Hartman Institute for Therapeutic Organ Regeneration

STAT5 acts as a repressor to regulate early embryonic erythropoiesis.

TitleSTAT5 acts as a repressor to regulate early embryonic erythropoiesis.
Publication TypeJournal Article
Year of Publication2006
AuthorsSchmerer M, Torregroza I, Pascal A, Umbhauer M, Evans T
JournalBlood
Volume108
Issue9
Pagination2989-97
Date Published2006 Nov 01
ISSN0006-4971
KeywordsAnimals, Embryo, Nonmammalian, Embryonic Development, Erythropoiesis, Fibroblast Growth Factors, Gene Expression Regulation, Developmental, Phosphorylation, Reverse Transcriptase Polymerase Chain Reaction, STAT5 Transcription Factor, Xenopus, Xenopus Proteins
Abstract

STAT5 regulates definitive (adult stage) erythropoiesis through its ability to transduce signals from the erythropoietin receptor. A function for STAT-dependent signaling during primitive (embryonic) erythropoiesis has not been analyzed. We tested this in the Xenopus system, because STAT5 is expressed at the right time and place to regulate development of the embryonic primitive ventral blood island. Depletion of STAT5 activity results in delayed accumulation of the first globin-expressing cells, indicating that the gene does regulate primitive erythropoiesis. Our results suggest that in this context STAT5 functions as a repressor, since forced expression of an activator isoform blocks erythropoiesis, while embryos expressing a repressor isoform develop normally. The erythroid phenotype caused by the activator isoform of STAT5 resembles that caused by overexpression of fibroblast growth factor (FGF). We show that STAT5 isoforms can function epistatic to FGF and can be phosphorylated in response to hyperactivated FGF signaling in Xenopus embryos. Therefore, our data indicate that STAT5 functions in both primitive and definitive erythropoiesis, but by different mechanisms.

DOI10.1182/blood-2006-05-022137
Alternate JournalBlood
PubMed ID16835375
PubMed Central IDPMC1895518
Grant ListGM07491 / GM / NIGMS NIH HHS / United States
HL056182 / HL / NHLBI NIH HHS / United States

Weill Cornell Medicine
Hartman Institute for Therapeutic Organ Regeneration
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