Development of the spatial pattern of retinoic acid receptor-beta transcripts in embryonic chick facial primordia

Retinoic acid causes a range of embryonic defects, including craniofacial 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 primordia 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. RAR-beta transcripts were present in a subset of migrating neural-crest-derived cells in the head of the stage 10 embryo. These cells were situated in pathways followed by cells that migrate from the neural crest overlying the posterior prosencephalic/anterior mesencephalic region of the developing brain. Cells containing RAR-beta transcripts accumulated around the developing eyes and in the regions of the ventral head from which the upper beak primordia later develop. We mapped the distribution of RAR-beta transcripts as the facial primordia were forming, with particular reference to the development of the maxillary primordia. We found that these form in a region of the ventral head that includes 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.(ABSTRACT TRUNCATED AT 250 WORDS)

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Retinoic acid treatment alters the distribution of retinoic acid receptor-beta transcripts in the embryonic chick face

Development ◽

10.1242/dev.111.4.1007 ◽

1991 ◽

Vol 111 (4) ◽

pp. 1007-1016 ◽

Cited By ~ 2

Author(s):

A. Rowe ◽

J.M. Richman ◽

P.M. Brickell

Keyword(s):

Retinoic Acid ◽

Retinoic Acid Receptor ◽

Anterior Part ◽

In Situ Hybridisation ◽

Cdna Clones ◽

Acid Receptor ◽

Facial Defect ◽

Retinoic Acid Receptor Beta ◽

Frontonasal Mass ◽

Receptor Beta

Retinoic acid is a metabolite of vitamin A that can act as a signalling molecule in a number of developmental systems. Retinoic acid is also known to be teratogenic in mammals, causing a range of defects including abnormalities in craniofacial development. Exposure of the developing chick face to retinoic acid released slowly from a bead implanted in the wing bud results in a specific facial defect, in which outgrowth of the frontonasal mass is inhibited. This results in clefting of the primary palate and absence of the upper beak. To investigate the role of nuclear retinoic acid receptors in normal and abnormal chick face morphogenesis, we isolated chick retinoic acid receptor-beta (RAR-beta) cDNA clones and probed northern blots of RNA isolated from chick embryos at stages 22, 24 and 25 and from adults. RAR-beta transcripts of 2.8 and 3.5 kb were present in several regions of the embryo, including the facial primordia, and were also present at much lower levels in adult tissues. In situ hybridisation showed that RAR-beta transcripts were present in all of the facial primordia at embryonic stages 20, 24 and 28, but that their distribution was not uniform. Transcripts were abundant in the lateral nasal processes, at the edges and corners of the frontonasal mass and in the anterior part of the maxillary primordia. Lower levels were present elsewhere. Treatment of stage 20 embryos with retinoic acid altered the distribution of RAR-beta transcripts in the maxillary primordia, such that high levels of transcripts were present throughout, rather than being confined to the anterior part. This change was detectable at stage 24, before any alterations in the morphology of the facial primordia were apparent. By stage 28, when the morphology of the facial primordia was clearly abnormal, there were more widespread changes in the distribution of RAR-beta transcripts. These results show that RAR-beta transcripts are particularly concentrated in regions of the primordia that give rise to the upper beak, the development of which is specifically affected by retinoic acid. In addition, they demonstrate that retinoic acid can induce changes in the pattern of expression of RAR-beta transcripts in vivo.

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