Perivascular extracellular vesicles induce bone repair, and do so via tetraspanin binding to recipient skeletal progenitor cells.

Basalins are intrinsically disordered proteins with astonishingly high-sequence divergence that are essential for building the transition zone basal plate and for proper central pair nucleation.

Large-scale skeletal regeneration requires Hh signaling in Sox9+ lineage cells to coordinate callus formation and bone repair.

Bone cells exposed to physiological forces release ATP through repairable membrane injury, generating an intercellular signal that conveys the destructive potential of forces and the adaptive capacity of endangered cells.

A detailed model of the T7 replisome with the precise positions of the helicase and polymerase at the replication fork explains how catalysis by the two enzymes is coordinated.

Despite differing by only one amino acid in the C-terminal tail, copy 1 of yeast histone 2A has a repair-specific role not shared by copy 2.

A periosteal Bmp2 signaling center couples bone length to bone width during development and must be reactivated by clinical bone anabolic therapies to reduce fracture risk and accelerate fracture repair.

Experiments on E. coli show that multiple mechanisms contribute to extreme resistance to ionizing radiation in bacteria, with mutations to three genes for DNA repair having a prominent role in one evolved population.

Biochemical reconstitution experiments uncover the ubiquitin-mediated function of a DNA repair protein, key to the understanding of Fanconi Anemia, a cancer-associated bone marrow failure syndrome.