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

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

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.

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.

Monogamous rodents of the genus Peromyscus, upon disruption of pair bonds, acquire increased oncogenic activity.

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.

Prdm9-generated meiotic asynapsis of homologous chromosomes in mouse subspecific hybrids causes hybrid sterility and can be reversed by introducing random stretches of consubspecific sequence (≥ 27Mb) on four chromosomes most sensitive to asynapsis.

Wounded epidermal keratinocytes emit a signal that activates a specialized T-cell in the skin, leading to an increase in hair follicle stem cell numbers that contributes to tissue repair.

A regulatory circuit that localizes to the synaptonemal complex, a liquid crystalline compartment between chromosomes, ensures crossing-over while limiting the number of crossovers between homologous chromosomes during meiosis.

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.