Alteration of CTCF-associated chromatin neighborhood inhibits TAL1-driven oncogenic transcription program and leukemogenesis.
作者： Ying Li , Ziwei Liao , Huacheng Luo , Aissa Benyoucef , Yuanyuan Kang
DOI: 10.1093/NAR/GKAA098
关键词:
摘要: Aberrant activation of the TAL1 is associated with up to 60% T-ALL cases and involved in CTCF-mediated genome organization within locus, suggesting that CTCF boundary plays a pathogenic role T-ALL. Here, we show -31-Kb binding site (-31CBS) serves as chromatin defines topologically associating domain (TAD) enhancer/promoter interaction required for activation. Deleted or inverted -31CBS impairs expression context-dependent manner. Deletion reduces accessibility blocks long-range between +51 erythroid enhancer promoter-1 leading inhibition cells, but not cells. However, TAL1-expressing leukemia-prone promoter-IV specifically interacts +19 stem cell located 19 Kb downstream this disrupted by inversion Inversion Jurkat cells alters accessibility, histone modifications TAD TAL1-driven leukemogenesis. Thus, our data reveal acts critical regulator define +19-enhancer leukemic prone promoter IV Manipulation can alter oncogenic transcription networks
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