No abstract

Several lines of evidence suggest that Wnt genes play a critical role in regulating development of the vertebrate embryo. To address the role that this family may play in the development of the chicken central nervous system (CNS), we have used a PCR based strategy to clone partial sequences for Wnt genes. At least six different Wnt genes are expressed in the developing CNS of the chick embryo. The domains of expression overlap either partially or completely, and are expressed in spatial domains that prefigure morphological subunits of the embryonic neural tube. Wnt-1 and Wnt-4 are first expressed in the open neural plate in the region of the presumptive mesencephalon. Wnt-3a expression is first observed in the rhombencephalic regions of the open neural plate. After neural tube closure, when the embryonic subdivisions of the neural tube became apparent, Wnt-1, Wnt-3a and Wnt-4 are all broadly expressed in partially overlapping domains in the mesencephalon and caudal diencephalon, as well as in the rhombencephalon and spinal cord. The mesencephalic expression patterns are subsequently modified such that Wnt-1 and Wnt-4 are expressed in a characteristic ring just rostral to the isthmus, at the mesencephalic/metencephalic junction; and Wnt-1 and Wnt-3a expression become restricted to the dorsal midline. Wnt-1, Wnt-3a, Wnt-4, Wnt-5a and Wnt-8b are expressed in one or two caudal subdivisions of the developing diencephalon, the synencephalon and posterior parencephalon, but do not extend ventral to the zona limitans interparencephalica. In contrast, Wnt-7b is expressed in the anterior parencephalon. Both Wnt-7b and Wnt-8b are expressed in telencephalic portions of the secondary prosencephalon. The timing and spatial distribution of Wnt-gene expression in the chick embryo further support the general hypothesis that Wnt genes play key roles in patterning the developing vertebrate nervous system.

Motor hyperplasia following the enlargement of the periphery by implantation of a supernumerary leg is not due to "remote control" of proliferation, as shown by motor neuron counts in 6-day chick embryos. We have tested the alternative hypothesis that we are dealing with reduction of the naturally occurring cell death. In normal development, the lumbar lateral motor column (l.m.c.) undergoes motor neuron degeneration resulting in a cell loss of at least 40%, which occurs between six and one-half and nine and one-half days. Following transplantation of supernumerary legs, cases selected for vigorous motility showed a numerical difference between experimental and contralateral (control) sides amounting to +11.0% to +27.5%. The transplants were innervated by varying combinations of thoracic and rostral lumbar nerves. We interpret our data in terms of survival of motor neurons which normally would have failed in a competition at the periphery but which were sustained by the enlarged peripheral fields. Our data do not permit a decision between the two alternatives: competition for synaptic sites or for a trophic agent. The surviving motor neurons are not limited to the rostral segments of the motor column but in most instances distributed along its entire rostro-caudal extent, implying a redistribution of all l.m.c. axons. The term "hyperplasia" is no longer appropriate for the phenomenon under consideration and should be replaced by the term "hypothanasia.""

No abstract

Motor pool positions for individual leg muscles were mapped in hatched chicks using intramuscular injections of HRP. Several leg muscles were also mapped in stage 38 (12-day) embryos. The results indicate that an adult map is formed by stage 38. The adult motor pool map can be viewed as being composed of two maps, one for muscles derived from the embryonic ventral muscle mass, the other for muscles derived from the dorsal mass. Each of these maps is a continuous, although distorted, representation of muscle precursor position on the original sheets of dorsal and ventral muscle mass. The developmental implications of these findings are discussed.