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

GSE269322 Mus musculus Expression profiling by high throughput sequencing 9 samples Submitted 2025/06/09 Platform GPL34290
Summary
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.
Published in
XPR1 regulates fetal liver macrophage development, identity, and pyrenocyte clearance
Stifter SA, Bijnen M, Tuzlak S et al. · The Journal of experimental medicine 2026 · PMID 41335223 · doi:10.1084/jem.20241587
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Also filed as BioProject PRJNA1121216 and SRA study SRP512397. Searching any of these in the dataset finder brings you back here.

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