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PMID: 7568185 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Transcription factor GATA-1 permits survival and maturation of erythroid precursors by preventing apoptosis.

Proceedings of the National Academy of Sciences of the United States of America ·Vol. 92 ·No. 21 ·1995-10-10 ·Pages 9623-7

Weiss MJ, Orkin SH

Abstract

The transcription factor GATA-1 recognizes a consensus motif present in regulatory regions of numerous erythroid-expressed genes. Mouse embryonic stem cells lacking GATA-1 cannot form mature red blood cells in vivo. In vitro differentiation of GATA-1- embryonic stem cells gives rise to a population of committed erythroid precursors that exhibit developmental arrest and death. We show here that the demise of GATA-1- erythroid cells is accompanied by several features characteristics of apoptosis. This process occurs despite normal expression of all known GATA target genes examined, including the erythropoietin receptor, and independent of detectable accumulation of the tumor suppressor protein p53. Thus, in addition to its established role in regulating genes that define the erythroid phenotype, GATA-1 also supports the viability of red cell precursors by suppressing apoptosis. These results illustrate the multifunctional nature of GATA-1 and suggest a mechanism by which other hematopoietic transcription factors may ensure the development of specific lineages.

MeSH Terms
Animals Apoptosis Cell Differentiation Cell Survival DNA-Binding Proteins/metabolism Erythroblasts/pathology,physiology Erythroid-Specific DNA-Binding Factors Fluorescent Antibody Technique GATA1 Transcription Factor Mice Transcription Factors/metabolism Tumor Suppressor Protein p53/metabolism
Chemicals
DNA-Binding Proteins Erythroid-Specific DNA-Binding Factors GATA1 Transcription Factor Gata1 protein, mouse Transcription Factors Tumor Suppressor Protein p53
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Weiss M J
Children's Hospital, Dana-Farber Cancer Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Orkin S H
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Article Info
Journal
Proceedings of the National Academy of Sciences of the United States of America
Abbr.
Proc Natl Acad Sci U S A
ISSN
0027-8424
DOI
10.1073/pnas.92.21.9623
Published
1995-10-10
Pages
9623-7
Language
English
Region
United States
NLM ID
7505876
PMCID
PMC40854
Subset
IM
Grants
NHLBI NIH HHS · K08 HL03364-01 · United States
External Links
PubMed source DOI: 10.1073/pnas.92.21.9623 PMC Full Text View journal details
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