{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lee D"],"funding":["National Research Foundation of Korea (NRF)","National Research Foundation of Korea"],"pagination":["e70181"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11698014"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["38(22)"],"pubmed_abstract":["Topologically associating domains (TADs) are chromatin domains in the eukaryotic genome. TADs often comprise several sub-TADs. The boundaries of TADs and sub-TADs are enriched in CTCF, an architectural protein. Deletion of CTCF-binding motifs at one boundary disrupts the domains, often resulting in a transcriptional decrease in genes inside the domains. However, it is not clear how TAD and sub-TAD affect each other in the domain formation. Unaffected gene transcription was observed in the β-globin locus when one boundary of TAD or sub-TAD was destroyed. Here, we disrupted β-globin TAD and sub-TAD by deleting CTCF motifs at both boundaries in MEL/ch11 cells. Disruption of TAD impaired sub-TAD, but sub-TAD disruption did not affect TAD. Both TAD and sub-TAD disruption compromised the β-globin transcription, accompanied by the loss of enhancer-promoter interactions. However, histone H3 occupancy and H3K27ac were largely maintained across the β-globin locus. Genome-wide analysis showed that putative enhancer-promoter interactions and gene transcription were decreased by the disruption of CTCF-mediated topological domains in neural progenitor cells. Collectively, our results indicate that there is unequal relationship between TAD and sub-TAD formation. TAD is likely not sufficient for gene transcription, and, therefore, sub-TAD appears to be required. TAD-dependently formed sub-TADs are considered to provide chromatin environments for enhancer-promoter interactions enabling gene transcription."],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["TAD-dependent sub-TAD is required for enhancer-promoter interaction enabling the β-globin transcription."],"pmcid":["PMC11698014"],"funding_grant_id":["NRF‐2020R1I1A3054808","2022R1C1C2006355","NRF-2020R1I1A3054808"],"pubmed_authors":["Kim A","Kang J","Lee D"],"additional_accession":[]},"is_claimable":false,"name":"TAD-dependent sub-TAD is required for enhancer-promoter interaction enabling the β-globin transcription.","description":"Topologically associating domains (TADs) are chromatin domains in the eukaryotic genome. TADs often comprise several sub-TADs. The boundaries of TADs and sub-TADs are enriched in CTCF, an architectural protein. Deletion of CTCF-binding motifs at one boundary disrupts the domains, often resulting in a transcriptional decrease in genes inside the domains. However, it is not clear how TAD and sub-TAD affect each other in the domain formation. Unaffected gene transcription was observed in the β-globin locus when one boundary of TAD or sub-TAD was destroyed. Here, we disrupted β-globin TAD and sub-TAD by deleting CTCF motifs at both boundaries in MEL/ch11 cells. Disruption of TAD impaired sub-TAD, but sub-TAD disruption did not affect TAD. Both TAD and sub-TAD disruption compromised the β-globin transcription, accompanied by the loss of enhancer-promoter interactions. However, histone H3 occupancy and H3K27ac were largely maintained across the β-globin locus. Genome-wide analysis showed that putative enhancer-promoter interactions and gene transcription were decreased by the disruption of CTCF-mediated topological domains in neural progenitor cells. Collectively, our results indicate that there is unequal relationship between TAD and sub-TAD formation. TAD is likely not sufficient for gene transcription, and, therefore, sub-TAD appears to be required. TAD-dependently formed sub-TADs are considered to provide chromatin environments for enhancer-promoter interactions enabling gene transcription.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2025-04-22T09:04:00.611Z","creation":"2025-04-05T22:51:05.891Z"},"accession":"S-EPMC11698014","cross_references":{"pubmed":["39545685"],"doi":["10.1096/fj.202401526RR"]}}