Michael J. Conboy

TL;DR: Heterochronic parabiosis increased aged hepatocyte proliferation and restored the cEBP-α complex to levels seen in young animals, suggesting that the age-related decline of progenitor cell activity can be modulated by systemic factors that change with age.

TL;DR: It is shown that muscle stem cells from aged mice tend to convert from a myogenic to a fibrogenic lineage as they begin to proliferate and that this conversion is mediated by factors in the systemic environment of the old animals.

TL;DR: Analysis of injured muscle revealed that, with age, resident precursor cells had a markedly impaired propensity to proliferate and to produce myoblasts necessary for muscle regeneration, and Notch signaling is a key determinant of muscle regenerative potential that declines with age.

TL;DR: It is demonstrated that the temporal balance between Notch and Wnt signaling orchestrates the precise progression of muscle precursor cells along the myogenic lineage pathway, through stages of proliferative expansion and then differentiation, during postnatal myogenesis.

TL;DR: It is demonstrated that a delivery vehicle composed of gold nanoparticles conjugated to DNA and complexed with cationic endosomal disruptive polymers can deliver Cas9 ribonucleoprotein and donor DNA into a wide variety of cell types and efficiently correct the DNA mutation that causes Duchenne muscular dystrophy in mice via local injection, with minimal off-target DNA damage.