NFI transcription factors provide chromatin access to maintain stem cell identity while preventing unintended lineage fate choices
- Authors
- Adam, Rene C.; Yang, Hanseul; Ge, Yejing; Infarinato, Nicole R.; Gur-Cohen, Shiri; Miao, Yuxuan; Wang, Ping; Zhao, Yilin; Lu, Catherine P.; Kim, Jeong E.; Ko, Joo Y.; Paik, Seung S.; Gronostajski, Richard M.; Kim, Jaehwan; Krueger, James G.; Zheng, Deyou; Fuchs, Elaine
- Issue Date
- Jun-2020
- Publisher
- NATURE PORTFOLIO
- Citation
- NATURE CELL BIOLOGY, v.22, no.6, pp.640 - 650
- Indexed
- SCIE
SCOPUS
- Journal Title
- NATURE CELL BIOLOGY
- Volume
- 22
- Number
- 6
- Start Page
- 640
- End Page
- 650
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/145568
- DOI
- 10.1038/s41556-020-0513-0
- ISSN
- 1465-7392
- Abstract
- Tissue homeostasis and regeneration rely on resident stem cells (SCs), whose behaviour is regulated through niche-dependent crosstalk. The mechanisms underlying SC identity are still unfolding. Here, using spatiotemporal gene ablation in murine hair follicles, we uncover a critical role for the transcription factors (TFs) nuclear factor IB (NFIB) and IX (NFIX) in maintaining SC identity. Without NFI TFs, SCs lose their hair-regenerating capability, and produce skin bearing striking resemblance to irreversible human alopecia, which also displays reduced NFIs. Through single-cell transcriptomics, ATAC-Seq and ChIP-Seq profiling, we expose a key role for NFIB and NFIX in governing super-enhancer maintenance of the key hair follicle SC-specific TF genes. When NFIB and NFIX are genetically removed, the stemness epigenetic landscape is lost. Super-enhancers driving SC identity are decommissioned, while unwanted lineages are de-repressed ectopically. Together, our findings expose NFIB and NFIX as crucial rheostats of tissue homeostasis, functioning to safeguard the SC epigenome from a breach in lineage confinement that otherwise triggers irreversible tissue degeneration.
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