Fos licenses early events in stem cell activation promoting skeletal muscle regeneration
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA490635 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7825570.fastq.gz | Fastqsanger.gz | |||
| SRR7825571.fastq.gz | Fastqsanger.gz | |||
| SRR7825572.fastq.gz | Fastqsanger.gz | |||
| SRR7825573.fastq.gz | Fastqsanger.gz | |||
| SRR7825564.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Fos licenses early events in stem cell activation promoting skeletal muscle regeneration [array]
| PRJNA490031 | ENA
Project description:Fos licenses early events in stem cell activation promoting skeletal muscle regeneration [RNA-seq]
| PRJNA490637 | ENA
Project description:Muscle stem cells, also known as satellite cells, are largely non-proliferative in uninjured skeletal muscle but transition at sites of injury into rapidly dividing progenitors that mediate muscle repair. As early events in satellite cell activation are rate-limiting for recovery from muscle damage, there is substantial interest in discovering their molecular driver(s). Using a comparative transcriptomic approach, we identified a prominent Fos signature in recently activated muscle satellite cells, which was rapidly and transiently induced by muscle damage. Functional interrogation using complementary genetic mouse models revealed that FOS is required for efficiently initiating key stem cell functions, including cell cycle entry, stem/progenitor cell expansion, and regeneration of muscle after injury. Transcriptional profiling further revealed that FOS activates critical gene circuits that stimulate cell migration, proliferation, and differentiation while simultaneously repressing quiescence-promoting gene signatures. Pharmacological and genetic disruption of one of these FOS-activated target genes, mono-ADP Ribosyl-Transferase 1 (Art1), in freshly isolated satellite cells substantially diminished cell cycle entry and expansion of the pool of regenerative stem cells. Together, these data implicate FOS as a crucial inducer of early-acting, pro-regenerative gene targets and highlight new transcriptional and post-translational modification events necessary for optimal injury-activated muscle stem cell regenerative responses.
2021-01-27 | GSE119695 | GEO
Project description:Muscle stem cells, also known as satellite cells, are largely non-proliferative in uninjured skeletal muscle but transition at sites of injury into rapidly dividing progenitors that mediate muscle repair. As early events in satellite cell activation are rate-limiting for recovery from muscle damage, there is substantial interest in discovering their molecular driver(s). Using a comparative transcriptomic approach, we identified a prominent Fos signature in recently activated muscle satellite cells, which was rapidly and transiently induced by muscle damage. Functional interrogation using complementary genetic mouse models revealed that FOS is required for efficiently initiating key stem cell functions, including cell cycle entry, stem/progenitor cell expansion, and regeneration of muscle after injury. Transcriptional profiling further revealed that FOS activates critical gene circuits that stimulate cell migration, proliferation, and differentiation while simultaneously repressing quiescence-promoting gene signatures. Pharmacological and genetic disruption of one of these FOS-activated target genes, mono-ADP Ribosyl-Transferase 1 (Art1), in freshly isolated satellite cells substantially diminished cell cycle entry and expansion of the pool of regenerative stem cells. Together, these data implicate FOS as a crucial inducer of early-acting, pro-regenerative gene targets and highlight new transcriptional and post-translational modification events necessary for optimal injury-activated muscle stem cell regenerative responses.
2021-01-27 | GSE119895 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-01-27 | GSE119896 | GEO
Project description:Notch signaling licenses allergic airway inflammation by promoting lymph node egress of Th2 cells
| PRJNA515916 | ENA
Project description:Expression analyses comparing c-Fos expressing keratinocytes vs non-expressing controls. Skin squamous cell carcinomas (SCCs) are the second most prevalent skin cancers. Chronic skin inflammation has been associated with the development of SCCs, but the contribution of skin inflammation to SCC development remains largely unknown. In this study we demonstrate that inducible expression of c-fos in the epidermis of adult mice is sufficient to promote inflammation-mediated epidermal hyperplasia leading to the development of pre-neoplastic lesions. Interestingly, c-Fos transcriptionally controls mmp10 and s100a7a15 expression in keratinocytes subsequently leading to CD4 T cell recruitment to the skin, thereby promoting epidermal hyperplasia. Combining inducible c-fos expression in the epidermis with a single dose of the carcinogen 7,12-Dimethylbenz(a)anthracene (DMBA) leads to the development of highly invasive SCCs, which are prevented by using the anti-inflammatory drug Sulindac. Moreover, human SCCs display a correlation between c-FOS expression and elevated levels of MMP10 and S100A15 proteins as well as CD4 T cell infiltration. Our studies demonstrate a bidirectional crosstalk between pre-malignant keratinocytes and infiltrating CD4 T cells in SCC development. Therefore, targeting inflammation along with the newly identified targets, such as MMP10 and S100A15, represent promising therapeutic strategies to treat SCCs. 5 different time points measured in triplicate comparing Dox-treated vs untreated c-FostetON keratinocytes
2013-09-05 | E-GEOD-50621 | biostudies-arrayexpress
Project description:Acinetobacter baumannii is a highly pathogenic and multidrug-resistant Gram-negative bacterium that causes severe nosocomial infections. To better understand the mechanism of pathogenesis, we compare the proteomes of uninfected and infected human cells, revealing that transcription factor FOS is the host protein most strongly induced by A. baumannii infection. Pharmacological inhibition of FOS reduces the cytotoxicity of A. baumannii in cell-based models, and similar results are also observed in a mouse infection model. A. baumannii outer membrane vesicles (OMVs) are shown to activate the aryl hydrocarbon receptor (AHR) of host cells by inducing the host enzyme tryptophan-2,3-dioxygenase (TDO), producing the ligand kynurenine, which binds AHR. Following ligand binding, AHR is a direct transcriptional activator of the FOS gene. Our results suggest that bacterial infection interacts with host tryptophan metabolism and the transcription factor FOS.
2024-08-05 | PXD053768 | Pride
Project description:Expression analyses comparing c-Fos expressing keratinocytes vs non-expressing controls. Skin squamous cell carcinomas (SCCs) are the second most prevalent skin cancers. Chronic skin inflammation has been associated with the development of SCCs, but the contribution of skin inflammation to SCC development remains largely unknown. In this study we demonstrate that inducible expression of c-fos in the epidermis of adult mice is sufficient to promote inflammation-mediated epidermal hyperplasia leading to the development of pre-neoplastic lesions. Interestingly, c-Fos transcriptionally controls mmp10 and s100a7a15 expression in keratinocytes subsequently leading to CD4 T cell recruitment to the skin, thereby promoting epidermal hyperplasia. Combining inducible c-fos expression in the epidermis with a single dose of the carcinogen 7,12-Dimethylbenz(a)anthracene (DMBA) leads to the development of highly invasive SCCs, which are prevented by using the anti-inflammatory drug Sulindac. Moreover, human SCCs display a correlation between c-FOS expression and elevated levels of MMP10 and S100A15 proteins as well as CD4 T cell infiltration. Our studies demonstrate a bidirectional crosstalk between pre-malignant keratinocytes and infiltrating CD4 T cells in SCC development. Therefore, targeting inflammation along with the newly identified targets, such as MMP10 and S100A15, represent promising therapeutic strategies to treat SCCs.
2013-09-05 | GSE50621 | GEO
Project description:Behavioral experiences activate the Fos transcription factor (TF) in sparse populations of neurons that are critical for encoding and recalling specific events. However, there is limited understanding of the mechanisms by which experience drives circuit reorganization to establish a network of Fos-activated cells. Additionally, it is unknown if Fos is required in this process beyond serving as a marker of recent neural activity and, if so, which of its many gene targets underlie circuit reorganization. Here we demonstrate that when mice engage in spatial exploration of novel environments, perisomatic inhibition of Fos-expressing hippocampal CA1 pyramidal neurons by parvalbumin (PV)-interneurons (INs) is enhanced, while perisomatic inhibition by cholecystokinin (CCK)-INs is weakened. This bidirectional modulation of inhibition is specific to Fos-expressing neurons and is abolished when the function of the Fos TF complex is disrupted. Single-cell RNA-sequencing, ribosome-associated mRNA profiling, and chromatin analyses, combined with electrophysiology reveal that Fos activates the transcription of Scg2 (secretogranin II), a gene that encodes multiple distinct neuropeptides, to coordinate these changes in inhibition. As PV- and CCK-INs mediate distinct features of pyramidal cell activity, the Scg2-dependent reorganization of inhibitory synaptic input might be predicted to affect network function in vivo. Consistent with this prediction, hippocampal gamma rhythms and pyramidal cell coupling to CA1 theta are significantly altered with loss of Scg2. Together these findings reveal an instructive role for Fos and Scg2 in establishing a network of Fos-activated neurons via the rewiring of local inhibition from an initially broad to a selectively modulated state. The opposing plasticity mechanisms on distinct inhibitory pathways may support the consolidation of memories over time.
2020-10-04 | GSE158841 | GEO