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P63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling

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

ORGANISM(S): Mus musculus

PROVIDER: GSE145268 | GEO | 2020/09/23

REPOSITORIES: GEO

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p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [scRNA-seq]

Project description:Np63+ve cells are multipotent and maintain all epithelial cell lineages of the embryonic and adult salivary gland (SG). However, the molecular mechanisms by which Np63 regulates stem/progenitor (SP) cell populations in the SG remains elusive. To better understand Np63 s role in directing cell fate choices, here we have utilized Np63-null adult mice and primary salivary cell cultures to probe alterations in SP cell differentiation and function. Specifically, we have generated bulk RNA-seq and scRNA-seq data from Np63-null adult mice and p63 and H3K27Ac ChIP-seq data from primary salivary cell cultures. These genomic and epigenomic data sets were leveraged to interrogate altered SG cellular identities and differentiation states resulting from the loss of Np63. Our studies reveal that ablation of Np63 results in a loss of the SP cell population and skewed SG differentiation that is modulated by dysregulated TGF- /Activin signaling. Our findings offer new molecular revelations into the SP cell gene regulatory networks that are likely to be relevant for normal or diseased SG states.

2020-09-23 | GSE145267 | GEO

p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [RNA-seq]

2020-09-23 | GSE145266 | GEO

p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [ChIP-seq]

2020-09-23 | GSE145264 | GEO

p63 and Its Target Follistatin Maintain Salivary Gland Stem/Progenitor Cell Function through TGF-β/Activin Signaling.

Project description:Multipotent ΔNp63-positive cells maintain all epithelial cell lineages of the embryonic and adult salivary gland (SG). However, the molecular mechanisms by which ΔNp63 regulates stem/progenitor (SP) cell populations in the SG remains elusive. To understand the role of ΔNp63 in directing cell fate choices in this gland, we have generated ΔNp63-deleted adult mice and primary salivary cell cultures to probe alterations in SP cell differentiation and function. In parallel, we have leveraged RNA-seq and ChIP-seq-based characterization of the ΔNp63-driven cistrome and scRNA-seq analysis to molecularly interrogate altered SG cellular identities and differentiation states dependent on ΔNp63. Our studies reveal that ablation of ΔNp63 results in a loss of the SP cell population and skewed differentiation that is mediated by Follistatin-dependent dysregulated TGF-β/Activin signaling. These findings offer new revelations into the SP cell gene regulatory networks that are likely to be relevant for normal or diseased SG states.

| S-EPMC7498843 | biostudies-literature

p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling

Project description:p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling

| PRJNA606576 | ENA

p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [ChIP-seq]

Project description:p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [ChIP-seq]

| PRJNA606548 | ENA

p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [RNA-seq]

Project description:p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [RNA-seq]

| PRJNA606573 | ENA

p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [scRNA-seq]

Project description:p63 Maintains the Proliferative Potential of Salivary Gland Stem/Progenitor Cells by Regulating Follistatin, a Key Mediator of TGF-b/Activin Signaling [scRNA-seq]

| PRJNA606579 | ENA

p63 maintains keratinocyte proliferative capacity through regulation of Skp2-p130 levels.

Project description:p63 is a master regulator of proliferation and differentiation in stratifying epithelia, and its expression is frequently altered in carcinogenesis. However, its role in maintaining proliferative capacity remains unclear. Here, we demonstrate that hypoproliferation and loss of differentiation in organotypic raft cultures of primary neonatal human foreskin keratinocytes (HFKs) depleted of the α and β isoforms of p63 result from p53-p21-mediated accumulation of retinoblastoma (Rb) family member p130. Hypoproliferation in p63-depleted HFKs can be rescued by depletion of p53, p21(CIP1) or p130. Furthermore, we identified the gene encoding S-phase kinase-associated protein 2 (Skp2), the recognition component of the SCF(Skp2) E3 ubiquitin ligase, as a novel target of p63, potentially influencing p130 levels. Expression of Skp2 is maintained by p63 binding to a site in intron 2 and mRNA levels are downregulated in p63-depleted cells. Hypoproliferation in p63-depleted cells can be restored by re-expression of Skp2. Taken together, these results indicate that p63 plays a multifaceted role in maintaining proliferation in the mature regenerating epidermis, in addition to being required for differentiation.

| S-EPMC3085435 | biostudies-literature

Proliferative stem cells maintain quiescence of their niche by secreting the Activin inhibitor Follistatin.

Project description:Aging causes stem cell dysfunction as a result of extrinsic and intrinsic changes. Decreased function of the stem cell niche is an important contributor to this dysfunction. We use the Drosophila testis to investigate what factors maintain niche cells. The testis niche comprises quiescent "hub" cells and supports two mitotic stem cell pools: germline stem cells and somatic cyst stem cells (CySCs). We identify the cell-cycle-responsive Dp/E2f1 transcription factor as a crucial non-autonomous regulator required in CySCs to maintain hub cell quiescence. Dp/E2f1 inhibits local Activin ligands through production of the Activin antagonist Follistatin (Fs). Inactivation of Dp/E2f1 or Fs in CySCs or promoting Activin receptor signaling in hub cells causes transdifferentiation of hub cells into fully functional CySCs. This Activin-dependent communication between CySCs and hub regulates the physiological decay of the niche with age and demonstrates that hub cell quiescence results from signals from surrounding stem cells.

| S-EPMC8387025 | biostudies-literature

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