Cooperative and antagonistic interplay between PU.1 and GATA-2 in the specification of myeloid cell fates

Jonathan C. Walsh; Rodney P. DeKoter; Hyun Jun Lee; Erica D. Smith; David W. Lancki; Michael F. Gurish; Daniel S. Friend; Richard L. Stevens; John Anastasi; Harinder Singh

doi:10.1016/S1074-7613(02)00452-1

Cooperative and antagonistic interplay between PU.1 and GATA-2 in the specification of myeloid cell fates

Jonathan C. Walsh, Rodney P. DeKoter, Hyun Jun Lee, Erica D. Smith, David W. Lancki, Michael F. Gurish, Daniel S. Friend, Richard L. Stevens, John Anastasi, Harinder Singh^*

^*Corresponding author for this work

Cell & Developmental Biology

Research output: Contribution to journal › Article › peer-review

224 Scopus citations

Abstract

PU.1 and GATA transcription factors appear to antagonize each other's function in the development of distinct lineages of the hematopoietic system. In contrast, we demonstrate that PU.1, like GATA-2, is essential for the generation of mast cells. PU.1-/- hematopoietic progenitors can be propagated in IL-3 and differentiate into mast cells or macrophages upon restoration of PU.1 activity. Using these progenitors and a conditionally activatable PU.1 protein, we show that PU.1 can negatively regulate expression of the GATA-2 gene. In the absence of GATA-2, PU.1 promotes macrophage but not mast cell differentiation. Reexpression of GATA-2 in such progenitors enables the generation of mast cells. We propose a developmental model in which cooperative function or antagonistic crossregulation by PU.1 of GATA-2 promotes distinct myeloid cell fates.

Original language	English (US)
Pages (from-to)	665-676
Number of pages	12
Journal	Immunity
Volume	17
Issue number	5
DOIs	https://doi.org/10.1016/S1074-7613(02)00452-1
State	Published - Nov 1 2002

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Infectious Diseases

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/S1074-7613(02)00452-1

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title = "Cooperative and antagonistic interplay between PU.1 and GATA-2 in the specification of myeloid cell fates",

abstract = "PU.1 and GATA transcription factors appear to antagonize each other's function in the development of distinct lineages of the hematopoietic system. In contrast, we demonstrate that PU.1, like GATA-2, is essential for the generation of mast cells. PU.1-/- hematopoietic progenitors can be propagated in IL-3 and differentiate into mast cells or macrophages upon restoration of PU.1 activity. Using these progenitors and a conditionally activatable PU.1 protein, we show that PU.1 can negatively regulate expression of the GATA-2 gene. In the absence of GATA-2, PU.1 promotes macrophage but not mast cell differentiation. Reexpression of GATA-2 in such progenitors enables the generation of mast cells. We propose a developmental model in which cooperative function or antagonistic crossregulation by PU.1 of GATA-2 promotes distinct myeloid cell fates.",

author = "Walsh, {Jonathan C.} and DeKoter, {Rodney P.} and Lee, {Hyun Jun} and Smith, {Erica D.} and Lancki, {David W.} and Gurish, {Michael F.} and Friend, {Daniel S.} and Stevens, {Richard L.} and John Anastasi and Harinder Singh",

note = "Funding Information: We thank Abe Brass, Steven Kosak, and Celeste Simon for critical comments on the manuscript. This work was supported by the Howard Hughes Medical Institute (R.P.D., D.W.L., and H.S.) and NIH grants AI-23483, AI-31599, GM-07151, HL-07237, and HL-36110 (D.S.F, J.C.W., M.F.G., and R.L.S.). Flow cytometry services were provided by the University of Chicago Cancer Research Center core facility.",

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doi = "10.1016/S1074-7613(02)00452-1",

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T1 - Cooperative and antagonistic interplay between PU.1 and GATA-2 in the specification of myeloid cell fates

AU - Walsh, Jonathan C.

AU - DeKoter, Rodney P.

AU - Lee, Hyun Jun

AU - Smith, Erica D.

AU - Lancki, David W.

AU - Gurish, Michael F.

AU - Friend, Daniel S.

AU - Stevens, Richard L.

AU - Anastasi, John

AU - Singh, Harinder

N1 - Funding Information: We thank Abe Brass, Steven Kosak, and Celeste Simon for critical comments on the manuscript. This work was supported by the Howard Hughes Medical Institute (R.P.D., D.W.L., and H.S.) and NIH grants AI-23483, AI-31599, GM-07151, HL-07237, and HL-36110 (D.S.F, J.C.W., M.F.G., and R.L.S.). Flow cytometry services were provided by the University of Chicago Cancer Research Center core facility.

PY - 2002/11/1

Y1 - 2002/11/1

N2 - PU.1 and GATA transcription factors appear to antagonize each other's function in the development of distinct lineages of the hematopoietic system. In contrast, we demonstrate that PU.1, like GATA-2, is essential for the generation of mast cells. PU.1-/- hematopoietic progenitors can be propagated in IL-3 and differentiate into mast cells or macrophages upon restoration of PU.1 activity. Using these progenitors and a conditionally activatable PU.1 protein, we show that PU.1 can negatively regulate expression of the GATA-2 gene. In the absence of GATA-2, PU.1 promotes macrophage but not mast cell differentiation. Reexpression of GATA-2 in such progenitors enables the generation of mast cells. We propose a developmental model in which cooperative function or antagonistic crossregulation by PU.1 of GATA-2 promotes distinct myeloid cell fates.

AB - PU.1 and GATA transcription factors appear to antagonize each other's function in the development of distinct lineages of the hematopoietic system. In contrast, we demonstrate that PU.1, like GATA-2, is essential for the generation of mast cells. PU.1-/- hematopoietic progenitors can be propagated in IL-3 and differentiate into mast cells or macrophages upon restoration of PU.1 activity. Using these progenitors and a conditionally activatable PU.1 protein, we show that PU.1 can negatively regulate expression of the GATA-2 gene. In the absence of GATA-2, PU.1 promotes macrophage but not mast cell differentiation. Reexpression of GATA-2 in such progenitors enables the generation of mast cells. We propose a developmental model in which cooperative function or antagonistic crossregulation by PU.1 of GATA-2 promotes distinct myeloid cell fates.

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Cooperative and antagonistic interplay between PU.1 and GATA-2 in the specification of myeloid cell fates

Abstract

ASJC Scopus subject areas

UN SDGs

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