Ontology highlight
ABSTRACT:
PROVIDER: PRJNA733846 | ENA |
REPOSITORIES: ENA
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Project description:We reveal that Axin2 mediates stem cell competition in developing brain.
2023-03-10 | GSE178509 | GEO
Project description:Axin2 mediates stem cell competition in developing brain
| PRJNA739456 | ENA
Project description:Axin2-expressing calvarial suture stem cells can contribute to calvarial development, homeostatic maintenance, repair, and regeneration. We used microarray to examine the gene expression profiles of Axin2-expressing suture stem cells and Axin2-negative cells in suture mesenchyme. Three of Axin2+/GFP+ and three of Axin2-/GFP- cell samples were collected from mice carrying Axin2rtTA and TREH2BGFP transgenes. Each samples were isolated from 6-8 Axin2rtTA; TRE-H2BGFP mice and sorted by the GFP intensity.
2015-11-11 | E-GEOD-74849 | biostudies-arrayexpress
Project description:Stem cell competition controls organ size, maintains tissue homeostasis and optimizes long-term tissue function through eliminating cells less fit than their neighbors, but whether competitive interaction occurs between neural stem cells in the developing brain and its mechanistic drivers remains enigmatic. We applied single-cell RNA sequencing of mouse E11.5 medial cortex and bulk RNA sequencing of AnnexinV positive, PI negative cells to identify the loser cell in the natural state.
2023-03-10 | GSE203163 | GEO
Project description:A tendon’s ordered extracellular matrix (ECM) is integral for transmitting force and highly prone to injury. Whether and how tendon cells, or tenocytes, embedded within this dense ECM mobilize and contribute to healing is unknown. Here, we identify a specialized Axin2+ tenocyte population in mouse and human tendons that remains latent in homeostasis yet serves as a major source of tendon progenitors during healing. We show that Axin2+ tenocytes readily expand in vitro and express stem cell markers. In vivo, Axin2+ cells are major functional contributors to repair: Axin2+ tenocytes de-differentiate, expand, and re-adopt a tenocyte fate post-injury. Specific loss of Wnt secretion in Axin2+ cells alters their stem cell identity and disrupts their activation upon injury, severely compromising healing. Our work highlights Axin2+ tenocytes as quiescent stem cells embedded in dense matrix, which are uniquely regulated in an autocrine manner and are central organizers of robust tendon healing.
2024-10-22 | GSE188598 | GEO
Project description:Axin2-expressing calvarial suture stem cells can contribute to calvarial development, homeostatic maintenance, repair, and regeneration. We used microarray to examine the gene expression profiles of Axin2-expressing suture stem cells and Axin2-negative cells in suture mesenchyme.
2015-11-11 | GSE74849 | GEO
Project description:The gastrointestinal epithelial crypts are clonal units with a high cell turnover, driven by a small population of long-lived, Lgr5-expressing stem cells located in the crypt base. Despite this, depletion of Lgr5+ cells does not lead to severe pathology. Instead, other cell populations, such as secretory and enterocyte precursors are able to de-differentiate, replace Lgr5+ cells, and regenerate the crypt. However, the signals that regulate this epithelial plasticity are not well understood. Here we illuminate the hierarchical organization and regulation of stem cell plasticity in the colonic crypt. Using in vivo lineage tracing, we find that the classic Wnt target gene Axin2 is expressed in colonic Lgr5+ cells and adjacent Lgr5-negative cells that give rise to entire crypts upon Lgr5+ cell depletion. The identity of Lgr5+ cells is controlled by by R-spondin 3 (Rspo3) produced by myofibroblasts and the recovery of Lgr5+ cells upon depletion required functional Rspo3 signaling. In contrast, expression of Axin2 and the reserve stem cell function of Axin2+ cells is not dependent on Rspo3. Accordingly, upon knockout of Rspo3, Lgr5-negative Axin2+ cells are able to compensate the loss of the Lgr5+ cell compartment and maintain epithelial integrity. In contrast, Rspo3 is essential for maintaining epithelial integrity in the context of injury of the entire Axin2+ cell pool, as observed in the context of DSS colitis. We demonstrate that DSS induces a progressive loss of the Lgr5+ stem cells as well as Axin2+ Lgr5-negative reserve stem cell compartment. While Rspo3 deficient animals are unable to withstand this injury, in Rspo3 competent animals, crypt homeostasis and regeneration are fueled by the remaining Axin2-negative, differentiated cells. These cells can be reprogrammed by Rspo3 to proliferate and act as stem cells. Thus, we identity Rspo3 as a major regulator of the Lgr5 stem cell signature. While loss of this signature can be compensated by Rspo3-independent reserve stem cells under healthy conditions, it is essential for re-establishment of epithelial integrity upon crypt injury.
2019-06-01 | GSE115752 | GEO
Project description:Summary: RNAseq analysis of Axin2+ hepatocyte stem cells versus Axin2- mature hepatocytes shows that Axin2+ cells have a distinct gene expression profile compared to Axin2- hepatocytes. Methods: Hepatocytes were isolated from 8 week old Axin2rtTA;TetO-H2B-GFP mice (n = 3) given doxycycline in drinking water for 7 days. After removal of non-parenchymal cells, the hepatocytes were sorted into GFP+ versus GFP- populations by FACS. mRNA was isolated and RNAseq profiles were generated using Illumina HiSeq 2000. The reads were mapped to the mouse genome (mm10) using TopHat (v2.0.11) and differential gene expression analysis was performed using CuffDiff (v.2.2.2). Results: We mapped about 60 million sequence reads per sample to the mouse genome (build mm10) and identified more than 30,000 transcripts in the Axin2+ and Axin2- cell populations. Differential gene expression analysis using CuffDiff identified 96 genes with signficantly different expression levels between the two populations. Several of these were confirmed by RNA in situ and qRT-PCR analysis. mRNA profiles of Axin2+ and Axin2- cells from uninjured adult mouse liver were analysed by deep sequencing, in triplicate, using Illumina HiSeq 2000.
2015-08-07 | E-GEOD-68806 | biostudies-arrayexpress
Project description:Summary: RNAseq analysis of Axin2+ and Axin2- endometrial epithelial cells shows that Axin2+ cells have a distinct gene expression profile compared to Axin2- cells. Methods: Four-week-old Axin2rtTA; tetOH2BJGFP mice (n=3) were ovariectomized. After 2 weeks of rest, H2BJGFP was induced in Axin2+ cells by a single dose of doxycycline administered intraperitoneally and uteri were collected 4 days post-doxycycline administration. Endometrial epithelial cells were isolated, digested into single cell suspension and Axin2+ (GFPhigh) and Axin2- (GFP-) cells were FACS sorted. The respective Axin2+ and Axin2- cells from each of the three mice used in this experiment were pooled together (Axin2- cells = C1, C2, C3; Axin2+ cells = M1, M2, M3, Arabic numeral represents the mouse number). Total RNA was isolated using RNeasy Micro kit (Qiagen) as per manufacturer instructions. RNA quality and concentration were determined using Nanodrop ND-1000 Spectrophotometer. RNAseq profiles were generated using Illumina NovaSeq platform. The reads were mapped to the mouse genome (Build version mm10) using the STAR aligner (v2.5.3a) and differential gene expression analysis was performed using edgeR (version 3.22.5) tool. Results: Differential gene expression analysis using edgeR identified 4458 genes that were differentially expressed by more than twofold in the Axin2high population compared with Axin2- population. Several of these differentially expressed genes include some of the well-known stem cell markers.
2020-01-14 | GSE140222 | GEO
Project description:Cell competition is a new notion of old theory Darwinian theory in cell level. It is notorious as its function on cancer promotion, actually, cell competition is a critical checkpoint machinery in development, its proper operation roles out suboptimal cells and makes sure the high quality of basic materials make up organism. Although its function has been revealed on other organs, it remains mysterious in brain development. In this paper, we get a compromised cell competitional model by knocking out endothelial Brd4, the lack of Brd4 in endothelial cell induces less neural stem cells deaths and compromised cell competition, endothelial Brd4 regulates cell competition is Testican2 dependent, Testican2 can deposit Sparc. We find a noncanonical role of the canonical negative cell competitional regulator Sparc in the fate decision of neural stem cells, neural stem cells highly expressing Sparc steps forward differentiation. We also find a compromised cell competition in AD patients, by cloning a point mutant of Brd4 found in a group of AD, we reveals that the mutant lose the potential of cell competition promotion. We put forward a new strategy for the treatment of aging related diseases by enhancing cell competitional state.
2023-01-25 | GSE223131 | GEO