIN OCCUPANCY; TRANSCRIPTIONAL REPRESSION; HEMATOPOIETIC DEFECT; GLOBIN LOCUS; GENE LOCUS; EXPRESSION; COMPLEXES; PROMOTER;
D O I
10.1097/MOH.0b013e32833800b8
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Purpose of review Efforts have been made to understand how erythroid differentiation is regulated, and recent discoveries have clarified that lineage-specific transcription factor networks are essential for proper differentiation of erythroid cells. The transcription factors GATA1 and GATA2 are involved in such networks that regulate erythroid gene expression. Importantly, expression of Gata1 and Gata2 genes is also under the control of such regulatory networks. The present review is focused on the mechanism of Gata1 and Gata2 gene regulation during erythropoiesis and the physiological significance of their dynamic regulation. Recent findings Gata1 and Gata2 genes are regulated by multiple transcription factors, including their own products GATA1 and GATA2. GATA1 and GATA2 recognize specific regulatory GATA motifs, and their expression levels change dynamically during erythroid differentiation, leading to diversified gene expression during erythropoiesis. Summary Strict regulations of the Gata1 and Gata2 genes are critical for proper lineage commitment and development of erythroid cells. It has been shown in transgenic mouse analyses that cis-acting GATA binding motifs are critical for the expression of Gata1 and Gata2 genes. Furthermore, expression of Gata1 and Gata2 genes along with a set of erythroid genes appeared to be regulated by GATA factor switching.
引用
收藏
页码:163 / 168
页数:6
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