Gene Center Munich, Ludwig-Maximilians-Universität München, Munich, Germany.
Nucleic Acids Res. 2024 Jun 24;52(11):6490-6506. doi: 10.1093/nar/gkae391.
CTCF is a zinc finger protein associated with transcription regulation that also acts as a barrier factor for topologically associated domains (TADs) generated by cohesin via loop extrusion. These processes require different properties of CTCF-DNA interaction, and it is still unclear how CTCF's structural features may modulate its diverse roles. Here, we employ single-molecule imaging to study both full-length CTCF and truncation mutants. We show that CTCF enriches at CTCF binding sites (CBSs), displaying a longer lifetime than observed previously. We demonstrate that the zinc finger domains mediate CTCF clustering and that clustering enables RNA recruitment, possibly creating a scaffold for interaction with RNA-binding proteins like cohesin's subunit SA. We further reveal a direct recruitment and an increase of SA residence time by CTCF bound at CBSs, suggesting that CTCF-SA interactions are crucial for cohesin stability on chromatin at TAD borders. Furthermore, we establish a single-molecule T7 transcription assay and show that although a transcribing polymerase can remove CTCF from CBSs, transcription is impaired. Our study shows that context-dependent nucleic acid binding determines the multifaceted CTCF roles in genome organization and transcription regulation.
CTCF 是一种锌指蛋白,与转录调控有关,同时也作为环挤出(cohesin)产生的拓扑关联域(TADs)的障碍因子。这些过程需要 CTCF-DNA 相互作用的不同特性,目前尚不清楚 CTCF 的结构特征如何调节其多种作用。在这里,我们采用单分子成像技术来研究全长 CTCF 和截断突变体。我们表明 CTCF 在 CTCF 结合位点(CBSs)处富集,其寿命比之前观察到的要长。我们证明锌指结构域介导 CTCF 聚集,并且聚集使 RNA 募集成为可能,可能为与 RNA 结合蛋白(如 cohesin 的亚基 SA)的相互作用创建支架。我们进一步揭示了直接募集和 CTCF 在 CBS 处结合的 SA 居留时间增加,表明 CTCF-SA 相互作用对于 TAD 边界处染色质上 cohesin 的稳定性至关重要。此外,我们建立了一个单分子 T7 转录测定法,并表明尽管转录聚合酶可以将 CTCF 从 CBSs 中移除,但转录会受到损害。我们的研究表明,依赖于上下文的核酸结合决定了 CTCF 在基因组组织和转录调控中的多方面作用。