Multiple functions of SWI/SNF chromatin remodeling complex in plant-pathogen interactions

AbstractThe SWI/SNF chromatin remodeling complex utilizes the energy of ATP hydrolysis to facilitate chromatin access and plays essential roles in DNA-based events. Studies in animals, plants and fungi have uncovered sophisticated regulatory mechanisms of this complex that govern development and various stress responses. In this review, we summarize the composition of SWI/SNF complex in eukaryotes and discuss multiple functions of the SWI/SNF complex in regulating gene transcription, mRNA splicing, and DNA damage response. Our review further highlights the importance of SWI/SNF complex in regulating plant immunity responses and fungal pathogenesis. Finally, the potentials in exploiting chromatin remodeling for management of crop disease are presented.

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Cryo-electron microscopy structure of a nucleosome-bound SWI/SNF chromatin remodeling complex

10.1101/805184 ◽

2019 ◽

Cited By ~ 2

Author(s):

Yan Han ◽

Alexis A Reyes ◽

Sara Malik ◽

Yuan He

Keyword(s):

Electron Microscopy ◽

Chromatin Remodeling ◽

Atp Hydrolysis ◽

Protein Complexes ◽

Gene Activation ◽

The Body ◽

Cellular Processes ◽

Cryo Electron Microscopy ◽

Chromatin Remodeling Complex ◽

High Resolution Structure

AbstractThe multi-subunit chromatin remodeling complex SWI/SNF1–3 is highly conserved from yeast to humans and plays critical roles in various cellular processes including transcription and DNA damage repair4, 5. It uses the energy from ATP hydrolysis to remodel chromatin structure by sliding and evicting the histone octamer6–10, creating DNA regions that become accessible to other essential protein complexes. However, our mechanistic understanding of the chromatin remodeling activity is largely hindered by the lack of a high-resolution structure of any complex from this family. Here we report the first structure of SWI/SNF from the yeast S. cerevisiae bound to a nucleosome at near atomic resolution determined by cryo-electron microscopy (cryo-EM). In the structure, the Arp module is sandwiched between the ATPase and the Body module of the complex, with the Snf2 HSA domain connecting all modules. The HSA domain also extends into the Body and anchors at the opposite side of the complex. The Body contains an assembly scaffold composed of conserved subunits Snf12 (SMARCD/BAF60), Snf5 (SMARCB1/BAF47/ INI1) and an asymmetric dimer of Swi3 (SMARCC/BAF155/170). Another conserved subunit Swi1 (ARID1/BAF250) folds into an Armadillo (ARM) repeat domain that resides in the core of the SWI/SNF Body, acting as a molecular hub. In addition to the interaction between Snf2 and the nucleosome, we also observed interactions between the conserved Snf5 subunit and the histones at the acidic patch, which could serve as an anchor point during active DNA translocation. Our structure allows us to map and rationalize a subset of cancer-related mutations in the human SWI/SNF complex and propose a model of how SWI/SNF recognizes and remodels the +1 nucleosome to generate nucleosome-depleted regions during gene activation11–13.

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BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration

Nature Communications ◽

10.1038/s41467-019-12573-z ◽

2019 ◽

Vol 10 (1) ◽

Cited By ~ 9

Author(s):

Min Liu ◽

Tongyu Sun ◽

Ni Li ◽

Junjie Peng ◽

Da Fu ◽

...

Keyword(s):

Chromatin Remodeling ◽

Stress Responses ◽

Inflammatory Diseases ◽

Central Component ◽

Intestinal Epithelial ◽

Potential Therapeutic Target ◽

Atpase Subunit ◽

Colon Inflammation ◽

Chromatin Remodeling Complex ◽

Inflammatory Bowel

Abstract Autophagy is a central component of integrated stress responses that influences many inflammatory diseases, including inflammatory bowel disease (IBD) and colorectal cancer (CRC). While the core machinery is known, the molecular basis of the epigenetic regulation of autophagy and its role in colon inflammation remain largely undefined. Here, we report that BRG1, an ATPase subunit of the SWI/SNF chromatin remodeling complex, is required for the homeostatic maintenance of intestinal epithelial cells (IECs) to prevent the inflammation and tumorigenesis. BRG1 emerges as a key regulator that directly governs the transcription of Atg16l1, Ambra1, Atg7 and Wipi2, which are important for autophagosome biogenesis. Defective autophagy in BRG1-deficient IECs results in excess reactive oxygen species (ROS), which leads to the defects in barrier integrity. Together, our results establish that BRG1 may represent an autophagy checkpoint that is pathogenetically linked to colitis and is therefore likely a potential therapeutic target for disease intervention.

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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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