Wnt1 was expressed in B220-positive cells of the B-cell lineage and to a lesser extent in the lineage-detrimental cells that represent hematopoietic progenitor cells, but not in the myeloid and erythroid lineages. We performed extra lineage-tracing experiments using Wnt1-Cre transgenic mice intercrossed with RosamT/mG reporter mice, which express cell-type particular green fluorescent proteins on Cre-mediated activation.9,10 Fluorescence analysis showed strong expression in a subset of osteocytic cells in the subchondral bone and weaker expression in cortical bone . Discussion Several lines of evidence indicate that canonical WNT signaling is essential for regular skeletal development and homeostasis.6,14 WNT signaling induces osteoblast differentiation and bone formation in early osteoblast progenitors and regulates osteoblast-dependent osteoclastogenesis in mature osteoblasts and osteocytes.15-18 Moreover, mice lacking the WNT receptor Fzd9 have a cell-autonomous defect in bone development.19 The patients defined here have a kind of autosomal dominant osteoporosis the effect of a missense mutation in WNT1 and a serious type of osteogenesis imperfecta caused by a homozygous truncation mutation in WNT1.When FMRP is certainly lacking, mGluR5 pathways are overactive resulting in unusual connections in the mind and the behavioral and cognitive impairments connected with Fragile X. Related StoriesCHOP researchers delay symptoms, lengthen lifespan in animal model of Batten diseaseNew study examines previously unknown secret to DNA repairCrucial modification in single DNA bottom predisposes children to aggressive form of cancerThe research team, led by Sebastien Jacquemont of Vaudois University in Switzerland in collaboration with Baltazar Gomez-Mancilla of Novartis, found no significant effects of treatment when the complete group of 30 patients was analyzed.