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Here we show that CFP1, an integral component of the Setd1A\/B methyltransferase complex, is critically required for functional H3K4me3-BD installation and B cell fate determination. Cfp1 deletion impairs H3K4me3-BDs on a subset of B lineage genes and redistributes H3K4me3 from active genes to bivalent promoters. Transcription of subsets of the H3K4me3-BD-bound genes is diminished in part due to reduced RNA polymerase II at the promoter and gene body. Specifically, CFP1 ablation abolishes H3K4me3-BD at the recombination center and distal\u00a0PAIR elements in the immunoglobulin heavy chain (IgH) gene, severely compromises its locus contraction for efficient V-to-DJ recombination, and consequently arrests cells at the pro-B stage. Moreover, Cfp1-deficient pro-B cells up-regulate a panel of progenitor and myeloid-specific genes with elevated H3K4me3 marks and can trans-differentiate into various myeloid cell types. Therefore, our study reveals pivotal roles for CFP1-mediated H3K4me3-BDs in the transcriptional regulation of cell lineage fate specification and commitment.<\/jats:p>","DOI":"10.1093\/nar\/gkag125","type":"journal-article","created":{"date-parts":[[2026,2,4]],"date-time":"2026-02-04T12:46:34Z","timestamp":1770209194000},"source":"Crossref","is-referenced-by-count":1,"title":["CFP1-mediated H3K4me3 broad domains control early B cell lineage fate determination"],"prefix":"10.1093","volume":"54","author":[{"given":"Wanyu","family":"Bai","sequence":"first","affiliation":[{"name":"Pediatric Hematology Laboratory, Division of Hematology\/Oncology, Department of Pediatrics, The Seventh Affiliated Hospital of Sun Yat-Sen University , Shenzhen 518107 ,","place":["China"]},{"name":"Department of Immunology and Microbiology, Zhongshan School of Medicine, Sun Yat-sen University , Guangzhou 510080 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