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

Multivariate genotype-phenotype mapping enables quantification of pathway and process-level effects on complex phenotypes and predicts phenotypic effects of novel mutations.

Disruption of the intracellular vimentin network upon cellular stress results in enhanced cell surface vimentin on human osteoarthritic chondrocytes and might represent a novel membrane-associated marker of stress-induced premature senescence.

Through the interaction between PCP signaling and N-cadherin, oriented cell division and cell rearrangement are coordinated to establish the appropriate tissue architecture critical for limb skeletal morphogenesis.

In cooperatively breeding Damaraland mole-rats, transitioning to 'queen' results in extensive gene regulatory and morphological remodeling, but also costs to skeletal integrity that scale with reproductive investment.

A newly identified adipose lineage cell population, MALP, regulates marrow vasculature and osteogenesis in bone.

A GWAS meta-analysis for OPLL identified fourteen significant genomic loci and a subsequent Mendelian randomization study provided genetic evidence for a causal effect of obesity on the pathogenesis of OPLL, especially one of its subtypes, thoracic OPLL.

Full spectrum flow cytometry reveals a high degree of placental mesenchymal cell heterogeneity, which is lost with culture, highlighting the importance of detailed ex vivo phenotyping to optimise the use of these cells in downstream applications.

MMP14 activity-mediated cleavage of the ectodomain of PTH1R modulates PTH signaling in the chondrocyte-derived osteoblast lineage, regulating osteogenesis and thereby bone metabolism, with therapeutic significance for bone-wasting diseases.

Meniscal Gli1+ cells are mesenchymal progenitors that contribute to the development and injury repair of meniscus.