Universlty of Manitoba, ln Partîal Fulfiìlment - MSpace at the ...

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et al. 1961). tríth the single exception of a severely affected embryo
wlth myelodysplasia (showi.ng loss of all structures due to cystic
changes ln the caudal region), no notochordal abnormal i ties were seen in
the present series of chick embryos.
Howeve r the embryos with establ ished myeloschlsis showed separation
of the notochord from neural tissue at the cránial end of the leslon. ln
the looptal I mutant mouse open neural defects are a predomlnant expresslon
of the gene, and appear to arise by non-closure representlng a myeloschlsis.
Embryos lllustrated by Stein and Rudin (t953) sho" separat¡on of notochord
from the open neural defect at 10 days. Dav¡s (1942, 1944) by ,ultraviolet
lrradlation of Stage 7-9 chick embryos produced nryeloschlsls, similar to
the defects in the present embryos, also associated wìth notochordal
separation. A similar finding was reported by Ancel (1946-\7,1956), who
suggested that the separat¡on arose by incomplete separation of mesodern
lnto somltes at the end of gastrulation. .ln the.present embryos, however,
the gap was filled by a loose mesenchyme after the establ îshment of myeloschisis,
rather than by fused somitlc mesoderm before the formation of
the neural' defect.
Notochordal separation from the neural tube occurs as a normal
developmental process upon somíte díspersal and migration of sclerotome
cells. Even ôt Stage 10 in the present enbryos ¡t was seen at tbe
cephal ic end of the notochord, and by Stage 20 had extended into the
sornite region. Separatíon,rjid not occur in the early stages of myeloschisls,
and so appears to follow rather than cêuse non-closure. This
suggests a reduced adhesion between notochord and neural plate, but
it mlght reflect the fallure of some essent¡al inductlve process êt
an earl lei srase r¡jllán (1968).