Limb development in the polydactylous talpid³ mutant of the fowl

Talpid² limb development is characterized by excessive elongation of the apical ectodermal ridge (AER). In the forelimb the talpid² AER is of normal length during stages 22 and 23, but at stage 28 it exceeds the normal by about 65%. In the hindlimb the talpid² AER is of normal length during stages 22 – 24, but at stage 27 it exceeds the normal by about 20%.

Massive cell death is absent from the superficial mesenchyme of both fore and hind talpid² limbs. Histological and histochemical studies show that areas of dead cell groups rich in acid phosphatase activity are absent in talpid² from the positions in the superficial limb mesenchyme in which they occur in the normal.

This absence of cell death in the limb superficial mesenchyme is thought to account for (a) the abnormal sculpturing of talpid² limbs, and (b) the excessive elongation of the talpid² AER, through apical ectodermal maintenance factor (AEMF) being available from areas of mesenchyme normally undergoing necrosis and lacking AEMF.

The abnormal talpid² forelimb skeleton originates in an anomalous pattern of mesenchymal condensation forming the membranous skeleton at stage 26. Talpid² limb mesenchyme shows an abnormal pattern of alkaline phosphatase distribution beginning at stage 26.

The relationship between the abnormal pattern of limb mesenchymal condensation and the absence of massive cell death in the superficial mesenchyme is not understood.

Talpid³ limb development is discussed in relation to other cases where genes affect the pattern of cell death, and in relation to other examples of polydactyly.