“…These changes were related to the physiological increase in the level of protein synthesis within these cells. However, when marked and irregular dilations of the RER are observed in chondrocytes in growth plates from patients with endochondral growth defects, this finding is pathologic [8] and may reflect inability to transport material from the RER to the Golgi because of production of an abnormal product, a primary defect in the intracellular transport mechanism [18,34], or a rate of synthesis which exceeds the rate of intracellular transport from the cell. Dilated RER profiles have been found in chondrocytes from patients with several forms of spondyloepiphyseal dysplasia [22,26,29], Kniest syndrome [16,18,20], pseudoachondroplasia [11,20], metaphyseal dysostosis [9], thanatophoric dwarfism [21], and in the cho mutant in mice [27,28].…”