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Non-coding Transcription Instructs Chromatin Folding and Compartmentalization to Dictate Enhancer-Promoter Communication and T Cell Fate.

Cell | Sep 21, 2017

It is now established that Bcl11b specifies T cell fate. Here, we show that in developing T cells, the Bcl11b enhancer repositioned from the lamina to the nuclear interior. Our search for factors that relocalized the Bcl11b enhancer identified a non-coding RNA named ThymoD (thymocyte differentiation factor). ThymoD-deficient mice displayed a block at the onset of T cell development and developed lymphoid malignancies. We found that ThymoD transcription promoted demethylation at CTCF bound sites and activated cohesin-dependent looping to reposition the Bcl11b enhancer from the lamina to the nuclear interior and to juxtapose the Bcl11b enhancer and promoter into a single-loop domain. These large-scale changes in nuclear architecture were associated with the deposition of activating epigenetic marks across the loop domain, plausibly facilitating phase separation. These data indicate how, during developmental progression and tumor suppression, non-coding transcription orchestrates chromatin folding and compartmentalization to direct with high precision enhancer-promoter communication.

Pubmed ID: 28938112 RIS Download

Mesh terms: Animals | CCCTC-Binding Factor | Chromatin | Enhancer Elements, Genetic | Leukemia | Locus Control Region | Lymphoma | Mice | Nuclear Lamina | Promoter Regions, Genetic | RNA, Untranslated | Repressor Proteins | T-Lymphocytes | Thymus Gland | Transcription, Genetic | Tumor Suppressor Proteins

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Associated grants

  • Agency: NIAID NIH HHS, Id: R01 AI109599
  • Agency: NIAID NIH HHS, Id: P01 AI102853
  • Agency: NIAID NIH HHS, Id: R01 AI100880
  • Agency: NIDDK NIH HHS, Id: U54 DK107977
  • Agency: NIAID NIH HHS, Id: R01 AI082850

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