P34(CDC2) AND MITOTIC CYCLIN EXPRESSION IN THE DEVELOPING QUAIL NEURORETINA

After an initial proliferation phase, neurons of the central nervous s ystem (CNS) of higher eukaryotes remain postmitotic during their entir e lifespan. This requires that a very stringent control be exerted on the cell division apparatus, whose molecular mechanisms remain quite e lusive. Here we have used quail neuroretina as a model to study the co ntrol of cell division in the developing CNS. In vertebrates, embryoni c neuroretinal cells (NR cells) stop their proliferation at different times depending on the cell type. Most NR cells in the quail embryo be come postmitotic between E7 and E8. To acquire a better understanding of the molecular events leading to quiescence in NR cells, we have ana lyzed the expression of cdc2 and of two activators of p34(cdc2): cycli n A and cyclin B2 in the developing neuroretina. We report that these three proteins are downregulated between E7 and E9, suggesting that a common mechanism could block their transcription in differentiating ne urons. We also report, using an immunohistochemical approach, that p34 (cdc2) downregulation is correlated with the appearance of the microtu bule-associated protein tau. These results strongly suggest that inhib ition of cdc2 gene expression is closely linked to the achievement of terminal differentiation in neurons. However, we also show that postmi totic ganglion cells precursors begin to synthesize the early neuronal differentiation marker beta(3)-tubulin while p34(cdc2) is Still detec table in these cells, suggesting that p34(cdc2) or a closely related k inase could play a role in some ''young'' postmitotic neurons.