SWI/SNF complex-mediated ZNF410 cooperative binding maintains chromatin accessibility and enhancer activity

The clustering of multiple transcription factor binding sites (TFBSs) for the same TF has proved to be a pervasive feature of cis-regulatory elements in the eukaryotic genome. However, the contribution of binding sites within the homotypic clusters of TFBSs (HCTs) to TF binding and target gene expression remains to be understood. Here, we characterize the CHD4 enhancers that harbor unique functional ZNF410 HCTs genome wide. We uncover that ZNF410 controls chromatin accessibility and activity of the CHD4 enhancer regions. We demonstrate that ZNF410 binds to the HCTs in a collaborative fashion, further conferring transcriptional activation. In particular, three ZNF410 motifs (sub-HCTs) located at 3' end of the distal enhancer act as "switch motifs" to control chromatin accessibility and enhancer activity. Mechanistically, the SWI/SNF complex is selectively required to mediate cooperative ZNF410 binding for CHD4 expression. Together, our findings expose a complex functional hierarchy of homotypic clustered motifs, which cooperate to fine-tune target gene expression.

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Publication Details

Journal
Cell Reports
Published
2025-03-31
DOI
https://doi.org/10.1016/j.celrep.2025.115476
Citations
1
Primary Topic
Chromatin Remodeling and Cancer
Type
article
Field-Weighted Citation Impact
0.81
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SWI/SNF complex-mediated ZNF410 cooperative binding maintains chromatin accessibility and enhancer activity

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1 citations
Cell Reports
Chromatin Remodeling and Cancer
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article

SWI/SNF complex-mediated ZNF410 cooperative binding maintains chromatin accessibility and enhancer activity

Haoyue Zhang, Xianjiang Lan, Xiaodong Cheng, Ren Ren, Gerd A. Blobel, Han Zhao, Sijian Xia, Yijie Shen, Bin Xu, Haowen Lu, Siyuan Xu, Chuxuan Peng
article en
1 citations

Abstract

The clustering of multiple transcription factor binding sites (TFBSs) for the same TF has proved to be a pervasive feature of cis-regulatory elements in the eukaryotic genome. However, the contribution of binding sites within the homotypic clusters of TFBSs (HCTs) to TF binding and target gene expression remains to be understood. Here, we characterize the CHD4 enhancers that harbor unique functional ZNF410 HCTs genome wide. We uncover that ZNF410 controls chromatin accessibility and activity of the CHD4 enhancer regions. We demonstrate that ZNF410 binds to the HCTs in a collaborative fashion, further conferring transcriptional activation. In particular, three ZNF410 motifs (sub-HCTs) located at 3' end of the distal enhancer act as "switch motifs" to control chromatin accessibility and enhancer activity. Mechanistically, the SWI/SNF complex is selectively required to mediate cooperative ZNF410 binding for CHD4 expression. Together, our findings expose a complex functional hierarchy of homotypic clustered motifs, which cooperate to fine-tune target gene expression.

Cell ReportsVol. 44(4)
Children's Hospital of Philadelphia (US), The University of Texas MD Anderson Cancer Center (US), Capital Medical University (CN), Fudan University (CN), Shenzhen Bay Laboratory (CN), Zhongda Hospital Southeast University (CN), Zhongshan Hospital (CN), University of Pennsylvania (US)
Openalex Percentile: Top 30%
Chromatin Remodeling and Cancer
0.81
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