Cell behaviour and cleft palate in the mutant mouse, amputated.

Cleft palate with a genetic origin normally arises because of a failure of the palatal shelves to elevate or fuse. Until now attention in studies of palatal development development has been focused on two critical phases, those of elevation and fusion. In the mutant mouse, amputated, however, cleft palate arise because of a failure of the palatal shelves to make any significant outgrowth between the 12th day after conception when the palatal shelves are first observed and the 14th day when elevation and fusion normally occur. When cell proliferation (mitotic index) was measured in the palatal shelves on days 12, 13 and 14 no difference was found between mutant and normal. The failure of the mutant palate to grow cannot be accounted for on grounds of reduced cell proliferation. For this reason the palatal mesenchyme in 12.5-day and 14.5-day normal and amputated mice has been studied wit the scanning electron microscope. This work shows that the mesenchymal cells in the mutant palate are clumped together and have much greater areas of cell contact than are observed in the normal palate. The abnormal cell behaviour described in mutant palatal mesenchyme is typical of amputated embryonic mesenchyme in general, and in other cases has been shown to cause abnormal morphogenesis. We propose that aberrant cell behaviour causing an aggregation through increased cell adhesion inhibits palatal outgrowth in the mutant, and for this reason the palatal shelves subsequently fail to elevate and fuse.