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ABC‐me: a novel mitochondrial transporter induced by GATA‐1 during erythroid differentiation
Author(s) -
Shirihai Orian S.,
Gregory Todd,
Yu Channing,
Orkin Stuart H.,
Weiss Mitchell J.
Publication year - 2000
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/19.11.2492
Subject(s) - biology , atp binding cassette transporter , gata2 , transcription factor , microbiology and biotechnology , gata1 , globin , haematopoiesis , erythropoiesis , embryonic stem cell , mitochondrion , stem cell , gene , transporter , genetics , medicine , anemia
Transcription factor GATA‐1 is essential for normal erythropoiesis. GATA‐binding sites are consistently found in promoters or enhancers of genes expressed selectively in erythroid cells. To discover novel GATA‐1‐regulated genes, we searched for GATA‐1‐activated transcripts in G1E cells, an erythroid line derived from GATA‐1 − embryonic stem cells. By subtractive analysis, we identified a new ATP‐binding cassette (ABC) transporter that is strongly and rapidly induced by GATA‐1. This protein, named ABC‐me (for ABC ‐ m itochondrial e rythroid), localizes to the mitochondrial inner membrane and is expressed at particularly high levels in erythroid tissues of embryos and adults. ABC‐me is induced during erythroid maturation in cell lines and primary hematopoietic cells, and its overexpression enhances hemoglobin synthesis in erythroleukemia cells. The ABC proteins participate in diverse physiological processes by coupling ATP hydrolysis to the transport of a variety of substrates across cell membranes. We speculate that ABC‐me, a newly identified erythroid‐expressed ABC superfamily member, may mediate critical mitochondrial transport functions related to heme biosynthesis.