Nuclear actin structure regulates chromatin accessibility.
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ABSTRACT:
PROVIDER: PRJNA1015586 | ENA |
REPOSITORIES: ENA
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Project description:Nuclear actin structure regulates chromatin accessibility [ATAC-seq]
| PRJNA1015599 | ENA
Project description:Nuclear actin structure regulates chromatin accessibility [RNA-seq]
| PRJNA1015598 | ENA
Project description:Polymerized B-actin may provide a structural basis for chromatin accessibility and actin transport into the nucleus can guide mesenchymal stem cell (MSC) differentiation. Using MSC, we show that using CK666 to inhibit Arp2/3 directed secondary actin branching results in decreased nuclear actin structure, and significantly alters chromatin access measured with ATACseq at 24 h. The ATAC-seq results due to CK666 are distinct from those caused by cytochalasin D (CytoD), which enhances nuclear actin structure. In addition, nuclear visualization shows Arp2/3 inhibition decreases pericentric H3K9me3 marks. CytoD, alternatively, induces redistribution of H3K27me3 marks centrally. Such alterations in chromatin landscape are consistent with differential gene expression associated with distinctive differentiation patterns. Further, knockdown of the non-enzymatic monomeric actin binding protein, Arp4, leads to extensive chromatin unpacking, but only a modest increase in transcription, indicating an active role for actin-Arp4 in transcription. These data indicate that dynamic actin remodeling can regulate chromatin interactions.
2024-04-12 | GSE242944 | GEO
Project description:Polymerized b-actin may provide a structural basis for chromatin accessibility. Nuclear actin transport into the nucleus can determine mesenchymal stem cell (MSC) differentiative outcomes through regulated control of gene expression. Using MSC, we show that inhibiting Arp2/3 directed secondary actin branching with CK666, which results in decreased nuclear actin structure, significantly alters chromatin access measured with ATAC-seq at 24 h. The ATAC-seq results due to CK666 are distinct from those caused by cytochalasin D (CytoD), which increases nuclear actin structure. Nuclear visualization shows Arp2/3 inhibition is associated with decreased pericentric H3K9me3 marks. CytoD, in contrast, induces relocation of H3K27me3 marks away from the inner membrane. Treatment induced alterations in the chromatin landscape at 24 hours prompts differential gene expression associated with decreased proliferation and increased differentiation. Further, knockdown of the non-enzymatic monomeric actin binding protein, Arp4, leads to extensive chromatin unpacking, but only a modest change in transcription, indicating an active role for actin-Arp4 in transcription. These data indicate that dynamic actin remodeling can regulate chromatin interactions.
2024-04-12 | GSE242943 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-04-12 | GSE242945 | GEO
Project description:Actin dynamically shuttles between the nucleus and cytosplasm and regulates a wide range of transcriptional processes within the nucleus We used gene expression profiling of keratinocytes overexpressing wild type actin or actin tagged with a nuclear localisation sequence to identify genes specifically regulated by nuclear actin
2016-09-22 | GSE78028 | GEO
Project description:The mechanisms underlying cancer metastasis remain poorly understood. Here, we report that TFAM deficiency rapidly and stably induced spontaneous lung metastasis in mice with liver cancer. Interestingly, unexpected polymerization of nuclear actin was observed in TFAM-knockdown HCC cells when cytoskeleton was examined. Polymerization of nuclear actin is causally linked to the high-metastatic ability of HCC cells by modulating chromatin accessibility and coordinating the expression of genes associated with extracellular matrix remodeling, angiogenesis, and cell migration. Mechanistically, TFAM deficiency blocked the TCA cycle and increased the intracellular malonyl-CoA levels. Malonylation of mDia2, which drives actin assembly, promotes its nuclear translocation. Importantly, inhibition of malonyl-CoA production or nuclear actin polymerization significantly impeded the spread of HCC cells in mice. Moreover, TFAM was significantly downregulated in metastatic HCC tissues and was associated with overall survival and time to tumor recurrence of HCC patients. Taken together, our study connects mitochondria to the metastasis of human cancer via uncovered mitochondria-to-nucleus retrograde signaling, indicating that TFAM may serve as an effective target to block HCC metastasis.
2022-06-23 | MTBLS4307 | MetaboLights
Project description:Nuclear actin dynamics regulate enhanced RNA polymerase II clustering on specific genes upon serum stimulation, thus establishing the serum-induced transcriptional program.
2017-12-01 | GSE82320 | GEO
Project description:T cell antigen receptor (TCR) signaling triggers selective cytokine expression to drive T cell proliferation and differentiation required for immune defense and surveillance. The nuclear signaling events responsible for specificity in cytokine gene expression upon T cell activation are largely unknown. Here, we uncover formation of a dynamic actin filament network in the nucleus that regulates cytokine expression for effector functions of CD4 T lymphocytes. TCR engagement triggers the rapid and transient formation of a nuclear actin filament network via nuclear Arp2/3 complex, induced by elevated nuclear Ca2+ levels and regulated via N-Wasp and NIK. Specific interference with TCR-induced formation of nuclear actin filaments impairs production of effector cytokines and prevents generation of antigen-specific antibodies, but does not interfere with immune synapse formation and cell proliferation. Ca2+-regulated actin polymerization in the nucleus allows CD4 T cells the rapid conversion of TCR signals into effector functions required for T cell help Identification of nuclear F-actin sensitive genes upon TCR signaling
2018-11-15 | GSE122531 | GEO
Project description:The mechanisms underlying cancer metastasis remain poorly understood. Here, we report that TFAM deficiency rapidly and stably induced spontaneous lung metastasis in mice with liver cancer. Interestingly, unexpected polymerization of nuclear actin was observed in TFAM-knockdown HCC cells when cytoskeleton was examined. Polymerization of nuclear actin is causally linked to the high-metastatic ability of HCC cells by modulating chromatin accessibility and coordinating the expression of genes associated with extracellular matrix remodeling, angiogenesis and cell migration. Mechanistically, TFAM deficiency blocked the TCA cycle and increased the intracellular malonyl-CoA levels. Malonylation of mDia2, which drives actin assembly, promotes its nuclear translocation. Importantly, inhibition of malonyl-CoA production or nuclear actin polymerization significantly impeded the spread of HCC cells in mice. Moreover, TFAM was significantly downregulated in metastatic HCC tissues and was associated with overall survival and time to tumor recurrence of HCC patients. Taken together, our study connects mitochondria to the metastasis of human cancer via uncovered mitochondria-to-nucleus retrograde signaling, indicating that TFAM may serve as an effective target to block HCC metastasis.
2024-01-01 | GSE197830 | GEO