Nuclear actin structure regulates chromatin accessibility [ATAC-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1015599 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26038512_1.fastq.gz | Fastqsanger.gz | |||
| SRR26038512_2.fastq.gz | Fastqsanger.gz | |||
| SRR26038513_1.fastq.gz | Fastqsanger.gz | |||
| SRR26038513_2.fastq.gz | Fastqsanger.gz | |||
| SRR26038514_1.fastq.gz | Fastqsanger.gz |
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Project description:Nuclear actin structure regulates chromatin accessibility.
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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.
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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.
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Project description:β-actin is a crucial component of several chromatin remodeling complexes which control chromatin structure and accessibility. The mammalian Brahma-associated factor (BAF) is one such complex that plays essential roles in development and differentiation by regulating the chromatin state of critical genes and opposing the repressive activity of polycomb repressive complexes. While previous work has shown that β-actin loss can lead to extensive changes in gene expression and heterochromatin organization, it is not known if changes in β-actin levels can directly influence chromatin remodeling activities of BAF and polycomb proteins. Here we conduct a comprehensive genomic analysis of β-actin knockout mouse embryonic fibroblasts (MEFs) using ATAC-Seq, HiC-seq, RNA-Seq and ChIP-Seq of various epigenetic marks. We demonstrate that β-actin levels can affect the complex interplay between chromatin remodelers such as BAF/BRG1 and EZH2 in a dosage-dependent manner. Our results show that changes in β-actin levels and associated chromatin remodeling activities can not only impact local chromatin accessibility but also induce reversable changes in 3D genome architecture. Our findings support a novel role for β-actin levels in shaping the chromatin landscape during development and differentiation.
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