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The Bcl11-Cxxc1 axis regulates stage-specific chromatin accessibility during lymphocyte development
Kazuki Okuyama1, Wooseok Seo2, Hirotaka Takahashi3
1Laboratory for Transcriptional Regulation, RIKEN Center for Integrative Medical Sciences (IMS), Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan; kaokuyam@ncc.go.jp ichiro.taniuchi@riken.jp.
Genes & Development
|August 3, 2026
Summary
Bcl11b protein is vital for T-cell development. Its interaction with Cxxc1 regulates chromatin structure, impacting T-cell maturation and B-cell development.
Area of Science:
- Immunology
- Molecular Biology
- Epigenetics
Background:
- Bcl11b is a zinc finger transcription factor essential for T-lymphopoiesis.
- A truncated Bcl11b disrupts chromatin accessibility in developing T-cells.
Purpose of the Study:
- To identify chromatin modifiers associated with the Bcl11b zinc finger.
- To elucidate the role of Cxxc1 in lymphopoiesis and chromatin regulation.
Main Methods:
- Chromatin immunoprecipitation (ChIP) assays to identify protein binding sites.
- Analysis of thymocyte development in wild-type and knockout mouse models.
- Assessment of chromatin structure and gene expression.
Main Results:
- Cxxc1, a component of the Set1 complex, was identified as a key interacting protein.
- Cxxc1 deficiency impairs the transition from double-negative to double-positive thymocytes, maintaining a double-negative chromatin state.
- Genomic regions bound by Cxxc1 significantly overlap with Bcl11b binding sites and are affected by Bcl11b deficiency.
Conclusions:
- Bcl11b family proteins recruit Cxxc1 to modulate chromatin structure during lymphopoiesis.
- This mechanism is conserved in both T-cell and B-cell development, involving Bcl11a in B-lymphocytes.
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