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Continuous expression of the transcription factor E2-2 maintains the cell fate of mature plasmacytoid dendritic cells

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE24726: Gene expression profile of mature plasmacytoid dendritic cells (PDC) after the deletion of transcription factor E2-2 GSE24740: Binding targets of transcription factor E2-2 in human plasmacytoid dendritic cells Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Boris Reizis

PROVIDER: E-GEOD-24785 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profile of mature plasmacytoid dendritic cells (PDC) after the deletion of transcription factor E2-2

Project description:The interferon-producing plasmacytoid dendritic cells (PDC) share common progenitors with antigen-presenting classical dendritic cells (cDC), yet they possess distinct morphology and molecular features resembling those of lymphocytes. It is unclear whether the unique cell fate of PDC is actively maintained in the steady state. We report that the deletion of transcription factor E2-2 from mature peripheral PDC caused their spontaneous differentiation into cells with cDC properties. This included the loss of PDC markers, increase in MHC class II expression and T cell priming capacity, acquisition of dendritic morphology and induction of cDC signature genes. Genome-wide chromatin immunoprecipitation revealed direct binding of E2-2 to key PDC-specific and lymphoid genes, as well as to certain genes enriched in cDC. Thus, E2-2 actively maintains the cell fate of mature PDC and opposes the “default” cDC fate, in part through direct regulation of lineage-specific gene expression programs. Inducible deletion of E2-2 (Tcf4) has been performed by administering tamoxifen to conditional E2-2flox/flox Rosa26-CreER+ mice or to E2-2flox/flox Rosa26-CreER- control littermates. Four or six days later total splenocytes were isolated, pooled from 2-3 mice and PDC (CD11b- B220+ CD11clow Bst2+) were isolated by sorting. Global gene expression profiles of E2-2-deficient (null) and control (Ctrl) PDC were compared using Affymetrix microarrays (GPL1261).

2010-12-21 | E-GEOD-24726 | biostudies-arrayexpress

Binding targets of transcription factor E2-2 in human plasmacytoid dendritic cells

Project description:The interferon-producing plasmacytoid dendritic cells (PDC) share common progenitors with antigen-presenting classical dendritic cells (cDC), yet they possess distinct morphology and molecular features resembling those of lymphocytes. It is unclear whether the unique cell fate of PDC is actively maintained in the steady state. We report that the deletion of transcription factor E2-2 from mature peripheral PDC caused their spontaneous differentiation into cells with cDC properties. This included the loss of PDC markers, increase in MHC class II expression and T cell priming capacity, acquisition of dendritic morphology and induction of cDC signature genes. Genome-wide chromatin immunoprecipitation revealed direct binding of E2-2 to key PDC-specific and lymphoid genes, as well as to certain genes enriched in cDC. Thus, E2-2 actively maintains the cell fate of mature PDC and opposes the “default” cDC fate, in part through direct regulation of lineage-specific gene expression programs. Cells of the human PDC lymphoma line CAL-1 (Maeda et al., Int J Hematol 2005) were crosslinked with formaldehyde, sonicated, and subjected to immunoprecipitation with anti-E2-2 mAb (Bain et al., Mol Cell Biol 1993) or mouse IgG control as described (Cisse et al., Cell 2008). After crosslink reversal, the isolated chromatin was amplified, labeled and hybridized to Human Promoter ChIP-on-chip Microarray Set (Agilent Technologies). Hybridized microarrays were scanned and analyzed using DNA Analytics software (Agilent Technologies).

2010-12-21 | E-GEOD-24740 | biostudies-arrayexpress

Transcription profiling of mouse Plasmacytoid dendritic cells (pDCs) from E2-2 heterozygotes

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Transcription profiling of human pDC cell line

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Ring1B Promotes Hepatic Stem/Progenitor Cell Expansion via Simultaneous Suppression of Cdkn1a and Cdkn2a

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Distinct distributions of histone marks shape cell identities of murine hepatic progenitors and adult hepatocytes

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2011-11-30 | E-GEOD-34030 | biostudies-arrayexpress

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Origins of MLL cancer stem cells govern leukemic self-renewal mediated by -catenin and Hoxa9

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LRH-1 and PTF1-L coregulate an exocrine pancreas-specific transcriptional network for digestive function

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