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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

| PRJNA428953 | ENA

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)

| PRJNA428977 | ENA

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.

| S-EPMC4826298 | biostudies-literature

BCL7B, a SWI/SNF complex subunit, orchestrates cancer immunity and stemness.

Project description:Cancer is one of the main causes of human death. Here, we focus on the B-cell lymphoma 7 protein family member B (BCL7B) gene, an accessory subunit of the SWI/SNF chromatin-remodelling complex. To characterize the function of BCL7B, heterozygous BCL7B-deficient stomach cancer cell lines were generated with the CRISPR/Cas9 genome editing system. The comprehensive gene expression patterns were compared between parental cells and each ΔBCL7B cell line by RNA-seq. The results showed marked downregulation of immune-related genes and upregulation of stemness-related genes in the ΔBCL7B cell lines. Moreover, by ChIP-seq analysis with H3K27me3 antibody, the changes of epigenetic modification sequences were compared between parental cells and each ΔBCL7B cell line. After machine learning, we detected the centroid sequence changes, which exerted an impact on antigen presentation. The regulation of BCL7B expression in cancer cells gives rise to cancer stem cell-like characteristics and the acquisition of an immune evasion phenotype.

| S-EPMC10466690 | biostudies-literature

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.

| S-EPMC9827562 | biostudies-literature

SWI/SNF chromatin remodeling subunit Smarca4/BRG1 is essential for female fertility†.

Project description:Mammalian folliculogenesis is a complex process that involves the regulation of chromatin structure for gene expression and oocyte meiotic resumption. The SWI/SNF complex is a chromatin remodeler using either Brahma-regulated gene 1 (BRG1) or BRM (encoded by Smarca4 and Smarca2, respectively) as its catalytic subunit. SMARCA4 loss of expression is associated with a rare type of ovarian cancer; however, its function during folliculogenesis remains poorly understood. In this study, we describe the phenotype of BRG1 mutant mice to better understand its role in female fertility. Although no tumor emerged from BRG1 mutant mice, conditional depletion of Brg1 in the granulosa cells (GCs) of Brg1fl/fl;Amhr2-Cre mice caused sterility, whereas conditional depletion of Brg1 in the oocytes of Brg1fl/fl;Gdf9-Cre mice resulted in subfertility. Recovery of cumulus-oocyte complexes after natural mating or superovulation showed no significant difference in the Brg1fl/fl;Amhr2-Cre mutant mice and significantly fewer oocytes in the Brg1fl/fl;Gdf9-Cre mutant mice compared with controls, which may account for the subfertility. Interestingly, the evaluation of oocyte developmental competence by in vitro culture of retrieved two-cell embryos indicated that oocytes originating from the Brg1fl/fl;Amhr2-Cre mice did not reach the blastocyst stage and had higher rates of mitotic defects, including micronuclei. Together, these results indicate that BRG1 plays an important role in female fertility by regulating granulosa and oocyte functions during follicle growth and is needed for the acquisition of oocyte developmental competence.

| S-EPMC9930400 | biostudies-literature

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