Microarray analysis of gene expression during ESC cell competition
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PROVIDER: PRJNA431212 | ENA |
REPOSITORIES: ENA
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Project description:A fundamental question in developmental biology is whether there are mechanisms to detect stem cells with mutations that, although not adversely affecting viability, would compromise their ability to contribute to further development. Here, we show that cell competition is a mechanism regulating the fitness of embryonic stem cells (ESCs). We find that ESCs displaying defective bone morphogenetic protein signaling or defective autophagy or that are tetraploid are eliminated at the onset of differentiation by wild-type cells. This elimination occurs in an apoptosis-dependent manner and is mediated by secreted factors. Furthermore, during this process, we find that establishment of differential c-Myc levels is critical and that c-Myc overexpression is sufficient to induce competitive behavior in ESCs. Cell competition is, therefore, a process that allows recognition and elimination of defective cells during the early stages of development and is likely to play important roles in tissue homeostasis and stem cell maintenance.
2018-01-24 | GSE109494 | GEO
Project description:Deconstructing lincRNA regulation during ESC to NPC differentiation
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Project description:A fundamental question in developmental biology is whether there are mechanisms to detect stem cells with mutations that although do not adversely affect their viability, would compromise their ability to contribute to further development. Here we show that cell competition is a novel mechanism regulating the fitness of embryonic stem cells (ESCs). We find that ESCs displaying defective BMP signalling, defective autophagy or are tetraploid are eliminated at the onset of differentiation by wild-type cells. This elimination occurs in an apoptotic dependent manner and is mediated by secreted factors. Furthermore, during this process we find that establishment of differential cMyc levels is critical and that cMyc over-expression is sufficient to induce competitive behaviour in ESCs. Cell competition is therefore a process that allows recognition and elimination of defective cells during the early stages of development and is likely to play important roles in tissue homeostasis and stem cell maintenance. We used microarrays to compare the gene expression profiles of Bmpr1a-/- and control embryonic stem cells (ESCs) in the ESC state and after differentiation in N2B27 Microarray profiles of control and Bmpr1a-/- mouse embryonic stem cells in embryonic stem cell culture media and in N2B27
2013-06-20 | E-GEOD-48092 | biostudies-arrayexpress
Project description:Long noncoding RNAs (lncRNAs) have emerged as crucial regulators of gene expression during embryonic stem cell (ESC) self-renewal and differentiation. Here, we systemically analyzed the differentially regulated lncRNAs during ESC-derived cardiomyocyte (CM) differentiation. We established a perspicuous profile of lncRNA expression at four critical developmental stages and found that the differentially expressed lncRNAs were grouped into six distinct clusters. The cluster with specific expression in ESC enriches the largest number of lncRNAs. Investigation of lncRNA-protein interaction network revealed that they are not only controlled by classic key transcription factors, but also modulated by epigenetic and epitranscriptomic factors including N6-methyladenosine (m6A) effector machineries.
2022-03-01 | GSE197205 | GEO
Project description:Dynamic lncRNA expression pattern during ESC-derived cardiac differentiation
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Project description:Microarray expression data following the treatment of mouse ESC with Panobinostat/LBH589
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Project description:In early mammalian embryogenesis, the selective elimination of suboptimal cells is critical for developmental integrity. Cell competition is a non-autonomous quality control in which “winner” cells eliminate viable but suboptimal “loser” cells based on their relative difference in fitness. Due to its central role in fitness perception, loss of p53 results in the emergence of “supercompetitor” cells, which stand at the apex of cell competition and induce apoptosis in neighboring wild-type (WT) cells. Here, we investigate cell competition dynamics using mosaic 3D mouse gastruloids, an embryonic stem cell (ESC)-based in vitro model of gastrulation, composed of defined numbers of WT and p53-KO cells. In mosaic gastruloids, even low numbers of p53-KO cells robustly outcompete WT cells, and introduction of as few as two p53-KO cells is sufficient to measurably impair neighboring WT cell growth. Cell competition in gastruloids is independent of proliferation rates, nutrient availability, or reactive oxygen species, and not influenced by Nodal and ERK signaling. However, we observe that Wnt and BMP signaling protect from cell competition, which is exclusively driven by intrinsic apoptosis, as indicated by Bcl2-mediated complete rescue of WT cells. During gastruloid development, cell competition is temporally restricted to a window of 48–96 hours after aggregation, mirroring embryonic days E5.5–E7.5 in the mouse. Heterochronic mosaic gastruloid experiments demonstrate that relative differences in pluripotency levels are neither necessary nor sufficient to cause supercompetition, but that cell competition is contingent on both competitors residing within the developmental window permissive to competition. Neither pluripotent mosaic 3D aggregates, nor 3D EpiGastruloids, which model more advanced developmental processes, display any competition, supporting the hypothesis that developmental cell competition is specific to the onset of gastrulation. Our findings offer insights into the mechanisms of cell fitness evaluation in mammalian embryogenesis and establish gastruloids as a powerful 3D model for investigating developmental stage-specific cell competition.
2026-02-12 | GSE294530 | GEO
Project description:RNA-seq analysis of Streptococcus pneumoniae during intraspecies competition in broth culture
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Project description:LIN28a is an RNA binding protein that was initially characterized for its role in the negative regulation of let-7 microRNA biogenesis. In the last years a new role in the regulation of mRNA translation has been highlighted. This mechanism seems to be particularly relevant in the exit of embryonic stem cells (ESCs) from the naïve state and in the first phases of differentiation process. We have demonstrated that in the first step of ESC differentiation, i.e. the establishment of epiblast-like-cells and the formation of neural precursors, LIN28a enhances the translation of de novo DNA methyltransferase Dnmt3a [1] and blocks that of the chromatin architectural factor Hmga2 [2]. How LIN28a fulfils these opposite functions in ESC differentiation is still unknown. Our preliminary results indicated that LIN28a contributes in several ways to guide ESC differentiation possibly by changing molecular partners and regulating different targets. To explore this idea, we have generated Lin28a KO ESCs using CRISPR-Cas9 technology to study how Lin28a contributes to ESC differentiation. We have found that Lin28a KO ESCs are not able to properly exit from the naïve state to undergo a differentiation program. This effect seems to be due to the impairment of different cellular processes. To better characterize this role in ESC fate we have analyzed the molecular interactions of LIN28a at different steps of ESC differentiation through proteomics approaches. Moreover, to identify the direct mRNA targets of LIN28a we are developing an iCLIP protocol suitable to analyze the binding of LIN28a to RNAs during ESC differentiation. These data coupled with the phenotypic and proteomics analysis will contribute to understand the emerging fundamental role of RNA binding proteins in differentiation and development.
2026-05-05 | PXD049332 | Pride
Project description:Cell competition promotes the elimination of weaker cells from a growing population. Here we investigate how cells of Drosophila wing imaginal discs distinguish “winners” from “losers” during cell competition. Using genomic and functional assays we have identified Maxwell`s Demon (Mwd), a cell membrane protein conserved in multicellular animals. Our results suggest that the membrane protein Mwd is a dedicated component of the cell competition response that is required and sufficient to label cells as “winners” or “losers”. In Drosophila, the mwd locus produces three isoforms, mwdubi, mwdLose-A and mwdLose-B. Basal levels of mwdubi are constantly produced. During competition the mwdLose isoforms are upregulated in prospective loser cells. Cell-cell comparison of relative mwdLose and mwdubi levels ultimately determine which cell undergoes apoptosis. This “extracellular code” may constitute an ancient mechanism to terminate competitive conflicts among cells. Two samples have been analysed: tub>dmyc>Gal4 transgene cells (competitor) and tub>cd2>Gal4 control cells (non competitor) at different time points (0, 12, 24 and 48 hours). Each experiment was replicated 6 times, three of them by dye swap.
2011-02-09 | E-GEOD-21230 | biostudies-arrayexpress