The Core Subunit of A Chromatin-Remodeling Complex, ZmCHB101, Plays Essential Roles in Maize Growth and Development

AbstractSCHLAP1 is a long-noncoding RNA that is prognostic for progression to metastatic prostate cancer and promotes an invasive phenotype. SCHLAP1 is reported to function by depleting the core SWI/SNF subunit, SMARCB1, from the genome. SWI/SNF is a large, multi-subunit, chromatin remodeling complex that can be combinatorially assembled to yield hundreds to thousands of distinct complexes. Here, we investigated the hypothesis that SCHLAP1 affects only specific forms of SWI/SNF and that the remaining SWI/SNF complexes were important for the increased invasion in SCHLAP1 expressing prostate cells. Using several assays we found that SWI/SNF is not depleted from the genome by SCHLAP1 expression. We find that SCHLAP1 induces changes to chromatin openness but is not sufficient to drive changes in histone modifications. Additionally, we show that SWI/SNF binds many coding and non-coding RNAs. Together these results suggest that SCHLAP1 has roles independent of canonical SWI/SNF and that SWI/SNF broadly interacts with RNA.

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Piwi suppresses transcription of Brahma-dependent transposons via Maelstrom in ovarian somatic cells

Science Advances ◽

10.1126/sciadv.aaz7420 ◽

2020 ◽

Vol 6 (50) ◽

pp. eaaz7420

Author(s):

Ryo Onishi ◽

Kaoru Sato ◽

Kensaku Murano ◽

Lumi Negishi ◽

Haruhiko Siomi ◽

...

Keyword(s):

Rna Polymerase ◽

Rna Polymerase Ii ◽

Chromatin Remodeling ◽

Adenosine Triphosphatase ◽

Somatic Cells ◽

Pol Ii ◽

Heterochromatin Formation ◽

Rna Transcripts ◽

The Core ◽

Chromatin Remodeling Complex

Drosophila Piwi associates with PIWI-interacting RNAs (piRNAs) and represses transposons transcriptionally through heterochromatinization; however, this process is poorly understood. Here, we identify Brahma (Brm), the core adenosine triphosphatase of the SWI/SNF chromatin remodeling complex, as a new Piwi interactor, and show Brm involvement in activating transcription of Piwi-targeted transposons before silencing. Bioinformatic analyses indicated that Piwi, once bound to target RNAs, reduced the occupancies of SWI/SNF and RNA polymerase II (Pol II) on target loci, abrogating transcription. Artificial piRNA-driven targeting of Piwi to RNA transcripts enhanced repression of Brm-dependent reporters compared with Brm-independent reporters. This was dependent on Piwi cofactors, Gtsf1/Asterix (Gtsf1), Panoramix/Silencio (Panx), and Maelstrom (Mael), but not Eggless/dSetdb (Egg)–mediated H3K9me3 deposition. The λN-box B–mediated tethering of Mael to reporters repressed Brm-dependent genes in the absence of Piwi, Panx, and Gtsf1. We propose that Piwi, via Mael, can rapidly suppress transcription of Brm-dependent genes to facilitate heterochromatin formation.

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ATPase SRCAP is a new player in cell division, uncovering molecular aspects of Floating-Harbor syndrome

10.1101/2020.09.12.294645 ◽

2020 ◽

Cited By ~ 1

Author(s):

Giovanni Messina ◽

Yuri Prozzillo ◽

Francesca Delle Monache ◽

Maria Virginia Santopietro ◽

Maria Teresa Atterrato ◽

...

Keyword(s):

Cell Division ◽

Chromatin Remodeling ◽

Catalytic Subunit ◽

Current View ◽

Mitotic Apparatus ◽

Direct Role ◽

The Core ◽

Chromatin Remodeling Complex ◽

Evolutionarily Conserved ◽

Floating Harbor Syndrome

AbstractFloating-Harbor syndrome (FHS) is a rare genetic disease affecting human development caused by heterozygous truncating mutations in the Srcap gene, which encodes the ATPase SRCAP, the core catalytic subunit of the homonymous chromatin-remodeling complex. Using a combined approach, we studied the involvement of SRCAP protein in cell cycle progression in HeLa cells. In addition to the canonical localization in interphase nuclei, both SRCAP and its Drosophila orthologue DOMINO-A localized to the mitotic apparatus after nuclear envelope breakdown. Moreover, SRCAP and DOMINO-A depletion impaired mitosis and cytokinesis in human and Drosophila cells, respectively. Importantly, SRCAP interacted with several cytokinesis regulators at telophase, strongly supporting a direct role in cytokinesis, independent of its chromatin remodeling functions. Our results provide clues about previously undetected, evolutionarily conserved roles of SRCAP in ensuring proper mitosis and cytokinesis. We propose that perturbations in cell division contribute to the onset of developmental defects characteristic of FHS.SummarySignificance statementSrcap is the causative gene of the rare Floating Harbor syndrome (FHS). It encodes the ATPase SRCAP, the core catalytic subunit of the homonymous multiprotein chromatin-remodeling complex in humans, which promotes the exchange of canonical histone H2A with the H2A.Z variant. According to the current view on SRCAP protein functions, FHS is caused by chromatin remodeling defects. Our findings suggest that, in addition to the established function as epigenetic regulator, SRCAP plays previously undetected and evolutionarily conserved roles in cell division. Hence, we propose that perturbations in cell division produced by SRCAP mutations are important causative factors co-occurring at the onset of FHS.

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INO80 requires a polycomb subunit to regulate the establishment of poised chromatin in murine spermatocytes

Development ◽

10.1242/dev.200089 ◽

2022 ◽

Vol 149 (1) ◽

Author(s):

Prabuddha Chakraborty ◽

Terry Magnuson

Keyword(s):

Chromatin Remodeling ◽

Binding Sites ◽

Strand Break ◽

Rna Seq ◽

Genome Wide Analysis ◽

The Core ◽

Chromatin Remodeling Complex ◽

Genome Wide ◽

Dna Double Strand Break ◽

Transcription Program

ABSTRACT INO80 is the catalytic subunit of the INO80-chromatin remodeling complex that is involved in DNA replication, repair and transcription regulation. Ino80 deficiency in murine spermatocytes (Ino80cKO) results in pachytene arrest of spermatocytes due to incomplete synapsis and aberrant DNA double-strand break repair, which leads to apoptosis. RNA-seq on Ino80cKO spermatocytes revealed major changes in transcription, indicating that an aberrant transcription program arises upon INO80 depletion. In Ino80WT spermatocytes, genome-wide analysis showed that INO80-binding sites were mostly promoter proximal and necessary for the regulation of spermatogenic gene expression, primarily of premeiotic and meiotic genes. Furthermore, most of the genes poised for activity, as well as those genes that are active, shared INO80 binding. In Ino80cKO spermatocytes, most poised genes demonstrated de-repression due to reduced H3K27me3 enrichment and, in turn, showed increased expression levels. INO80 interacts with the core PRC2 complex member SUZ12 and promotes its recruitment. Furthermore, INO80 mediates H2A.Z incorporation at the poised promoters, which was reduced in Ino80cKO spermatocytes. Taken together, INO80 is emerging as a major regulator of the meiotic transcription program by mediating poised chromatin establishment through SUZ12 binding.

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A specialized condensin complex participates in somatic nuclear maturation in Tetrahymena thermophila

Molecular Biology of the Cell ◽

10.1091/mbc.e18-08-0487 ◽

2019 ◽

Vol 30 (11) ◽

pp. 1326-1338 ◽

Cited By ~ 3

Author(s):

Rachel Howard-Till ◽

Miao Tian ◽

Josef Loidl

Keyword(s):

Sexual Reproduction ◽

Chromatin Remodeling ◽

Nuclear Division ◽

Tetrahymena Thermophila ◽

Vegetative Cells ◽

Nuclear Maturation ◽

The Core ◽

Condensin Complex ◽

Chromatin Remodeling Complex ◽

Putative Member

Condensins are highly conserved proteins that are important for chromosome maintenance in nearly all forms of life. Although many organisms employ two forms of the condensin complex, the condensin genes in Tetrahymena have expanded even further. Here we report a form of condensin that is specifically active during sexual reproduction. This complex, condensin D, is composed of the core condensin proteins, Smc2 and Smc4, and two unique subunits, the kleisin Cph5 and Cpd2. Cpd2 is also found in somatic nuclei in vegetative cells, but is dispensable for growth and nuclear division. Immunoprecipitation experiments show that condensin D interacts with a putative member of a chromatin-remodeling complex during development. Condensin D is required for sexual reproduction and for endoreplication and genome reduction of the progeny’s somatic nuclei. Altogether, Tetrahymena possesses at least four forms of condensin to fulfill the needs of maintaining chromosomes in two different nuclei containing the somatic and germline genomes.

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Faculty Opinions recommendation of The chromatin-remodeling complex WINAC targets a nuclear receptor to promoters and is impaired in Williams syndrome.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1014780.194751 ◽

2003 ◽

Author(s):

Giovanni Neri

Keyword(s):

Nuclear Receptor ◽

Chromatin Remodeling ◽

Williams Syndrome ◽

Chromatin Remodeling Complex

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Regulation of Egr1 Target Genes by the Nurd Chromatin Remodeling Complex

10.21236/ada486655 ◽

2008 ◽

Author(s):

John Svaren

Keyword(s):

Chromatin Remodeling ◽

Target Genes ◽

Chromatin Remodeling Complex

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Actin-Related Protein 4 Interacts with PIE1 and Regulates Gene Expression in Arabidopsis

Genes ◽

10.3390/genes12040520 ◽

2021 ◽

Vol 12 (4) ◽

pp. 520

Author(s):

Wenfeng Nie ◽

Jinyu Wang

Keyword(s):

Gene Expression ◽

Plant Growth ◽

Chromatin Remodeling ◽

Leaf Size ◽

Early Flowering ◽

Physical Interaction ◽

Loss Of Function ◽

Single Nucleotide Change ◽

Chromatin Remodeling Complex ◽

Related Proteins

As essential structural components of ATP-dependent chromatin-remodeling complex, the nucleolus-localized actin-related proteins (ARPs) play critical roles in many biological processes. Among them, ARP4 is identified as an integral subunit of chromatin remodeling complex SWR1, which is conserved in yeast, humans and plants. It was shown that RNAi mediated knock-down of Arabidopsis thaliana ARP4 (AtARP4) could affect plant development, specifically, leading to early flowering. However, so far, little is known about how ARP4 functions in the SWR1 complex in plant. Here, we identified a loss-of-function mutant of AtARP4 with a single nucleotide change from glycine to arginine, which had significantly smaller leaf size. The results from the split luciferase complementation imaging (LCI) and yeast two hybrid (Y2H) assays confirmed its physical interaction with the scaffold and catalytic subunit of SWR1 complex, photoperiod-independent early flowering 1 (PIE1). Furthermore, mutation of AtARP4 caused altered transcription response of hundreds of genes, in which the number of up-regulated differentially expressed genes (DEGs) was much larger than those down-regulated. Although most DEGs in atarp4 are related to plant defense and response to hormones such as salicylic acid, overall, it has less overlapping with other swr1 mutants and the hta9 hta11 double-mutant. In conclusion, our results reveal that AtARP4 is important for plant growth and such an effect is likely attributed to its repression on gene expression, typically at defense-related loci, thus providing some evidence for the coordination of plant growth and defense, while the regulatory patterns and mechanisms are distinctive from other SWR1 complex components.

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Interplay of BAF and MLL4 promotes cell type-specific enhancer activation

Nature Communications ◽

10.1038/s41467-021-21893-y ◽

2021 ◽

Vol 12 (1) ◽

Cited By ~ 1

Author(s):

Young-Kwon Park ◽

Ji-Eun Lee ◽

Zhijiang Yan ◽

Kaitlin McKernan ◽

Tommy O’Haren ◽

...

Keyword(s):

Cell Differentiation ◽

Chromatin Remodeling ◽

Direct Evidence ◽

Cell Type ◽

Chromatin Regulators ◽

Chromatin Remodeling Complex ◽

Histone H3k4 ◽

Cell Type Specific ◽

Pioneer Transcription Factor ◽

Factor C

AbstractCell type-specific enhancers are activated by coordinated actions of lineage-determining transcription factors (LDTFs) and chromatin regulators. The SWI/SNF chromatin remodeling complex BAF and the histone H3K4 methyltransferase MLL4 (KMT2D) are both implicated in enhancer activation. However, the interplay between BAF and MLL4 in enhancer activation remains unclear. Using adipogenesis as a model system, we identify BAF as the major SWI/SNF complex that colocalizes with MLL4 and LDTFs on active enhancers and is required for cell differentiation. In contrast, the promoter enriched SWI/SNF complex PBAF is dispensable for adipogenesis. By depleting BAF subunits SMARCA4 (BRG1) and SMARCB1 (SNF5) as well as MLL4 in cells, we show that BAF and MLL4 reciprocally regulate each other’s binding on active enhancers before and during adipogenesis. By focusing on enhancer activation by the adipogenic pioneer transcription factor C/EBPβ without inducing cell differentiation, we provide direct evidence for an interdependent relationship between BAF and MLL4 in activating cell type-specific enhancers. Together, these findings reveal a positive feedback between BAF and MLL4 in promoting LDTF-dependent activation of cell type-specific enhancers.

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