신보영 (California Institute of Technology)

한빛사논문

조회663

California Institute of Technology

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Nat. Immunol., 10 August 2023 | https://doi.org/10.1038/s41590-023-01585-z Runx factors launch T cell and innate lymphoid programs via direct and gene network-based mechanisms

Boyoung Shin¹, Wen Zhou^1,2,4, Jue Wang^1,2, Fan Gao^1,3,5 & Ellen V. Rothenberg^1,*

¹Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA, USA.
²Program in Biochemistry and Molecular Biophysics, California Institute of Technology, Pasadena, CA, USA.
³Bioinformatics Resource Center, Beckman Institute of California Institute of Technology, Pasadena, CA, USA.
⁴Present address: BillionToOne, Menlo Park, CA, USA.
⁵Present address: Lyterian Therapeutics, South San Francisco, CA, USA.

^*Corresponding author: correspondence to Ellen V. Rothenberg

Abstract

Runx factors are essential for lineage specification of various hematopoietic cells, including T lymphocytes. However, they regulate context-specific genes and occupy distinct genomic regions in different cell types. Here, we show that dynamic Runx binding shifts in mouse early T cell development are mostly not restricted by local chromatin state but regulated by Runx dosage and functional partners. Runx cofactors compete to recruit a limited pool of Runx factors in early T progenitor cells, and a modest increase in Runx protein availability at pre-commitment stages causes premature Runx occupancy at post-commitment binding sites. This increased Runx factor availability results in striking T cell lineage developmental acceleration by selectively activating T cell-identity and innate lymphoid cell programs. These programs are collectively regulated by Runx together with other, Runx-induced transcription factors that co-occupy Runx-target genes and propagate gene network changes.

논문정보

형식Research article
게재일2023년 08월 (BRIC 등록일 2023-08-14)
연구진국외 연구진
분야 생명과학 > 면역학

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