Mus musculus
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ABSTRACT:
PROVIDER: PRJNA348104 | ENA |
REPOSITORIES: ENA
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Project description:Zeb2 regulates commitment to plasmacytoid dendritic cell and monocyte fate (part 2)
| PRJNA348103 | ENA
Project description:Zeb2 regulates commitment to plasmacytoid dendritic cell and monocyte fate
| PRJNA348101 | ENA
Project description:Recent studies have identified Zeb2 as a transcription factor important for the final maturation of natural killer cells and effector CD8+ T cells. We show that Zeb2 is required for the development of two myeloid cell types, the monocyte and the plasmacytoid dendritic cell, and clarify that this factor is not required for the development of classical dendritic cells.
2016-11-01 | GSE87883 | GEO
Project description:Recent studies have identified Zeb2 as a transcription factor important for the final maturation of natural killer cells and effector CD8+ T cells. We show that Zeb2 is required for the development of two myeloid cell types, the monocyte and the plasmacytoid dendritic cell, and clarify that this factor is not required for the development of classical dendritic cells.
2016-11-01 | GSE87882 | GEO
Project description:Plasmacytoid dendritic cells (pDCs) develop from pre-pDCs, while two lineages of conventional DCs (cDC1s and cDC2s) develop from lineage-committed pre-cDCs. A number of transcription factors (TFs) have been implicated in regulating the development of pDCs (E2-2, Id2) and cDC1s (IRF8, Id2 and Batf3) however, those required for the early commitment of pre-cDCs towards the cDC2 lineage are unknown. Here we identified the TF Zinc finger E box binding homeobox 2 (Zeb2), to play a crucial role in regulating DC development. Zeb2 was expressed from the pre-pDC and pre-cDC stage onwards, and highly expressed in mature pDCs and cDC2s. Mice conditionally lacking Zeb2 in CD11c+ cells had a cell intrinsic reduction in pDCs and cDC2s, coupled with an increase in cDC1s. Conversely, mice in which CD11c+ cells overexpressed Zeb2 displayed a reduction in cDC1s. This was accompanied by altered expression of Id2, which was upregulated in cDC2s and pDCs from conditional knock-out mice. Zeb2 ChIP analysis revealed Id2 to be a direct target of Zeb2. Thus, we conclude that Zeb2 regulates commitment to both the cDC2 and pDC lineages through repression of Id2.
2016-05-01 | GSE79903 | GEO
Project description:The transcription factor Zeb2 regulates development of conventional and plasmacytoid DCs by repressing Id2
| PRJNA317353 | ENA
Project description:The transcriptional regulator ID2 is required for type 1 classical dendritic cell (cDC1) specification, yet the mechanism has remained obscure. We previously identified the Zeb2 -165-kb enhancer as key to normal hematopoiesis, controlled by competing CEBP and NFIL3 inputs during myeloid dendritic cell divergence. Here, we uncover an unprecedented role for E proteins in myelopoiesis and demonstrate that ID2 promotes cDC1 development by antagonizing E protein activity at E-boxes within the Zeb2 enhancer. Deleting these E-boxes abolishes lymphoid B cell and plasmacytoid dendritic cell (pDC) development while skewing myelopoiesis toward cDC1s. Remarkably, E-box deletion rescues cDC1 development in Id2-deficient mice. These findings support a two-step model in which NFIL3 transiently represses Zeb2, followed by ID2-mediated inhibition of E proteins to stabilize cDC1 fate specification. Further, this work defines a paradigm of “site-specific pleiotropy,” wherein distinct transcription factor motifs–E-boxes and CEBP sites–within a single enhancer direct diverse cell fates.
2026-04-24 | GSE326954 | GEO
Project description:The transcriptional regulator ID2 is required for type 1 classical dendritic cell (cDC1) specification, yet the mechanism has remained obscure. We previously identified the Zeb2 -165-kb enhancer as key to normal hematopoiesis, controlled by competing CEBP and NFIL3 inputs during myeloid dendritic cell divergence. Here, we uncover an unprecedented role for E proteins in myelopoiesis and demonstrate that ID2 promotes cDC1 development by antagonizing E protein activity at E-boxes within the Zeb2 enhancer. Deleting these E-boxes abolishes lymphoid B cell and plasmacytoid dendritic cell (pDC) development while skewing myelopoiesis toward cDC1s. Remarkably, E-box deletion rescues cDC1 development in Id2-deficient mice. These findings support a two-step model in which NFIL3 transiently represses Zeb2, followed by ID2-mediated inhibition of E proteins to stabilize cDC1 fate specification. Further, this work defines a paradigm of “site-specific pleiotropy,” wherein distinct transcription factor motifs–E-boxes and CEBP sites–within a single enhancer direct diverse cell fates.
2026-04-24 | GSE326868 | GEO
Project description:Retinoic acid determines the in vivo fate-commitment of splenic pre-dendritic cells
| PRJNA175555 | ENA