ArticleGenome biology2023
Auxin-inducible degron 2 system deciphers functions of CTCF domains in transcriptional regulation.
Article in Genome biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- An updated catalog ofFrontiers in molecular neuroscience · 2023Pooled it
- Genome-wide rotational and translational phasing of nucleosomes with human transcription factors.Molecular cell · 2026Article
- The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers.Nature communications · 2026Article
- Deciphering resistance mechanisms to auxin-inducible protein degradation in mammalian cells.The Journal of biological chemistry · 2026Article
- RFX5 as a regulator of spatial chromatin contacts and gene expression.Communications biology · 2026Article
- Transposable elements shape stemness in normal and leukemic hematopoiesis.Nature genetics · 2026Article
- Article
- Spatial Chromatin Organization Across the Cell Cycle: Insights from Auxin-Inducible Protein Depletion.Cells · 2025Review
- Deciphering acquired resistance mechanisms to sustained auxin-inducible protein degradation in cells and mice.bioRxiv : the preprint server for biology · 2025Article
- Wnt signaling activation induces CTCF binding and loop formation atGenome research · 2025Article
- Unfolding neural diversity: how dynamic three-dimensional genome architecture regulates brain function and disease.Molecular psychiatry · 2025Review
- Deciphering the role of RNA in regulating CTCF's DNA binding affinity in leukemia cells.Genome biology · 2025Article
- Roles for the 3D genome in the cell cycle, DNA replication, and double strand break repair.Frontiers in cell and developmental biology · 2025Review
- 3D Genome Engineering: Current Advances and Therapeutic Opportunities in Human Diseases.Research (Washington, D.C.) · 2025Review
- A negatively charged region within carboxy-terminal domain maintains proper CTCF DNA binding.iScience · 2024Article
- CTCF mutation at R567 causes developmental disorders via 3D genome rearrangement and abnormal neurodevelopment.Nature communications · 2024Article
- Cohesin regulation and roles in chromosome structure and function.Current opinion in genetics & development · 2024Review
- RNA-binding protein RBM5 plays an essential role in acute myeloid leukemia by activating the oncogenic protein HOXA9.Genome biology · 2024Article
- Auxin-inducible degron 2 system deciphers functions of CTCF domains in transcriptional regulation.Genome biology · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCTCF is a well-established chromatin architectural protein that also plays various roles in transcriptional regulation. While CTCF biology has been extensively studied, how the domains of CTCF function to regulate transcription remains unknown. Additionally, the original auxin-inducible degron 1 (AID1) system has limitations in investigating the function of CTCF.
resultsWe employ an improved auxin-inducible degron technology, AID2, to facilitate the study of acute depletion of CTCF while overcoming the limitations of the previous AID system. As previously observed through the AID1 system and steady-state RNA analysis, the new AID2 system combined with SLAM-seq confirms that CTCF depletion leads to modest nascent and steady-state transcript changes. A CTCF domain sgRNA library screening identifies the zinc finger (ZF) domain as the region within CTCF with the most functional relevance, including ZFs 1 and 10. Removal of ZFs 1 and 10 reveals genomic regions that independently require these ZFs for DNA binding and transcriptional regulation. Notably, loci regulated by either ZF1 or ZF10 exhibit unique CTCF binding motifs specific to each ZF.
conclusionsBy extensively comparing the AID1 and AID2 systems for CTCF degradation in SEM cells, we confirm that AID2 degradation is superior for achieving miniAID-tagged protein degradation without the limitations of the AID1 system. The model we create that combines AID2 depletion of CTCF with exogenous overexpression of CTCF mutants allows us to demonstrate how peripheral ZFs intricately orchestrate transcriptional regulation in a cellular context for the first time.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.