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Transcription Factors Form a Ternary Complex with NIPBL/MAU2 to Localize Cohesin at Enhancers

ABSTRACT: Transcription Factors Form a Ternary Complex with NIPBL/MAU2 to Localize Cohesin at Enhancers

PROVIDER: PRJNA1189196 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31439428_1.fastq.gz	Fastqsanger.gz
	SRR31439428_2.fastq.gz	Fastqsanger.gz
	SRR31439429_1.fastq.gz	Fastqsanger.gz
	SRR31439429_2.fastq.gz	Fastqsanger.gz
	SRR31439430_1.fastq.gz	Fastqsanger.gz

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Transcription factors form a ternary complex with NIPBL/MAU2 to localize cohesin at enhancers

Project description:While the cohesin complex is a key player in genome architecture, how it localizes to specific chromatin sites is not well understood. Recently, we and others have proposed that direct interactions with transcription factors (TFs) lead to the localization of the cohesin-loader complex (NIPBL/MAU2) within enhancers. Here, we identify two clusters of protein-protein interaction (PPI) motifs within the NIPBL sequence that regulate NIPBL dynamics, interactome, and NIPBL-dependent transcriptional programs. These PPIMs directly interact with chromatin-associated proteins, including TFs and one of them is necessary for the maintenance of the NIPBL-MAU2 heterodimer. Finally, using the glucocorticoid receptor (GR) as a model, we investigate its interaction surfaces with NIPBL and MAU2 using AlphaFold2 and surface plasmon resonance to uncover a TF-NIPBL-MAU2 ternary complex and present its importance in GR-dependent gene regulation.

2025-04-17 | PXD058574 | Pride

Transcription Factors Form a Ternary Complex with NIPBL/MAU2 to Localize Cohesin at Enhancers

Project description:The cohesin complex is a key player in dynamic genome architecture adjustments. The loading of the cohesin complex on chromatin is believed to be achieved by the cohesin-loader Nipped-B homolog (NIPBL). Recently, we and others proposed that direct interactions with transcriptions factors (TFs) would lead to accurate positioning of NIPBL on the DNA. In this study, we identified remarkable protein-protein interaction motifs (PPIMs) in the NIPBL sequence. Mutations of those motifs dramatically alters: (i) the global NIPBL chromatin binding, (ii) the NIPBL-dependent transcriptional program and (iii) the NIPBL proteome network including TFs. While we found that the MAU2/NIPBL interaction was relying on those PPIMs, we further discovered that MAU2 was directly interacting with dozens of TFs. Concomitantly, we found that numerous TFs were also able to interact with NIPBL through PPIMs. Finally, using nuclear receptors as models and then focusing on the Glucocorticoid Receptor (GR), we mechanistically dissect a trimeric complex formed by GR, NIPBL and MAU2 and investigate the importance of those interactions for GR transcriptional program.

2025-04-16 | GSE282583 | GEO

Transcription factors form a ternary complex with NIPBL/MAU2 to localize cohesin at enhancers.

Project description: Not available

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MAU2 and NIPBL variants in Cornelia de Lange syndrome reveal MAU2-independent loading of cohesin and uncover protective mechanisms against early truncating mutations in NIPBL

Project description:For its association with chromatin, the cohesin complex depends on a heterodimer formed by NIPBL and MAU2. Variants in NIPBL are the main cause of CdLS and result in NIPBL haploinsufficiency. Using CRISPR, we generated cells homozygous for an out-of-frame duplication in NIPBL. Remarkably, alternative translation initiation rescued NIPBL expression in these cells and produced an N-terminally truncated NIPBL that lacks MAU2-interaction domain, causing a dramatic reduction of MAU2 protein levels while a lot of NIPBL functions remain intact.

2020-06-10 | GSE122299 | GEO

ChIP-seq to measure binding of NIPBL/MAU2, RAD21, and CTCF in mouse embryonic stem cells and neural progenitor cells

Project description:Mammalian chromosomes are folded by the cohesin complex, which creates chromatin loops that are extruded as cohesin translocates along the chromatin fiber. This dynamic process regulates gene expression by controlling the frequency of contacts between enhancers and promoters. We analyzed where in the genome loop extrusion occurs to discover where extrusion initiates and whether particular regions are extruded more than others. We measured NIPBL/MAU2 binding in mouse embryonic stem cells and neural progenitor cells, and found that NIPBL/MAU2 is enriched at enhancers compared to promoters. We used the amount of cohesin binding at CTCF sites as a readout of cohesin traffic, and found that the NIPBL/MAU2 binding sites only modestly boost nearby cohesin levels.

2025-09-27 | GSE278338 | GEO

MAU2 and NIPBL variants in Cornelia de Lange syndrome reveal MAU2-independent loading of cohesin and uncover protective mechanisms against early truncating mutations in NIPBL

Project description:MAU2 and NIPBL variants in Cornelia de Lange syndrome reveal MAU2-independent loading of cohesin and uncover protective mechanisms against early truncating mutations in NIPBL

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Pioneer factors orchestrate tissue-specific cohesin-NIPBL chromatin entry and 3D genome organization

Project description:Cohesin complex shapes 3D genome organization by extruding DNA loops, yet the mechanisms underlying its chromatin entry remain poorly understood. Here, we reveal that the cohesin loader NIPBL exhibits highly tissue-specific chromatin binding, in stark contrast to the conserved binding profiles of CTCF and RAD21. We identify pioneer transcription factors (TFs), notably FOXA1, as key mediators of NIPBL recruitment to chromatin. FOXA1 directs NIPBL to intra-TAD regions, enabling symmetric loop extrusion, while factors like ETS1 target NIPBL to TAD boundaries, supporting one-sided extrusion. Rapid depletion of FOXA1 disrupts NIPBL binding and intra-TAD loops, whereas loss of NIPBL impairs both intra-TAD and inter-TAD interactions, highlighting their roles in 3D genome folding. Strikingly, a recurrent FOXA1 mutation (R219S) in prostate cancer redirects NIPBL to TAD boundaries by recognizing a non-canonical motif, fostering a more insulated and tumor-aggressive genome. Evolutionary analysis points to a potential conserved role for TF-NIPBL cooperation in cohesin chromatin entry across species with tissue-specific adaptations. Our findings reveal that pioneer factors orchestrate cohesin loading to shape tissue-specific chromatin accessibility and 3D genome dynamics, a mechanism hijacked in diseases like cancer to rewire gene expression.

2026-05-07 | GSE293071 | GEO