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Polycomb Repressive Complex 2 regulates basal cell fate during adult olfactory neurogenesis [EEDKO_H3K27me3_ChIP]

ABSTRACT: We show that Polycomb repressive complexes (PRCs) regulate lineage choice between neural and non-neural fates in the olfactory epithelium. Conditional loss of Polycomb repressive complex 2 perturbs lesion-induced neurogenesis and misexpression of lineage-specific transcription factors in multipotent olfactory globose basal cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE234634 | GEO | 2023/09/18

REPOSITORIES: GEO

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Polycomb Repressive Complex 2 regulates basal cell fate during adult olfactory neurogenesism [scRNA-seq]

Project description:We show that Polycomb repressive complexes (PRCs) regulate lineage choice between neural and non-neural fates in the olfactory epithelium. Conditional loss of Polycomb repressive complex 2 perturbs lesion-induced neurogenesis and misexpression of lineage-specific transcription factors in multipotent olfactory globose basal cells.

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Polycomb Repressive Complex 2 regulates basal cell fate during adult olfactory neurogenesis [ChIP-seq]

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Whole-transcriptome profiling of regenerating olfactory epithelium following loss of CBX paralogs

Project description:The polycomb group protein, CBX8, is a neuron-specific component of Polycomb repressive complex 1 (PRC1) in the adult olfactory epithelium. We performed loss of function assays in an in vitro model of the regeneratng olfactory epithelium to determine the role of CBX8 in adult olfactory neurogenesis. Whole-transcriptome analysis highlighted the importance of CBX8-PRC1 in the regulation of adult neurogenesis in the olfactory epithelium.

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Identification of neuron lineage-specific PRC1 targets in olfactory neuron precursors

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Direct Recruitment of Polycomb Repressive Complex 1 (PRC1) to Chromatin by Core Binding Transcription Factors (microarray)

Project description:Polycomb repressive complexes (PRCs) play key roles in developmental epigenetic regulation. Yet the mechanisms that target PRCs to specific loci in mammalian cells remain incompletely understood. In this study, we show that Bmi1, a core component of Polycomb Repressive Complex 1 (PRC1), binds directly to the Runx1/CBFbeta transcription factor complex. Genome-wide studies in megakaryocytic cells demonstrate considerable chromatin occupancy overlap between the PRC1 core component Ring1b and Runx1/CBFbeta and functional regulation of a significant fraction of commonly bound genes. Bmi1/Ring1b and Runx1/CBFbeta deficiency generate partial phenocopies of one another in vivo. We also show that Ring1b occupies key Runx1 binding sites in primary murine thymocytes and that this occurs via Polycomb Repressive Complex 2 (PRC2) independent mechanisms. Genetic depletion of Runx1 results in reduced Ring1b binding at these sites in vivo. These findings provide evidence for site-specific PRC1 chromatin recruitment by core binding transcription factors in mammalian cells. shRNA mediated knockdown of CBFb, Ring1b and control in biological triplicate

2012-02-10 | E-GEOD-33659 | biostudies-arrayexpress

Gene Expression Profiles of Adult Human Olfactory Bulb and Embryonic Neural Stem Cells

Project description:Global gene expression profiling was performed using RNA from human embryonic neural stem cells (hENSCs) and adult human olfactory bulb-derived neural stem cells (OBNSCs) to define a gene expression pattern and signaling pathways that are specific for each cell lineage. Subtractive gene expression profiling between both cell lineages provides a list of potential genes that are related to their multipotentiality, proliferation, migration, and alternative signaling pathways. To confirm the validity of our DNA microarray data, our results were compared with data from various databases. The gene expression profile of adult olfactory bulb neural stem cells (n=6) was compared with that of human embryonic neural stem cells (n=3).

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Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (scRNA-Seq)

Project description:A reduced sense of smell has been reported in people with cystic fibrosis (CF). These olfactory defects have largely been attributed to secondary manifestations of the disease, such as inflammation of the nasal mucosa. Here we show that CFTR, the gene responsible for CF, is expressed in proliferating olfactory human cells and that newborn CFTR null pigs display ultrastructural abnormalities in the olfactory epithelium and olfactory bulbs. In the absence of CFTR, olfactory sensory neurons still produce odor-evoked activity, but mutant animals display defective odor-guided suckling behavior after birth. Consistent with epithelial changes, we found a reduced expression of genes implicated in cell cycle and development in globose basal cells (GBCs), the neurogenic progenitor cells in the olfactory epithelium. Targeted sequencing revealed enhanced CFTR expression in the subpopulation of GBCs that is actively proliferating. Furthermore, CFTR loss caused a global reduction in the number of sensory neurons and altered olfactory receptors expression. Our findings highlight a previously unknown role of CFTR in olfactory system function by regulating progenitor cell proliferation in the olfactory epithelium.

2022-12-31 | GSE197189 | GEO

Direct Recruitment of Polycomb Repressive Complex 1 (PRC1) to Chromatin by Core Binding Transcription Factors (ChIP-Seq)

Project description:Polycomb repressive complexes (PRCs) play key roles in developmental epigenetic regulation. Yet the mechanisms that target PRCs to specific loci in mammalian cells remain incompletely understood. In this study, we show that Bmi1, a core component of Polycomb Repressive Complex 1 (PRC1), binds directly to the Runx1/CBFbeta transcription factor complex. Genome-wide studies in megakaryocytic cells demonstrate considerable chromatin occupancy overlap between the PRC1 core component Ring1b and Runx1/CBFbeta and functional regulation of a significant fraction of commonly bound genes. Bmi1/Ring1b and Runx1/CBFbeta deficiency generate partial phenocopies of one another in vivo. We also show that Ring1b occupies key Runx1 binding sites in primary murine thymocytes and that this occurs via Polycomb Repressive Complex 2 (PRC2) independent mechanisms. Genetic depletion of Runx1 results in reduced Ring1b binding at these sites in vivo. These findings provide evidence for site-specific PRC1 chromatin recruitment by core binding transcription factors in mammalian cells. ChIP-seq against Runx1, CBFb and Ring1b in L8057 cells (induced & uninduced with biological replicates) and thymocytes from control and Runx1 KO mice

2012-02-10 | E-GEOD-33653 | biostudies-arrayexpress

Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (Bulk RNA-Seq)

2022-12-31 | GSE197184 | GEO

YTHDF1 facilitates PRC1 mediated H2AK119ub in Human ES Cells

Project description:Polycomb repressive complexes( PRCs) play critical role in cell fate decisions during normal development as well as disease progression through mediate histone modifications such as H3K27me3 and H2AK119ub. How exactly PRCs recruited to chromatin remains to be fully illuminated. Here, we report that YTHDF1, a N6-methyladenine (m6A) RNA reader previously known being mainly cytoplasmic, associates with RNF2, a PRC1 protein that mediates H2AK119ub in human embryonic stem cells (hESCs). Specifically, a portion of YTHDF1 localizes in the nuclei and associates with RNF2/ H2AK119ub on a subset of gene loci related to neural development functions. Knock-down YTHDF1 attenuates H2AK119ub modification on these genes and promotes neural differentiation in hESCs. Our findings provide another non-canonical mechanism of YTHDF1 to participate in PRC1 mediated chromatin modification in hESCs.

2023-12-30 | GSE204824 | GEO

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