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The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE117081 | GEO | 2018/07/14

REPOSITORIES: GEO

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The Transcription Factor ZEB2 Is Required to Maintain the Tissue-Specific Identities of Macrophages.

Project description:Heterogeneity between different macrophage populations has become a defining feature of this lineage. However, the conserved factors defining macrophages remain largely unknown. The transcription factor ZEB2 is best described for its role in epithelial to mesenchymal transition; however, its role within the immune system is only now being elucidated. We show here that Zeb2 expression is a conserved feature of macrophages. Using Clec4f-cre, Itgax-cre, and Fcgr1-cre mice to target five different macrophage populations, we found that loss of ZEB2 resulted in macrophage disappearance from the tissues, coupled with their subsequent replenishment from bone-marrow precursors in open niches. Mechanistically, we found that ZEB2 functioned to maintain the tissue-specific identities of macrophages. In Kupffer cells, ZEB2 achieved this by regulating expression of the transcription factor LXR?, removal of which recapitulated the loss of Kupffer cell identity and disappearance. Thus, ZEB2 expression is required in macrophages to preserve their tissue-specific identities.

| S-EPMC6104815 | biostudies-literature

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [microarray]

Project description:Microarray, Bulk RNA Sequencing and Single cell RNA Sequencing of different murine tissue-resident macrophage populations to assess role of Zeb2 and LXRa

2018-07-14 | GSE117080 | GEO

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [bulk RNA-seq]

Project description:Microarray, Bulk RNA Sequencing and Single cell RNA Sequencing of different murine tissue-resident macrophage populations to assess role of Zeb2 and LXRa

2018-07-14 | GSE117078 | GEO

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [single-cell RNA-seq]

Project description:Microarray, Bulk RNA Sequencing and Single cell RNA Sequencing of different murine tissue-resident macrophage populations to assess role of Zeb2 and LXRa

2018-07-14 | GSE117079 | GEO

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages

Project description:The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages

| PRJNA481016 | ENA

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [microarray]

Project description:The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [microarray]

| PRJNA481018 | ENA

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [bulk RNA-seq]

Project description:The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [bulk RNA-seq]

| PRJNA481019 | ENA

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [single-cell RNA-seq]

Project description:The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [single-cell RNA-seq]

| PRJNA481017 | ENA

The transcription factor EGR2 is indispensable for tissue-specific imprinting of alveolar macrophages in health and tissue repair.

Project description:Alveolar macrophages are the most abundant macrophages in the healthy lung where they play key roles in homeostasis and immune surveillance against airborne pathogens. Tissue-specific differentiation and survival of alveolar macrophages rely on niche-derived factors, such as granulocyte-macrophage colony-stimulating factor (GM-CSF) and transforming growth factor–β (TGF-β). However, the nature of the downstream molecular pathways that regulate the identity and function of alveolar macrophages and their response to injury remain poorly understood. Here, we identify that the transcription factor EGR2 is an evolutionarily conserved feature of lung alveolar macrophages and show that cell-intrinsic EGR2 is indispensable for the tissue-specific identity of alveolar macrophages. Mechanistically, we show that EGR2 is driven by TGF-β and GM-CSF in a PPAR-γ–dependent manner to control alveolar macrophage differentiation. Functionally, EGR2 was dispensable for the regulation of lipids in the airways but crucial for the effective handling of the respiratory pathogen Streptococcus pneumoniae. Last, we show that EGR2 is required for repopulation of the alveolar niche after sterile, bleomycin-induced lung injury and demonstrate that EGR2-dependent, monocyte-derived alveolar macrophages are vital for effective tissue repair after injury. Collectively, we demonstrate that EGR2 is an indispensable component of the transcriptional network controlling the identity and function of alveolar macrophages in health and disease.

| S-EPMC7612216 | biostudies-literature

Homeodomain transcription factor and tumor suppressor Prep1 is required to maintain genomic stability.

Project description:Prep1 is a homeodomain transcription factor that is essential in embryonic development and functions in the adult as a tumor suppressor. We show here that Prep1 is involved in maintaining genomic stability and preventing neoplastic transformation. Hypomorphic homozygous Prep1(i/i) fetal liver cells and mouse embryonic fibroblasts (MEFs) exhibit increased basal DNA damage and normal DNA damage response after γ-irradiation compared with WT. Cytogenetic analysis shows the presence of numerous chromosomal aberrations and aneuploidy in very early-passage Prep1(i/i) MEFs. In human fibroblasts, acute Prep1 down-regulation by siRNA induces DNA damage response, like in Prep1(i/i) MEFs, together with an increase in heterochromatin-associated modifications: rapid increase of histone methylation and decreased transcription of satellite DNA. Ectopic expression of Prep1 rescues DNA damage and heterochromatin methylation. Inhibition of Suv39 activity blocks the chromatin but not the DNA damage phenotype. Finally, Prep1 deficiency facilitates cell immortalization, escape from oncogene-induced senescence, and H-Ras(V12)-dependent transformation. Importantly, the latter can be partially rescued by restoration of Prep1 level. The results show that the tumor suppressor role of Prep1 is associated with the maintenance of genomic stability.

| S-EPMC3141938 | biostudies-literature

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