Staphylococcus competition
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB69298 | ENA |
REPOSITORIES: ENA
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Project description:Competition between promoters within a shared regulatory landscape has been implicated in development and disease, but the determinants of promoter competition remain unclear. Here, we introduce diverse promoters into defined genomic sites within the Sox2 locus and measure how these insertions attenuate endogenous Sox2 expression. We find that the level of reduction in endogenous Sox2 transcription is correlated with the strength of the inserted promoter. Transcription from the inserted promoter is required for competition, with longer transcript resulting in more competition. The inserted active promoter and its associated transcriptional unit function as an insulator, rendering competition position-dependent. Finally, we observe HUSH-mediated silencing of the inserted promoters, which counteracts competition. Together, our work uncovers the rules governing promoter competition, highlights its impact on tuning gene expression levels and genome evolution, and suggests that transcripts of sufficient level and length can mediate insulation independently of CTCF and cohesin.
2026-05-02 | GSE296229 | GEO
Project description:Competition between promoters within a shared regulatory landscape has been implicated in development and disease, but the determinants of promoter competition remain unclear. Here, we introduce diverse promoters into defined genomic sites within the Sox2 locus and measure how these insertions attenuate endogenous Sox2 expression. We find that the level of reduction in endogenous Sox2 transcription is correlated with the strength of the inserted promoter. Transcription from the inserted promoter is required for competition, with longer transcript resulting in more competition. The inserted active promoter and its associated transcriptional unit function as an insulator, rendering competition position-dependent. Finally, we observe HUSH-mediated silencing of the inserted promoters, which counteracts competition. Together, our work uncovers the rules governing promoter competition, highlights its impact on tuning gene expression levels and genome evolution, and suggests that transcripts of sufficient level and length can mediate insulation independently of CTCF and cohesin.
2026-05-02 | GSE312207 | GEO
Project description:Cell competition was originally described in Drosophila as a process for selection of the fittest cells. Using genetic mosaic mouse models and bone marrow chimeras, we have characterized a form of cell competition that selects for the least damaged cells. This competition is controlled by p53 but is distinct from the classical p53-mediated DNA damage response: it persists for months, is specific to the hematopoietic stem and progenitor cells, and depends on the relative rather than absolute level of p53 in competing cells. The competition appears to be mediated by a non-cell autonomous induction of growth arrest and senescence-related gene expression in outcompeted cells with higher p53 activity. p53-mediated cell competition of this type could potentially contribute to the clonal expansion of incipient cancer cells. This microarray experiment is aimed at identification of candidate genes that mediate this competition. It compares mRNA expression patterns of HSCs with different levels of p53 activity in either competitive or non-competitive conditions (isolated from either wild type, mutant p53, or mosaic wt/mutant p53 mice (R26-mp53mice) after irradiation).
2010-04-01 | GSE20912 | GEO
Project description:we develop an interspecies pluripotent stem cell (PSC) co-culture strategy and uncover a previously unknown mode of cell competition. Interspecies PSC competition occurs during primed but not naive pluripotency, and between evolutionarily distant species. We identified genes related to NF-κB signaling pathways, among others, were upregulated in loser cells and genetic inactivation of RELA, a core component of canonical NF-κB pathway, could overcome interspecies PSC competition. We further showed that an upstream regulator of the NF-κB signaling, MYD88 innate immune signal transduction adaptor, was also involved in promoting loser PSC elimination. Suppressing interspecies PSC competition via genetic perturbation of MYD88 or P65 improved engraftment of human cells in early post-implantation mouse embryos. Our study discovers a new paradigm of cell competition and paves the way for studying evolutionarily conserved cell competition mechanisms during early mammalian development. Strategies developed here to overcome interspecies PSC competition may facilitate interspecies organogenesis between evolutionary distant species, including humans.
2020-12-31 | GSE142394 | GEO
Project description:Although increasing studies have proved cell competition widely involved in the growth and homeostasis of multicellular organisms is closely linked to tumorigenesis and development, the mechanistic contributions between drug resistance and tumor cell competition remain ill-defined. In this paper, we applied MS of cell competition group to determine the dominant characteristics of lenvatinib resistance and its metabolic differences in cell competition. Our results showed a vital role of HSP90-IDH1 mediated lipid accumulation in maintaining the competitive outcome of HCC drug-resistant cells via regulating lipid metabolism. HSP90-IDH1 axis could be a promising target to overcome HCC drug resistance.
2023-10-20 | PXD046294 |
Project description:Eukaryotic transcription factors (TFs) are key determinants of gene activity, yet they bind only a fraction of their corresponding DNA sequence motifs in any given cell type. Chromatin has the potential to restrict accessibility of binding sites; however, in which context chromatin states are instructive for TF binding remains mainly unknown. To explore the contribution of DNA methylation to constrained TF binding, we mapped DNase-I-hypersensitive sites in murine stem cells in the presence and absence of DNA methylation. Methylation-restricted sites are enriched for TF motifs containing CpGs, especially for those of NRF1. In fact, the TF NRF1 occupies several thousand additional sites in the unmethylated genome, resulting in increased transcription. Restoring de novo methyltransferase activity initiates remethylation at these sites and outcompetes NRF1 binding. This suggests that binding of DNA-methylationsensitive TFs relies on additional determinants to induce local hypomethylation. In support of this model, removal of neighbouring motifs in cis or of a TF in trans causes local hypermethylation and subsequent loss of NRF1 binding. This competition between DNA methylation and TFs in vivo reveals a case of cooperativity between TFs that acts indirectly via DNA methylation. Methylation removal by methylation-insensitive factors enables occupancy of methylation-sensitive factors, a principle that rationalizes hypomethylation of regulatory regions. DNase-seq (2 replicates) in mouse embryonic stem cells with (WT) and without DNA methylation (DNMT TKO). RNA-seq (3 replicates) in WT and DNMT TKO cells and in DNMT TKO cells after treatment with control siRNA or siRNA targeting Nrf1. H3K27ac ChIP-seq (2 replicates) in WT and DNMT TKO cells. NRF1 ChIP-seq (2 replicates) in WT and DNMT TKO cells, in WT upon culture in different conditions (adaptation to 2i and back to serum), upon transient overexpression of NRF1 and after differentiation into neuronal progenitor cells (NP). Whole-genome bisulfite sequencing in DNMT TKO cells and in WT upon culture in different conditions (adaptation to 2i and back to serum). NRF1 ChIP-seq (2 replicates) in human HMEC and HCC1954 cells.
2015-12-16 | E-GEOD-67867 | biostudies-arrayexpress
Project description:To identify new genetic elements required for S.aureus pathogenesis, we performed a transposon sequencing in the context of acute murine penumonia. We screened conditionally essential genes identified by Tn-seq and confirmed 6 previously uncharacterized genes were important during infection. As further study, we performed RNA-seq to identify uncharacterized genes.
2023-06-27 | GSE136543 | GEO
Project description:Identifying non-genetic determinants of malignant clonal fitness at single cell resolution (clonal competition scRNAseq)
| PRJNA679061 | ENA
Project description:Cytoplasmic competition between separate parental pronuclei in zygotes
| PRJNA1174679 | ENA
Project description:Cytoplasmic competition between separate parental pronuclei in zygotes
| PRJNA967384 | ENA