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. Mechaitsically, ATAC-seq revealed that BNC2 deletion reduced chromat

SUBMITTER: Zhong Zhang 

PROVIDER: S-SCDT-10_1038-S44318-025-00664-1 | biostudies-other |

REPOSITORIES: biostudies-other