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MafB is a conserved transcriptional regulator of macrophage development and identity across tissues and species [CUT&RUN 2]

ABSTRACT: Resident tissue macrophages (RTM) are characterized by a remarkable diversity but also share common features that are thought to be driven by conserved transcriptional programs. While the transcription factor MafB is highly expressed in the macrophage lineage, little is known about its role in establishing RTM identities. Here, we show that the absence of MafB results in a profound imbalance across many RTM populations and in a disruption of global and tissue-specific RTM signatures in mice. Furthermore, we found that MafB was required for the differentiation of bone-marrow-derived macrophages (BMDMs) ex vivo and of RTM populations from monocytes in vivo. Mechanistically, epigenetic profiling of MafB binding sites in BMDMs revealed that MafB directly regulated expression of key RTM differentiation and identity genes, including Csf1r and Fcgr1. Finally, in silico analyses showed that MafB binding sites were highly conserved across vertebrates. Our findings demonstrate the crucial and evolutionarily conserved role of MafB as regulator of RTM development and identity, connecting MafB-dependent transcriptional programs with unique defining features of RTM.

ORGANISM(S): Mus musculus

PROVIDER: GSE287476 | GEO | 2026/02/25

REPOSITORIES: GEO

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MafB is a conserved transcriptional regulator of macrophage development and identity across tissues and species [CUT&Run]

Project description:Resident tissue macrophages (RTM) are characterized by a remarkable diversity but also share common features that are thought to be driven by conserved transcriptional programs. While the transcription factor MafB is highly expressed in the macrophage lineage, little is known about its role in establishing RTM identities. Here, we show that the absence of MafB results in a profound imbalance across many RTM populations and in a disruption of global and tissue-specific RTM signatures in mice. Furthermore, we found that MafB was required for the differentiation of bone-marrow-derived macrophages (BMDMs) ex vivo and of RTM populations from monocytes in vivo. Mechanistically, epigenetic profiling of MafB binding sites in BMDMs revealed that MafB directly regulated expression of key RTM differentiation and identity genes, including Csf1r and Fcgr1. Finally, in silico analyses showed that MafB binding sites were highly conserved across vertebrates. Our findings demonstrate the crucial and evolutionarily conserved role of MafB as regulator of RTM development and identity, connecting MafB-dependent transcriptional programs with unique defining features of RTM.

2026-02-25 | GSE287346 | GEO

MafB is a conserved transcriptional regulator of macrophage development and identity across tissues and species [RNA-seq]

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MafB is a conserved transcriptional regulator of macrophage development and identity across tissues and species [scRNA-Seq]

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Non adherent macrophage of mafb null and WT

Project description:MafB is a member of the large Maf family of transcription factors that share similar basic region/leucine zipper DNA binding motifs and N-terminal activation domains.Although it is well known that MafB is specifically expressed in macrophages, characterization of the null mutant phenotype in these tissues has not been previously reported. To investigate suspected MafB functions macrophages, we generated mafB/green fluorescent protein (GFP) knock-in null mutant mice. MafB deficiency was found to dramatically suppress F4/80 expression in nonadherent macrophages. To investigate detail function of MafB in nonadherent macrophages, we performed microarray analysis. Macrophages were derived from day 14.5 fetal livers of mafB- /- and WT mice. Suspensions of single fetal liver cells were prepared by mechanical disruption . A total of 106 cells in suspension were centrifuged at 1,200 rpm for 5 min, and the cell pellet was resuspended in Dulbeccoâs modified Eagleâs medium supplemented with 10% fetal calf serum (heat inactivated), streptomycin and penicillin (100 units/ml), and macrophage colony-stimulating factor (M-CSF) (10 ng/ml) and then seeded either onto a nonadhesive dishes coated with hydrophilic polymers (Hydrocell; Cell Seed, Tokyo). The culture medium was not changed throughout the experiment. M-CSF (final concentration, 10 ng/ml) was added every day from day 4 onwards. One, 2, 4, and 6 days after seeding, the cells were harvested and analyzed by flow cytometry. After 6 day culture, macrophages of Mafb-/- and WT were use microarray analysis .

2010-02-27 | E-GEOD-20419 | biostudies-arrayexpress

Non adherent macrophage of mafb null and WT

2010-02-23 | GSE20419 | GEO

Effects of depletion of Irf8 and Mafb on gene expression of adult microglia and CNS border associtated macrophages (CAMs)

Project description:The central nervous system (CNS) includes anatomically distinct macrophage populations including parenchyma microglia and CNS-associated macrophages (CAMs). The stepwise development and specification of macrophage populations in the CNS rely on several key transcription factors, such as IRF8 and MAFB. In order to better understand the roles of IRF8 and MAFB for phenotypic determination of homeostatic microglia and CAMs, we performed quantitative bulk RNA sequencing of microglia and CAMs isolated from mouse models with myeloid cell-specific deletion of IRF8 or MAFB transcription factors. We found the distinct transcriptional machinery, mediated by IRF8 and MAFB, which underlies the diversity of macrophages in the CNS.

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MAFB controls the acquisition of the anti-inflammatory transcriptional profile of M-MØ.

Project description:Macrophage phenotypic and functional heterogeneity derives from tissue-specific transcriptional signatures shaped by the local microenvironment. Most studies addressing the molecular basis for macrophage heterogeneity have focused on murine cells, while the factors controlling the functional specialization of human macrophages are less known. M-CSF drives the generation of human monocyte-derived macrophages with a potent anti-inflammatory activity upon stimulation. We now report that knock-down of MAFB impairs the acquisition of the anti-inflammatory profile of human macrophages, identify the MAFB-dependent gene signature in human macrophages and illustrate the co-expression of MAFB and MAFB-target genes in CD163+ tissue-resident and tumor associated macrophages. The contribution of MAFB to the homeostatic/anti-inflammatory macrophage profile is further supported by the skewed polarization of monocyte-derived macrophages from Multicentric Carpo Tarsal Osteolysis (OMIM#166300), a pathology caused by mutations in the MAFB gene. Our results demonstrate that MAFB critically determines the acquisition of the anti-inflammatory transcriptional and functional profiles of human macrophages.

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MafB maintains β-cell identity under MafA-deficient condition

Project description:The transcription factor MafB plays an essential role in β-cell differentiation during the embryonic stage in rodents. Although MafB disappears from β-cells after birth, it has been reported that MafB can be evoked in β-cells and is involved in insulin+ β-cell number and islet architecture maintenance in adult mice under diabetic conditions. However, the underlying mechanism by which MafB protects β-cells remains unknown. To elucidate this, we performed RNA sequencing using an inducible diabetes model (A0BΔpanc mice) that we previously generated. We found that the deletion of Mafb can induce β-cell dedifferentiation, characterized by the upregulation of dedifferentiation markers, Slc5a10 and Cck, and several β-cell-disallowed genes; and the downregulation of mature β-cell markers, Slc2a2 and Ucn3. However, there is no re-expression of well-known progenitor cell markers, Foxo1 and Neurog3. Furtherly, the appearance of ALDH1A3+ cell and disappearance of UCN3+ cell also verify the β-cell de-differentiation state. Together, our results suggest that MafB can maintain β-cell identity under certain pathological conditions in adult mice, providing novel insight into the role of MafB in β-cell identity maintenance.

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Effect of c-Maf mutation on Mafb-GFP-positive FACS-purified cells in the E12.5 mouse gonad

Project description:Morphogenesis of the gonad requires cell-cell adhesion changes between diverse cell types. In the Drosophila gonad, the gene traffic jam regulates cell adhesion changes required for gonad formation and germ cell development (Li et al., 2003. Nature Cell Biol). To determine if the mammalian homologs of traffic jam in mammals, c-Maf and Mafb, also play a role in the transcription regulation of cell adhesion molecules in the mouse gonad, we performed a microarray analysis of FACS-purified Mafb-GFP-positive cells in E12.5 male control and c-Maf/Mafb mutant gonads. We used microarrays to determine genes affected by c-Maf mutation in E12.5 mouse gonad/mesonephros interstitial cells and macrophages E12.5 XY control (c-Maf+/-;Mafb-GFP+/-) and c-mutant (c-Maf-/-;Mafb-GFP+/-) gonad/interstitial interstitial cells and macrophages were obtained by FACS sorting of Mafb-GFP-positive cells. RNA was extracted for subsequent hybridization on Affymetrix microarrays.

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Mutations in MAFB that cause Multicentric Carpo Tarsal Osteolysis (MCTO) affect the transcriptome of M-MØ

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