Prevention of Genetic Polydactyly in Polydactyly Nagoya (Pdn) Mice in Vitro by Surgical Treatment of Foot Plate during Embryogenesis

Abstract Pdn/Pdn fetuses show preaxial Polydactyly of duplicated or triplicated metacarpal/metatarsal type in the fore- and hindlimbs. Pdn /+ fetuses show one extra digit of distal phalangeal type preaxially in the hindlimb and deformity of distal phalanx of the 1st digit in the forelimb. Normal patterns of physiological cell death in the preaxial apical ectodermal ridge (AER) and the deep preaxial mesoderm (fpp) were disrupted in Pdn/Pdn embryos. It was supposed that delayed involution of preaxial AER might have caused the abolishment of fpp, which in turn could have induced polydactyly in Pdn/Pdn .
In order to induce cell death in the fpp region artificially, tissue destruction of the fpp region of right fore- and hindfoot plates of Pdn/Pdn , Pdn /+ and +/+ embryos was performed by an electric knife on day 11.5 of gestation, and the embryos were cultured in the rotator culture system for 20 hours. The non-treated left foot plates served as the controls.
In Pdn/Pdn embryos, the non-treated left foot plates showed abnormal protuberance and/or the extra digital rays preaxially. But the treated right foot plates did not exhibit these abnormal characteristics. Instead they revealed 5 digital rays of mesodermal condensation in the histological sections.
These results indicated that the restriction of the artificial tissue destruction in the fpp region could prevent the manifestation of preaxial extra digits in Pdn mice.