Abstract
This Paper describes the development of theluxate syndrome in mice. The manifold detects of limbs, urogenital system and lumbar vertebrae are traced back to three underlying causes, namely, (i) a craniad shift of the hind-limb girdle, with (ii) imperfect morphogenetic control, or (iii) loss, of the anterior end of the limb field. Craniad shift of the hind-limb region is demonstrable in 101/2-day embryos. The limb defects give rise to defects of the umbilical arteries; these lead to the urogenital defects. A possible unitary hypothesis is discussed, whereby all the effects of theluxate gene could be attributed to a single gene effect, craniacl shift of the hind-limb inductor relative to a supposedly limited region of limb potency.
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