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Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [PPO1_Bulk_RNA-seq]

ABSTRACT: To investigate the glioma mouse model by knocking out Pten and Trp53 in embryonal Olig1 positive cells in glioma pathogenesis and track its evolution over multiple time-points. We then performed gene expression profiling analysis using data obtained from RNA-seq of 5 PPO1 tumor tissue with 3 Control cortex tissue.

ORGANISM(S): Mus musculus

PROVIDER: GSE200887 | GEO | 2023/01/03

REPOSITORIES: GEO

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Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [ATAC-seq]

Project description:To investigate the glioma mouse model by knocking out Pten and Trp53 in embryonal Olig2 and Olig1 positive cells in glioma pathogenesis. ATAC-seq

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Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [CUT&RUN]

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Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [PPO1_and PPO1_Cells_RNA-seq]

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Transit-amplifying lineage states convey the susceptibility of PTEN and P53 loss to gliomagenesis [PPO2_Bulk_RNA-seq]

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Transit-amplifying cells orchestrate stem cell activity and tissue regeneration.

Project description:Transit-amplifying cells (TACs) are an early intermediate in tissue regeneration. Here, using hair follicles (HFs) as a paradigm, we show that emerging TACs constitute a signaling center that orchestrates tissue growth. Whereas primed stem cells (SCs) generate TACs, quiescent SCs only proliferate after TACs form and begin expressing Sonic Hedgehog (SHH). TAC generation is independent of autocrine SHH, but the TAC pool wanes if they can't produce SHH. We trace this paradox to two direct actions of SHH: promoting quiescent-SC proliferation and regulating dermal factors that stoke TAC expansion. Ingrained within quiescent SCs' special sensitivity to SHH signaling is their high expression of GAS1. Without sufficient input from quiescent SCs, replenishment of primed SCs for the next hair cycle is compromised, delaying regeneration and eventually leading to regeneration failure. Our findings unveil TACs as transient but indispensable integrators of SC niche components and reveal an intriguing interdependency of primed and quiescent SC populations on tissue regeneration.

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Transit amplifying cells coordinate mouse incisor mesenchymal stem cell activation.

Project description:Stem cells (SCs) receive inductive cues from the surrounding microenvironment and cells. Limited molecular evidence has connected tissue-specific mesenchymal stem cells (MSCs) with mesenchymal transit amplifying cells (MTACs). Using mouse incisor as the model, we discover a population of MSCs neibouring to the MTACs and epithelial SCs. With Notch signaling as the key regulator, we disclose molecular proof and lineage tracing evidence showing the distinct MSCs contribute to incisor MTACs and the other mesenchymal cell lineages. MTACs can feedback and regulate the homeostasis and activation of CL-MSCs through Delta-like 1 homolog (Dlk1), which balances MSCs-MTACs number and the lineage differentiation. Dlk1's function on SCs priming and self-renewal depends on its biological forms and its gene expression is under dynamic epigenetic control. Our findings can be validated in clinical samples and applied to accelerate tooth wound healing, providing an intriguing insight of how to direct SCs towards tissue regeneration.

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Sex and mutation specific p53 gain-of-function activity in gliomagenesis [RNA-seq]

Project description:The goal of this study is to compare the sex specific effects of the expression of p53 missense mutations on the transcriptomes of male and female primary astrocytes. Primary cortical astrocytes harboring a single floxed Trp53 allele were harvested from male and female postnatal day one pups, and transduced with mutant p53;IRES GFP followed by CRE recombinase. mRNA was collected from male and female astrocytes transduce with mouse Trp53:R172H, Trp53:Y202C, or Trp53:Y217C. This study revealed sex specific gain-of-function effects on the transcriptomes of each cell line that correlated with cancer pathways.

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ID4 function antagonizes OLIG1 and OLIG2 to suppressive aggressive glioma

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A transit-amplifying population underpins the efficient regenerative capacity of the testis.

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HBEGF promotes gliomagenesis in the context of Ink4a/Arf and Pten loss.

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