Basonuclin-2 promotes fracture repair through NuRD-dependent chromatin remodeling in periosteal stem cells.

ABSTRACT: Bone fracture healing remains a significant challenge in orthopedics, as injury-responsive skeletal stem cell (SSC) populations and the regulatory mechanisms governing SSC activation during nonunion fracture repair remain poorly delineated. This study identifies zinc finger transcription factor basonuclin-2 (BNC2) as a skeletal fracture repair control factor in periosteal stem cells. BNC2 marks quiescent periosteal cells during homeostasis and is significantly upregulated upon injury in mice, driving endochondral ossification post-fracture via clonal expansion. Moreover, knockout of Bnc2 in Prx1-cre⁺ cells (not Ocn-cre⁺ osteoblasts or LepR-creER⁺ BMSCs) resulted in impaired fracture healing, suppressing SSC proliferation. Mechanistically, ATAC-seq revealed

SUBMITTER: Zhang Z 

PROVIDER: S-EPMC12910080 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature