Recent studies have demonstrated a link between limb reduction defects
and mesonephros removal [Geduspan and Solursh, 1992) Dev. Biol., 151:
242-250]. However, there is some question as to whether the limb-reduc
tion defects seen in that study resulted from the removal of mesonephr
os or from the formation of scar tissue medial to the limb territory.
The current study was conducted to test the hypothesis that eliminatio
n of the mesonephros without producing scar tissue adjacent to the lim
b will adversely affect limb morphogenesis. The hypothesis was tested
by the insertion of tantalum foil barriers into various levels of the
intermediate mesoderm of developing chick embryos to prevent the cauda
l elongation of the mesonephros. Limb reduction defects were obtained
when the mesonephros was prevented from forming caudal to somite 14. N
o limb defects were seen when a foil barrier was placed into the inter
mediate mesoderm at the level of somite 21 or 25. Our results support
the notion that a signal from the mesonephros is necessary for normal
limb development. In addition, it appears that a craniocaudal factor e
manating from the mesonephros prays a role in limb development. The li
mb reduction defects obtained in this study were also compared to the
pattern of thalidomide embryopathy in humans. There is a close corresp
ondence between the types of limb reduction anomalies seen with thalid
omide and mesonephric blocks and between the severity of defects vs. t
he timing of thalidomide intake or mesonephric blockage. A model for p
ossible thalidomide embryopathy is presented. (C) 1996 Wiley-Liss, Inc
.