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Fetal liver macrophage development and function require Xpr1

ABSTRACT: Erythroblastic island macrophages (EBI-Macs) support the development of red blood cells by recycling iron, producing growth factors,and clearing nuclei expelled from erythroblasts. In the developing embryo, the liver is the primary site of hematopoiesis,andfetal liver macrophagesperform the function ofEBI-Macs.Here, weshowthatthephosphate exporterXpr1is critical for the development offetal macrophagesin the liver and the spleen.Single-cellRNA-seqand flow cytometryanalysesin conditional mice lackingXpr1in hematopoietic and/orCD206+cellsrevealedloss of the Kupffercelltranscriptional program anda shift in the development offetal livermonocytes towards an interferon-activated monocyte/macrophage state.Functionally, thisled tothefailure to clear pyrenocytes.In adulthood,splenic red pulp and bone marrow macrophages were alsoabsent upon lossof intrinsicXpr1.Collectively,these findings reveal thatXpr1is required for the development, identity, and function ofEBI-Macs.

ORGANISM(S): Mus musculus

PROVIDER: GSE269382 | GEO | 2025/06/09

REPOSITORIES: GEO

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Fetal liver macrophage development and function require Xpr1 [RNA-Seq]

Project description:Erythroblastic island macrophages (EBI-Macs) support the development of red blood cellsby recycling iron, producing growth factors,and clearing nuclei expelled from erythroblasts. In the developing embryo, the liver is the primary site of hematopoiesis,andfetal liver macrophagesperform the function ofEBI-Macs.Here, weshowthatthephosphate exporterXpr1is critical for the development offetal macrophagesin the liver and the spleen.Single-cellRNA-seqand flow cytometryanalysesin conditional mice lackingXpr1in hematopoietic and/orCD206+cellsrevealedloss of the Kupffercelltranscriptional program anda shift in the development offetal livermonocytes towards an interferon-activated monocyte/macrophage state.Functionally, thisled tothefailure to clear pyrenocytes.In adulthood,splenic red pulp and bone marrow macrophages were alsoabsent upon lossof intrinsicXpr1.Collectively,these findings reveal thatXpr1is required for the development, identity, and function ofEBI-Macs.

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