In a previous study we showed that COL2A1 mRNA is expressed in both ectodermally and mesodermally derived structures of second trimester human fetal cochlea, whereas type II collagen is present in mesodermally derived structures and in tectorial and basilar membranes. Because the tectorial membrane is acellular and therefore does not make its own proteins, the source of type II collagen and proteoglycans in this membrane has been of interest. We have attempted to address this issue, at least in part, by performing quantitative cRNA mRNA in situ hybridization on second trimester human fetal cochlear sections using a COL2A1 probe. By counting the number of silver grains cell in the interdental cells, inner sulcus cells and inner ridge Kolliker organ cells and by an analysis of variance of these quantitative data. inner ridge cells were found to have significantly higher levels of COL2A1 mRNA than interdental and inner sulcus cells (p < 0.0001). On the basis of significantly higher COL2A1 mRNA levels in inner ridge cells and their higher numbers than interdental and inner sulcus cells we postulate that type II collagen for human fetal tectorial membrane is derived mostly from inner ridge Kolliker organ cells. The lower COL2A1 mRNA in interdental cells appears to provide type II collagen for the spiral limbus and the tectorial membrane. The inner sulcus cells, hair cells. Deiter's and Hensen's cells also appear to contribute lesser amounts of type II collagen to the tectorial membrane. In analogy to these findings it is possible that other tectorial membrane proteins, including proteoglycans and other collagens, are also largely derived from these cells during human fetal development.