2026-07-01 理化学研究所
Cxxc1の従来知られていた遺伝子発現の制御機構（左）と今回明らかになった新規の制御機構
＜関連情報＞
- https://www.riken.jp/press/2026/20260701_1/index.html
- https://genesdev.cshlp.org/content/early/2026/06/25/gad.353082.125
Bcl11–Cxxc1軸はリンパ球発生中の段階特異的なクロマチンアクセシビリティを制御する The Bcl11–Cxxc1 axis regulates stage-specific chromatin accessibility during lymphocyte development
Kazuki Okuyama,,Wooseok Seo,,Hirotaka Takahashi,Sawako Muroi,Ning Hou,,Shinsuke Ito,Tatsuya Sawasaki,Haruhiko Koseki,Yibo Wu, andIchiro Taniuchi
Genes & Development Published:June 25, 2026
DOI:10.1101/gad.353082.125
Abstract
A zinc finger transcription factor, Bcl11b, is crucial for T-lymphopoiesis. A truncated Bcl11b lacking the C-terminal zinc finger disrupts chromatin accessibility in CD4+CD8+ double-positive thymocytes. Screening chromatin modifiers associated with this zinc finger identified Cxxc1, a component of the Set1 complex mediating H3K4me3. Cxxc1 deficiency arrests the CD4−CD8− double-negative-to-double-positive transition, retaining double-negative-like chromatin structure in double-positive thymocytes. Genomic regions bound by Cxxc1 largely overlapped with Bcl11b and were altered upon Bcl11bdeficiency. Similar effects are observed in B-lymphocytes via another Bcl11 family protein, Bcl11a, highlighting the role of Bcl11 family proteins in recruiting Cxxc1 in chromatin modulation during lymphopoiesis.
