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N-terminal arginine anchor in BCL7A Fine-tunes Chromatin Remodeling and Drives Tumor Suppression in DLBCL [RNA-seq]

ABSTRACT: The hSWI/SNF (BRG1/BRM-associated factor) chromatin remodeling complex plays a critical role in regulating chromatin accessibility and gene expression, with its dysfunction linked to cancer. However, the specific mechanisms by which its subunit BCL7A suppresses tumor growth, particularly in diffuse large B-cell lymphoma (DLBCL), remain unclear. We hypothesized that the N-terminal α-helix of BCL7A, containing a conserved arginine anchor, mediates its interaction with the nucleosome acidic patch to regulate chromatin remodeling and tumor suppression. Our findings reveal that the arginine anchor is essential for BCL7A’s binding to the hSWI/SNF complex and its chromatin remodeling activity. Disruption of this anchor, either through truncation or recurrent DLBCL-associated mutations, abolishes BCL7A’s tumor-suppressive function without affecting its incorporation into the hSWI/SNF complex. Loss of the arginine anchor globally reduces BCL7A occupancy at target loci, impairing chromatin accessibility and transcriptional regulation. In vivo and cellular assays further confirm that the arginine anchor is critical for BCL7A-mediated suppression of tumor growth. This study identifies the BCL7A arginine anchor as a key molecular switch linking nucleosome binding to chromatin remodeling and tumor suppression, offering insights for targeted therapeutic strategies in DLBCL.

ORGANISM(S): Homo sapiens

PROVIDER: GSE296461 | GEO | 2026/05/20

REPOSITORIES: GEO

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N-terminal arginine anchor in BCL7A Fine-tunes Chromatin Remodeling and Drives Tumor Suppression in DLBCL [CUT&Tag]

Project description:The hSWI/SNF (BRG1/BRM-associated factor) chromatin remodeling complex plays a critical role in regulating chromatin accessibility and gene expression, with its dysfunction linked to cancer. However, the specific mechanisms by which its subunit BCL7A suppresses tumor growth, particularly in diffuse large B-cell lymphoma (DLBCL), remain unclear. We hypothesized that the N-terminal α-helix of BCL7A, containing a conserved arginine anchor, mediates its interaction with the nucleosome acidic patch to regulate chromatin remodeling and tumor suppression. Our findings reveal that the arginine anchor is essential for BCL7A’s binding to the hSWI/SNF complex and its chromatin remodeling activity. Disruption of this anchor, either through truncation or recurrent DLBCL-associated mutations, abolishes BCL7A’s tumor-suppressive function without affecting its incorporation into the hSWI/SNF complex. Loss of the arginine anchor globally reduces BCL7A occupancy at target loci, impairing chromatin accessibility and transcriptional regulation. In vivo and cellular assays further confirm that the arginine anchor is critical for BCL7A-mediated suppression of tumor growth. This study identifies the BCL7A arginine anchor as a key molecular switch linking nucleosome binding to chromatin remodeling and tumor suppression, offering insights for targeted therapeutic strategies in DLBCL.

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N-terminal arginine anchor in BCL7A Fine-tunes Chromatin Remodeling and Drives Tumor Suppression in DLBCL [ATAC-seq]

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Frequent mutations on amino-terminal BCL7A domain compromise its tumor suppressor role in DLBCL.

Project description:Mutations in genes encoding the various subunits of the SWI/SNF chromatin remodeling complex are frequently observed in different human cancers. In diffuse large B-cell lymphoma (DLBCL), genetic changes in BCL7A, a subunit of the SWI/SNF complex, have been recently reported but the functional role of such genetic changes remains unknown. BCL7A mutations concentrate at the first exon and the most frequently mutated hotspot is the splice donor site of the first intron. By using in vitro and in vivo analyses, we show that restoration of BCL7A drives a tumor suppressor-like phenotype. Further, we found that splice site mutations block the tumor suppressor phenotype and prevent BCL7A from binding to the SWI/SNF complex. Finally, we identified that the SWI/SNF complex accumulates mutations in a third of DLBCL tumors, especially in the GCB subtype. These discoveries highlight the tumor suppressor role of BCL7A mutations in DLBCL, and suggest that the SWI/SNF complex is involved in DLBCL pathogenesis.

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Frequent mutations in the amino-terminal domain of BCL7A impair its tumor suppressor role in DLBCL

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BCL7A and BCL7B potentiate SWI/SNF-complex-mediated chromatin accessibility to regulate gene expression and vegetative phase transition in plants

Project description:Switch defective/sucrose non-fermentable (SWI/SNF) chromatin remodeling complexes are multi-subunit machineries that establish and maintain chromatin accessibility and gene expression by regulating chromatin structure. However, how the remodeling activities of SWI/SNF complexes are regulated in eukaryotes remains elusive. B-cell lymphoma/leukemia protein 7A/B/C (BCL7A/B/C) have been reported as subunits of SWI/SNF complexes for decades in animals and recently in plants; however, the role of BCL7 subunits in SWI/SNF function remains undefined. Here, we identify a unique role for plant BCL7A and BCL7B homologous subunits in potentiating the genome-wide chromatin remodeling activities of BRAHMA-SWI/SNF complexes in plants. BCL7A/B require the catalytic ATPase BRAHMA (BRM) to assemble with the signature subunits of the BRM-SWI/SNF complexes and for genomic binding at a subset of target genes. Loss of BCL7A and BCL7B diminishes BRM-mediated genome-wide chromatin accessibility without changing the stability and genomic targeting of the BRM-SWI/SNF complex, highlighting the specialized role of BCL7A/B in regulating remodeling activity. We further show that BCL7A/B fine-tunes the remodeling activity of BRM-SWI/SNF complexes to generate accessible chromatin at the juvenility resetting region (JRR) of the microRNAs MIR156A/C for plant juvenile identity maintenance. In summary, our work uncovers the function of previously elusive SWI/SNF subunits in multicellular eukaryotes and provides insights into the mechanisms whereby plants memorize the juvenile identity through SWI/SNF-mediated control of chromatin accessibility.

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The Swi/Snf tumor suppressor complex establishes nucleosome occupancy at target promoters [Mnase-Seq I]

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