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Pivotal Role of the NuRD Complex in Remodeling Chromatin Environment and Maintaining Genome Architecture at CTCF Sites [BS-seq]

ABSTRACT: The currently available data of CTCF binding in mammalian cells are exclusively obtained with ChIP-seq. In order to fully retain the dynamic information of CTCF binding, we have developed a new method called GpC-Methylation Assisted Tracing (G-MAT) of a nuclear protein, which leverages DNA cytosine methylation to record the footprints of a protein within a given period of time.

ORGANISM(S): Homo sapiens

PROVIDER: GSE176248 | GEO | 2026/05/04

REPOSITORIES: GEO

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Pivotal Role of the NuRD Complex in Remodeling Chromatin Environment and Maintaining Genome Architecture at CTCF Sites [Hi-C]

Project description:Interactions between nuclear proteins and chromatin are critical in transcriptional regulation. The state-of-the-art approaches provide merely snapshot information on their interactions, which impedes our understanding of the causality in the dynamic regulatory processes. Here, we developed a novel method termed G-MAT that profiles the footprints of a nuclear protein on chromatin and DNA methylome simultaneously in living mammalian cells. Utilizing G-MAT to transcription factor CTCF, we inferred that CTCF searches its binding sites in the genome through stochastic collision to the chromatin. Together with eBioID, which is an enhanced BioID method facilitated by the Suntag system, we found hundreds of proteins with distinct functions co-occupying CTCF binding sites on chromatin, including RNA splicing and chromatin remodeling. Intriguingly, two methyl-CpG binding domain (MBD) proteins were found as interacting partners of CTCF, largely leading CTCF to preferentially bound to methylated DNA segments, consistent with the co-occurrence of CTCF footprints and DNA hyper-methylation when analyzing the G-MAT data at the single-molecule resolution. MBD2, one of the MBD proteins shown to be associated with demethylases, could likely erase DNA methylation near CTCF binding sites, resulting in seemingly anti-correlations between CTCF binding and DNA methylation. Altogether, G-MAT has enabled us to investigate the causal relationship between CTCF target searching and DNA methylation at the single-molecule level, providing an important data resource and novel insights for advanced understanding of transcriptional regulation dynamics.

2026-05-04 | GSE178813 | GEO

Pivotal Role of the NuRD Complex in Remodeling Chromatin Environment and Maintaining Genome Architecture at CTCF Sites [CTCF_MBD2_HT_Me_CAP_SELEX]

Project description:CCCTC-binding factor (CTCF) is an evolutionarily conserved transcription factor with diverse regulatory roles. Around stable CTCF binding sites, nucleosomes are highly ordered and DNA methylation is reduced, yet the mechanisms establishing and maintaining this epigenetic environment remain unclear. Utilizing an innovative eBioID method, we identified that virtually all subunits of the nucleosome remodeling and deacetylase (NuRD) complex are associated with CTCF in cells. Further analyses revealed that the NuRD complex is necessary for the chromatin binding of CTCF, and emerges as a novel regulator of the genome architecture. Additionally, we discovered that MBD3-NuRD facilitates the recruitment of TET demethylases to CTCF sites, initiating local DNA demethylation essential for the activation of adjacent gene expression. Embryonic stem cells deficient in the NuRD complex showed impaired lineage commitment. In summary, this study elucidates a mechanism illustrating the interplay between CTCF binding and the epigenome including 3D genome organization and DNA methylation, with the NuRD complex serving as an indispensable mediator.

2026-05-04 | GSE253695 | GEO