Flexible and scalable control of T cell memory by a reversible epigenetic switch
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA996890 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25367400_1.fastq.gz | Fastqsanger.gz | |||
| SRR25367400_2.fastq.gz | Fastqsanger.gz | |||
| SRR25373500_1.fastq.gz | Fastqsanger.gz | |||
| SRR25373500_2.fastq.gz | Fastqsanger.gz | |||
| SRR25373600_1.fastq.gz | Fastqsanger.gz |
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Project description:Flexible and scalable control of T cell memory by a reversible epigenetic switch (ATAC-seq)
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Project description:In this study, we use a minimal ex vivo culture system to track CD8 T cell differentiation at the single cell and clonal lineage level during activation. To characterize early heterogeneity in memory and effector differentiation in this system, we subjected cells to temporally-resolved single-cell transcriptomic profiling using sci-fate-seq (Cao et al., Nature Biotech, 202).
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Project description:In this study, we find that the Tcf7+ CD8 T cells present following acute challenge can form either from cells that maintain Tcf7 expression throughout activation or from cells that silence Tcf7 and reactivate it after stimulation removal. In this experiment, we asked whether both pathways can give rise to cells with genomic characteristics of memory. To do this, we activated naive CD8 T cells ex vivo for 2 days followed by 1 day of culture without TCR stimulation. On day 3, we sorted Tcf7-YFP high and low populations, all from a single CellTrace peak representing cells that had undergone the same number of divisions. The sorted populations were cultured for an additional 6 days and sorted again on day 9 by Tcf7-YFP levels. These samples, as well as control naive, antigen-experienced, and effector samples, were processed for RNA-seq analysis.
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Project description:In this study, we find that the Tcf7+ CD8 T cells present following acute challenge can form either from cells that maintain Tcf7 expression throughout activation or from cells that silence Tcf7 and reactivate it after stimulation removal. In this experiment, we asked whether both pathways can give rise to cells with genomic characteristics of memory. To do this, we activated naive CD8 T cells ex vivo for 2 days followed by 1 day of culture without TCR stimulation. On day 3, we sorted Tcf7-YFP high and low populations, all from a single CellTrace peak representing cells that had undergone the same number of divisions. The sorted populations were cultured for an additional 6 days and sorted again on day 9 by Tcf7-YFP levels. These samples, as well as control naive, antigen-experienced, and effector samples, were processed for ATAC-seq analysis.
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Project description:This SuperSeries is composed of the SubSeries listed below.
2023-07-25 | GSE237830 | GEO
Project description:The life cycle of Trypanosoma brucei involves several cell differentiation transitions that allow transmission, survival and proliferation of these parasites. One of these transitions, the differentiation of growth-arrested stumpy forms in the mammalian blood into proliferating insect-stage procyclic forms, can be induced synchronously in vitro by addition of cis-aconitate (CA). Using single-cell analysis by flow-cytometry to follow differentiation, we show that this transition is an irreversible bistable switch where cells commit to differentiation after 1-3 hours of exposure to CA. This irreversibility implies the existence of positive feedback mechanisms that allow commitment to differentiation: i.e. the establishment of “memory” of exposure to the differentiation signal. Such mechanisms probably depend on post-translational modifications (e.g. phosphorylation) and/or synthesis of regulatory proteins. Using the reversible protein synthesis inhibitor cycloheximide, we find that protein synthesis is required for establishment of signal memory and normal commitment to differentiation. To characterize the ‘commitment proteome’, we performed SILAC phosphoproteomics to provide a detailed map of the protein expression and phosphorylation events during the early stages of differentiation in a synchronised parasite population. Using a rigorous candidate gene approach we have also demonstrated that the stumpy form enriched serine-throenine protein kinases TbNRKA/B stringently control the earliest events in differentiation identifying these kinases as major regulators of trypanosome development.
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Project description:Chickarmane2006 - Stem cell switch reversible
Kinetic modeling approach of the transcriptional dynamics of the embryonic stem cell switch.
This model is described in the article:
Transcriptional dynamics of the embryonic stem cell switch.
Chickarmane V, Troein C, Nuber UA, Sauro HM, Peterson C
PLoS Computational Biology. 2006; 2(9):e123
Abstract:
Recent ChIP experiments of human and mouse embryonic stem cells have elucidated the architecture of the transcriptional regulatory circuitry responsible for cell determination, which involves the transcription factors OCT4, SOX2, and NANOG. In addition to regulating each other through feedback loops, these genes also regulate downstream target genes involved in the maintenance and differentiation of embryonic stem cells. A search for the OCT4-SOX2-NANOG network motif in other species reveals that it is unique to mammals. With a kinetic modeling approach, we ascribe function to the observed OCT4-SOX2-NANOG network by making plausible assumptions about the interactions between the transcription factors at the gene promoter binding sites and RNA polymerase (RNAP), at each of the three genes as well as at the target genes. We identify a bistable switch in the network, which arises due to several positive feedback loops, and is switched on/off by input environmental signals. The switch stabilizes the expression levels of the three genes, and through their regulatory roles on the downstream target genes, leads to a binary decision: when OCT4, SOX2, and NANOG are expressed and the switch is on, the self-renewal genes are on and the differentiation genes are off. The opposite holds when the switch is off. The model is extremely robust to parameter changes. In addition to providing a self-consistent picture of the transcriptional circuit, the model generates several predictions. Increasing the binding strength of NANOG to OCT4 and SOX2, or increasing its basal transcriptional rate, leads to an irreversible bistable switch: the switch remains on even when the activating signal is removed. Hence, the stem cell can be manipulated to be self-renewing without the requirement of input signals. We also suggest tests that could discriminate between a variety of feedforward regulation architectures of the target genes by OCT4, SOX2, and NANOG.
This model is hosted on BioModels Database
and identified by: MODEL7957907314
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
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Project description:Inflammation is essential to the disruption of tissue homeostasis and can destabilize the identity of lineage-committed epithelial cells. Here, we employ lineage-traced mouse models, single-cell transcriptomic and chromatin analyses, and CUT&TAG to identify an epigenetic memory of inflammatory injury in the pancreatic acinar cell compartment. Despite resolution of pancreatitis, our data show that acinar cells fail to return to their molecular baseline, with retention of elevated chromatin accessibility and H3K4me1 at metaplasia genes, such that memory represents an incomplete cell fate decision. In vivo, we find this epigenetic memory controls lineage plasticity, with diminished metaplasia in response to a second insult but increased tumorigenesis with an oncogenic Kras mutation. The lowered threshold for oncogenic transformation, in turn, can be restored by blockade of MAPK signaling. Together, we define the chromatin dynamics, molecular encoding, and recall of a prolonged epigenetic memory of inflammatory injury that impacts future responses but remains reversible.
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