Journal
IMMUNITY
Volume 48, Issue 2, Pages 243-+Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2018.01.012
Keywords
-
Categories
Funding
- NIH [K22AI112570, R01AI047833, P01CA119070, AI105343, AI082630, AI112521, AI115712, AI117718, AI108545, AI117950]
- Sloan Foundation
- National Psoriasis Foundation
- LLS Fellow Award
- Parker Institute for Cancer Immunotherapy
- NATIONAL CANCER INSTITUTE [ZIABC011633, P01CA119070] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI115712, R21AI117718, P01AI112521, U19AI117950, U19AI082630, K22AI112570, R01AI047833, P01AI108545, R01AI105343] Funding Source: NIH RePORTER
Ask authors/readers for more resources
T cell development is orchestrated by transcription factors that regulate the expression of genes initially buried within inaccessible chromatin, but the transcription factors that establish the regulatory landscape of the T cell lineage remain unknown. Profiling chromatin accessibility at eight stages of T cell development revealed the selective enrichment of TCF-1 at genomic regions that became accessible at the earliest stages of development. TCF-1 was further required for the accessibility of these regulatory elements and at the single-cell level, it dictated a coordinate opening of chromatin in T cells. TCF-1 expression in fibroblasts generated de novo chromatin accessibility even at chromatin regions with repressive marks, inducing the expression of T cell-restricted genes. These results indicate that a mechanism by which TCF-1 controls T cell fate is through its widespread ability to target silent chromatin and establish the epigenetic identity of T cells.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available