Expression data of chondrocytes subpopulations from WT, 13del and 13del:Chop-/- mice at P10 stage

The human metaphyseal chondrodysplasia type Schmid is an autosomal dominant disorder associated with mutations in COL10A1 gene that result in ER retention of misfolded alpha(X) collagen in hypertrophic chondrocytes (HCs). In a MCDS transgenic mouse model (13del), we have previously implicated HC response and adaptation to ER stress as the underlying molecular pathogenesis of the disease. We generate microarray data from chondrocytes in WT, 13del and 13del:Chop-/- mice to elucidate the etiological role of ER stress signaling in MCDS. Proximal tibia growth plates from WT, 13del and 13del:Chop-/- mice at P10 stage were fractionated and global gene expression data were generated from different chondrocyte populations for systematic comparison to identify the key factors of chondrocyte adaptation to ER stress.