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SWI/SNF subunit CHR2 remodels pri-miRNAs via microprocessor component SE to inhibit miRNA production

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE108859 | GEO | 2018/05/18

REPOSITORIES: GEO

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SWI/SNF subunit CHR2 remodels pri-miRNAs via microprocessor component SE to inhibit miRNA production (miRNA-Seq)

Project description:We performed Illumina sequencing of sRNA libraries prepared from leaves of adult plants in Arabidopsis. Chromatin remodeling factor 2 (CHR2) positively regulates transcription of MIR loci whereas repressing microRNA (miRNA) accumulation in vivo. CHR2 can directly bind to and unwind primary miRNAs (pri-miRNAs) and inhibit their processing; and this inhibition entails its remodeling activity in vitro and in vivo.

2018-05-18 | GSE108858 | GEO

SWI/SNF subunit CHR2 remodels pri-miRNAs via microprocessor component SE to inhibit miRNA production DMS-MaPseq)

Project description:Here we present dimethyl sulfate mutational profiling with sequencing (DMS-MaPseq) prepared from leaves of adult plants in Arabidopsis. Chromatin remodeling factor 2 (CHR2) positively regulates transcription of MIR loci whereas repressing microRNA (miRNA) accumulation in vivo. CHR2 can directly bind to and unwind primary miRNAs (pri-miRNAs) and inhibit their processing; and this inhibition entails its remodeling activity in vitro and in vivo.

2018-05-18 | GSE108857 | GEO

SWI/SNF subunit CHR2 remodels pri-miRNAs via microprocessor component SE to inhibit miRNA production

Project description:SWI/SNF subunit CHR2 remodels pri-miRNAs via microprocessor component SE to inhibit miRNA production

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SWI/SNF subunit CHR2 remodels pri-miRNAs via microprocessor component SE to inhibit miRNA production (miRNA-Seq)

Project description:SWI/SNF subunit CHR2 remodels pri-miRNAs via microprocessor component SE to inhibit miRNA production (miRNA-Seq)

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SWI/SNF subunit CHR2 remodels pri-miRNAs via microprocessor component SE to inhibit miRNA production DMS-MaPseq)

Project description:SWI/SNF subunit CHR2 remodels pri-miRNAs via microprocessor component SE to inhibit miRNA production DMS-MaPseq)

| PRJNA428974 | ENA

A commercial antibody to the human condensin II subunit NCAPH2 cross-reacts with a SWI/SNF complex component.

Project description:Condensin complexes compact and disentangle chromosomes in preparation for cell division. Commercially available antibodies raised against condensin subunits have been widely used to characterise their cellular interactome. Here we have assessed the specificity of a polyclonal antibody (Bethyl A302-276A) that is commonly used as a probe for NCAPH2, the kleisin subunit of condensin II, in mammalian cells. We find that, in addition to its intended target, this antibody cross-reacts with one or more components of the SWI/SNF family of chromatin remodelling complexes in an NCAPH2-independent manner. This cross-reactivity, with an abundant chromatin-associated factor, is likely to affect the interpretation of protein and chromatin immunoprecipitation experiments that make use of this antibody probe.

| S-EPMC7863998 | biostudies-literature

Suppression of the SWI/SNF Component Arid1a Promotes Mammalian Regeneration.

Project description:Mammals have partially lost the extensive regenerative capabilities of some vertebrates, possibly as a result of chromatin-remodeling mechanisms that enforce terminal differentiation. Here, we show that deleting the SWI/SNF component Arid1a substantially improves mammalian regeneration. Arid1a expression is suppressed in regenerating tissues, and genetic deletion of Arid1a increases tissue repair following an array of injuries. Arid1a deficiency in the liver increases proliferation, reduces tissue damage and fibrosis, and improves organ function following surgical resection and chemical injuries. Hepatocyte-specific deletion is also sufficient to increase proliferation and regeneration without excessive overgrowth, and global Arid1a disruption potentiates soft tissue healing in the ear. We show that Arid1a loss reprograms chromatin to restrict promoter access by transcription factors such as C/ebpα, which enforces differentiation, and E2F4, which suppresses cell-cycle re-entry. Thus, epigenetic reprogramming mediated by deletion of a single gene improves mammalian regeneration and suggests strategies to promote tissue repair after injury.

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Paraspeckles interact with SWI/SNF subunit ARID1B to regulate transcription and splicing.

Project description:Paraspeckles are subnuclear RNA-protein structures that are implicated in important processes including cellular stress response, differentiation, and cancer progression. However, it is unclear how paraspeckles impart their physiological effect at the molecular level. Through biochemical analyses, we show that paraspeckles interact with the SWI/SNF chromatin-remodeling complex. This is specifically mediated by the direct interaction of the long-non-coding RNA NEAT1 of the paraspeckles with ARID1B of the cBAF-type SWI/SNF complex. Strikingly, ARID1B depletion, in addition to resulting in loss of interaction with the SWI/SNF complex, decreases the binding of paraspeckle proteins to chromatin modifiers, transcription factors, and histones. Functionally, the loss of ARID1B and NEAT1 influences the transcription and the alternative splicing of a common set of genes. Our findings reveal that dynamic granules such as the paraspeckles may leverage the specificity of epigenetic modifiers to impart their regulatory effect, thus providing a molecular basis for their function.

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The SWI/SNF subunit Bcl7a contributes to motor coordination and Purkinje cell function.

Project description:Chromatin remodelers have emerged as prominent regulators of epigenetic processes and potential drivers of various human pathologies. The multi-subunit chromatin-remodeling SWI/SNF complex determines gene expression programs and, consequently, contributes to the differentiation, maturation and plasticity of neurons. Here, we investigate the elusive biological function of Bcl7a and Bcl7b, two newly identified subunits of the SWI/SNF complex that are highly expressed throughout the brain. We generated ubiquitous and neuron-specific Bcl7a and Bcl7b single and double knockout mice. We provide evidence that Bcl7b is dispensable for animal survival as well as behavioral plasticity. Conversely, ubiquitous Bcl7a knockout results in perinatal lethality, while genetic deletion of Bcl7a in postmitotic neurons elicits motor abnormalities and affects dendritic branching of Purkinje cells, with no obvious synergistic relationship with Bcl7b. Collectively, our findings reveal novel insights into the cellular processes linked to BCL7-containing SWI/SNF complexes and their unrecognized roles in the brain.

| S-EPMC5719005 | biostudies-literature

The SWI/SNF chromatin-remodeling complex subunit SNF5 is essential for hepatocyte differentiation.

Project description:Regulation of gene expression underlies cell differentiation and organogenesis. Both transcription factors and chromatin modifiers are crucial for this process. To study the role of the ATP-dependent SWI/SNF chromatin-remodeling complex in cell differentiation, we inactivated the gene encoding the core complex subunit SNF5/INI1 in the developing liver. Hepatic SNF5 deletion caused neonatal death due to severe hypoglycemia; mutant animals fail to store glycogen and have impaired energetic metabolism. The formation of a hepatic epithelium is also affected in SNF5-deficient livers. Transcriptome analyses showed that SNF5 inactivation is accompanied by defective transcriptional activation of 70% of the genes that are normally upregulated during liver development. These include genes involved in glycogen synthesis, gluconeogenesis and cell-cell adhesion. A fraction of hepatic developmentally activated genes were normally expressed, suggesting that cell differentiation was not completely blocked. Moreover, SNF5-deleted cells showed increased proliferation and we identified several misexpressed genes that may contribute to cell cycle deregulation in these cells. Our results emphasize the role of chromatin remodeling in the activation of cell-type-specific genetic programs and driving cell differentiation.

| S-EPMC1224692 | biostudies-literature

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