Exploring the Interaction between the SWI/SNF Chromatin Remodeling Complex and the Zinc Finger Factor CTCF

Valletta, Mariangela; Russo, Rosita; Baglivo, Ilaria; Russo, Veronica; Ragucci, Sara; Sandomenico, Annamaria; Iaccarino, Emanuela; Ruvo, Menotti; Feis, Italia De; Angelini, Claudia; Iachettini, Sara; Biroccio, Annamaria; Pedone, Paolo V.

doi:10.3390/ijms21238950

Cited by 15 publications

(11 citation statements)

References 54 publications

(98 reference statements)

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“…As a consequence, the BRG1 ATPase subunit of the BAF complex continuously maintains enhancers with open chromatin for binding of OSK and promotes the removal of flanking nucleosomes for occupancy of additional TFs [ 66 , 67 ] . BRG1 also interacts directly with the transcription factor CCCTC-binding factor (CTCF), which plays a role in largescale genome organization [ 68 , 69 ] .…”

Section: Muc1-c Drives Lineage Plasticity and Epigenetic Remodeling I...mentioning

confidence: 99%

Chronic activation of MUC1-C in wound repair promotes progression to cancer stem cells

Küfe¹

2022

J Cancer Metastasis Treat

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The mucin 1 (MUC1) gene emerged in mammals to afford protection of barrier epithelial tissues from the external environment. MUC1 encodes a transmembrane C-terminal (MUC1-C) subunit that is activated by loss of homeostasis and induces inflammatory, proliferative, and remodeling pathways associated with wound repair. As a consequence, chronic activation of MUC1-C promotes lineage plasticity, epigenetic reprogramming, and carcinogenesis. In driving cancer progression, MUC1-C is imported into the nucleus, where it induces NF-κB inflammatory signaling and the epithelial-mesenchymal transition (EMT). MUC1-C represses gene expression by activating (i) DNA methyltransferase 1 (DNMT1) and DNMT3b, (ii) Polycomb Repressive Complex 1 (PRC1) and PRC2, and (iii) the nucleosome remodeling and deacetylase (NuRD) nucleosome complex. PRC1/2-mediated gene repression is counteracted by the SWI/SNF chromatin remodeling complexes. MUC1-C activates the SWI/SNF BAF and PBAF complexes in cancer stem cell (CSC) models with the induction of genome-wide differentially accessible regions and expressed genes. MUC1-C regulates chromatin accessibility of enhancer-like signatures in association with the induction of the Yamanaka pluripotency factors and recruitment of JUN and BAF, which promote increases in histone activation marks and opening of chromatin. These and other findings described in this review have uncovered a pivotal role for MUC1-C in integrating lineage plasticity and epigenetic reprogramming, which are transient in wound repair and sustained in promoting CSC progression.

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Section: Muc1-c Drives Lineage Plasticity and Epigenetic Remodeling I...mentioning

confidence: 99%

Chronic activation of MUC1-C in wound repair promotes progression to cancer stem cells

Küfe¹

2022

J Cancer Metastasis Treat

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“…BPTF is a subunit of the SNF2Lcontaining chromatin remodeler complex that has been shown to be involved in positioning nucleosomes around CTCF sites and keeping CTCF sites accessible (Barisic et al, 2019;Wiechens et al, 2016). BPTF has also been found to co-occupy CTCF sites (Valletta et al, 2020).…”

Section: Genetic Dependency Between Ctcf and Rna Processing Proteins Identified By A Loss Of Function Crispr Screen After Ctcf Depletionmentioning

confidence: 99%

A cohesin traffic pattern genetically linked to gene regulation

Valton

Venev

Mair

et al. 2021

Preprint

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Cohesin-mediated loop extrusion folds interphase chromosomes at the ten to hundreds kilobases scale. This process produces structural features such as loops and topologically associating domains. We identify three types of cis-elements that define the chromatin folding landscape generated by loop extrusion. First, CTCF sites form boundaries by stalling extruding cohesin, as shown before. Second, transcription termination sites form boundaries by acting as cohesin unloading sites. RNA polymerase II contributes to boundary formation at transcription termination sites. Third, transcription start sites form boundaries that are mostly independent of cohesin, but are sites where cohesin can pause. Together with cohesin loading at enhancers, and possibly other cis-elements, these loci create a dynamic pattern of cohesin traffic along the genome that guides enhancer-promoter interactions. Disturbing this traffic pattern, by removing CTCF barriers, renders cells sensitive to knock-out of genes involved in transcription initiation, such as the SAGA and TFIID complexes, and RNA processing such DEAD-Box RNA helicases. In the absence of CTCF, several of these factors fail to be efficiently recruited to active promoters. We propose that the complex pattern of cohesin movement along chromatin contributes to appropriate promoter-enhancer interactions and localization of transcription and RNA processing factors to active genes.

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“…The clustered heatmap of the proteins that were differentially expressed in at least one out of three treatments was generated by using CIMminer free tool ( accessed on 15 March 2021) with unsupervised clustering on both axes and the following parameters: average linkage, Euclidean distance and equal width binning. Molecular function enrichment analysis was performed by using the ClueGO plug-in of Cytoscape 3.6.0 to generate a functionally grouped GO/pathway term network of enriched molecular function categories for the identified proteins based on kappa statistics [ 44 ].…”

Section: Methodsmentioning

confidence: 99%

Deciphering Molecular Determinants Underlying Penicillium digitatum’s Response to Biological and Chemical Antifungal Agents by Tandem Mass Tag (TMT)-Based High-Resolution LC-MS/MS

Citores

Valletta

Singh

et al. 2022

IJMS

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Penicillium digitatum is a widespread pathogen responsible for the postharvest decay of citrus, one of the most economically important crops worldwide. Currently, chemical fungicides are still the main strategy to control the green mould disease caused by the fungus. However, the increasing selection and proliferation of fungicide-resistant strains require more efforts to explore new alternatives acting via new or unexplored mechanisms for postharvest disease management. To date, several non-chemical compounds have been investigated for the control of fungal pathogens. In this scenario, understanding the molecular determinants underlying P. digitatum’s response to biological and chemical antifungals may help in the development of safer and more effective non-chemical control methods. In this work, a proteomic approach based on isobaric labelling and a nanoLC tandem mass spectrometry approach was used to investigate molecular changes associated with P. digitatum’s response to treatments with α-sarcin and beetin 27 (BE27), two proteins endowed with antifungal activity. The outcomes of treatments with these biological agents were then compared with those triggered by the commonly used chemical fungicide thiabendazole (TBZ). Our results showed that differentially expressed proteins mainly include cell wall-degrading enzymes, proteins involved in stress response, antioxidant and detoxification mechanisms and metabolic processes such as thiamine biosynthesis. Interestingly, specific modulations in response to protein toxins treatments were observed for a subset of proteins. Deciphering the inhibitory mechanisms of biofungicides and chemical compounds, together with understanding their effects on the fungal physiology, will provide a new direction for improving the efficacy of novel antifungal formulations and developing new control strategies.

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Exploring the Interaction between the SWI/SNF Chromatin Remodeling Complex and the Zinc Finger Factor CTCF

Cited by 15 publications

References 54 publications

Chronic activation of MUC1-C in wound repair promotes progression to cancer stem cells

Chronic activation of MUC1-C in wound repair promotes progression to cancer stem cells

A cohesin traffic pattern genetically linked to gene regulation

Deciphering Molecular Determinants Underlying Penicillium digitatum’s Response to Biological and Chemical Antifungal Agents by Tandem Mass Tag (TMT)-Based High-Resolution LC-MS/MS

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