Involvement of cellular retinoic acid-binding proteins I and II (CRABPI and CRABPII) and of the cellular retinol-binding protein I (CRBPI) in odontogenesis in the mouse.
The coordination of the activities of individual cells during development is regulated in part by epigenetic signals either encoded in the insoluble extracellular matrix or provided by small diffusible factors such as growth factors peptides and retinoids. Odontogenesis offers a suitable model to correlate the temporospatial distributions of such molecules, and of their cell receptors and ligands, with particular developmental processes. We have analyzed, by in situ hybridization, the distribution patterns of CRABPI, CRABPII and CRBPI transcripts during odontogenesis in the mouse. CRABPI transcripts were restricted to the mitogenic regions of the dental mesenchyme during late bell stages and were absent from post-mitotic odontoblasts. The only epithelial site of CRABPI transcription was the labial epithelial loop of the continuously growing incisor. CRABPII transcription was preponderant in the mitogenic zones of the dental epithelium: differential labeling of the dental epithelium occurred as early as the dental bud stage and during subsequent molar morphogenesis, this labeling became confined in the epithelial loops. The graded distribution of CRABPII transcripts along the anteroposterior axis of the continuously growing incisor was superimposed with the gradient of mitoses. CRABPII transcripts were absent from post-mitotic ameloblasts. It is concluded that during odontogenesis the expressions of the CRABPI and CRABPII genes are confined to regions exhibiting the highest rate of cell proliferation whenever differential mitotic activity is required. Moreover, the putative effects of retinoic acid on the regulation of cell proliferation kinetics in the dental epithelium and in the dental mesenchyme imply distinct CRABPs. CRBPI transcripts were restricted to the dental mesenchyme prior to the onset of CRABPI transcription. This observation supports the hypothesis that the two proteins might perform antagonistic functions in some retinoic acid-mediated developmental processes.
Mark
M P
MP
Institut de Biologie Médicale, INSERM-Université Louis Pasteur, Faculté de Médecine, Strasbourg, France.
Bloch-Zupan
A
A
Wolf
C
C
Ruberte
E
E
Ruch
J V
JV
D000818:Animals; D002352:Carrier Proteins / Q000235:genetics / Q000502:physiology*; D004247:DNA / Q000235:genetics; D005455:Fluorescent Antibody Technique; D007180:Incisor / Q000737:chemistry / Q000196:embryology; D051379:Mice; D009693:Nucleic Acid Hybridization; D009805:Odontogenesis / Q000235:genetics / Q000502:physiology*; D015347:RNA Probes; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D018168:Receptors, Retinoic Acid; D012177:Retinol-Binding Proteins / Q000235:genetics / Q000502:physiology*; D054840:Retinol-Binding Proteins, Cellular; D014158:Transcription, Genetic / Q000235:genetics
D002352:Carrier Proteins; D015347:RNA Probes; D012333:RNA, Messenger; D018168:Receptors, Retinoic Acid; D012177:Retinol-Binding Proteins; D054840:Retinol-Binding Proteins, Cellular; D004247:DNA