Abstract
A riboflavin-deficient, galactoflavin-con-taining diet administered to pregnant females of strain DBA mice produced cleft palates in 42% of their offspring. Correlation of palate development with other developmental features in embryos at the time of normal palate closure showed that the movement of palatine shelves from a vertical to a horizontal position was delayed. Since no other major deviation in palate morphogenesis was detected at this critical time, the formation of cleft palate was attributed to retardation of palatine shelf movement.