Csf1r-T2A-Fred knock-in mice contain a CRISPR/Cas9-generated insertion of a T2A-FusionRed sequence into the STOP codon of the Csf1r gene. The insertion of the T2A-FusionRed is in-frame with the CSF1R to generate a fusion protein that marks the plasma membrane and allow analysis of intracellular trafficking. The T2A-FusionRed does not affect endogenous gene expression. Csf1r encodes Cd115 which acts as the receptor for colony stimulating factor 1, a cytokine which controls the production, differentiation, and function of macrophages and contains binding sites for numerous macrophage-expressed transcription factors. In these Csf1r-T2A-Fred mice, CSF1R-FRed is expressed in monocytes and macrophages, and is absent from granulocytes and lymphocytes. In bone marrow, CSF1R-FRed is present in osteoclasts, CD169+ resident macrophages, and megakaryocytes, but is absent in lineage-negative hematopoietic stem cells. It is highly expressed in marrow monocytes and common myeloid progenitors but significantly lower in granulocyte-macrophage progenitors. In lymphoid tissues, CSF1R-FRed highlights diverse mononuclear phagocyte system (MPS) populations, including classical dendritic cells. Fluorescence is detectable by direct microscopy and flow cytometry. Homozygous mice are viable and fertile.

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Csf1r-T2A-Fred knock-in mice contain a CRISPR/Cas9-generated insertion of a T2A-FusionRed sequence into the STOP codon of the Csf1r gene. These mice may be useful for tracking cells of the mononuclear phagocyte system (MPS).

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