A. Rowe et al., DEVELOPMENT OF THE SPATIAL PATTERN OF RETINOIC ACID RECEPTOR-BETA TRANSCRIPTS IN EMBRYONIC CHICK FACIAL PRIMORDIA, Development, 114(3), 1992, pp. 805-813
Retinoic acid causes a range of embryonic defects, including craniofac
ial abnormalities, in both birds and mammals and is believed to have a
number of roles in normal development. We have previously shown that
the distribution of retinoic acid receptor-beta (RAR-beta transcripts
is spatially restricted within the neural-crest-derived upper beak pri
mordia of the chick embryo. We have now used in situ hybridisation to
trace the distribution of RAR-beta transcripts during the migration of
cranial neural crest cells and during formation of these primordia. R
AR-beta transcripts were present in a subset of migrating neural-crest
-derived cells in the head of the stage 10 embryo. These cells were si
tuated in pathways followed by cells that migrate from the neural cres
t overlying the posterior prosencephalic/anterior mesencephalic region
of the developing brain. Cells containing RAR-beta transcripts accumu
lated around the developing eyes and in the regions of the ventral hea
d from which the upper beak primordia later develop. We mapped the dis
tribution of RAR-beta transcripts as the facial primordia were forming
, with particular reference to the development of the maxillary primor
dia. We found that these form in a region of the ventral head that inc
ludes the boundary between regions of high and low levels of RAR-beta
transcripts. The boundary between these two groups of cells persisted
as the maxillary primordia developed. The restriction of RAR-beta tran
scripts to a subset of migrating neural crest cells which arise from a
specific region of the neural crest, and which give rise to precisely
distributed populations of cells, provides further evidence that ther
e is some form of prepatterning in the neural crest from which the fac
ial primordia originate.