Evidence for endogenous proteases, mRNA level and insulin as multiple mechanisms of N-cadherin down-regulation during retinal development.

Our previous studies of the role of cell adhesion in retinal development have focused on the expression and function of N-cadherin, the predominant calcium-dependent intercellular adhesion protein of neural tissues. During the course of retinal development, N-cadherin expression undergoes significant qualitative and quantitative changes in its pattern of expression, most prominently a sharp down-regulation of expression throughout most of the retina. The present studies were directed at investigating the epigenetic mechanisms that could mediate this loss of N-cadherin from the retina. Using an in vitro intact retinal organ culture system, results were obtained which suggest that insulin enhances the down-regulation of N-cadherin expression in a protein-synthesis-dependent fashion. Furthermore, the metalloprotease inhibitor 1,10-phenanthroline inhibits the loss of N-cadherin from the retina. While N-cadherin is down-regulated in organ culture, other cell adhesion molecules, which are not down-regulated in vivo, are also not down-regulated in organ culture. The defined organ culture medium conditioned by the retina accumulates both a soluble 90 x 10(3) M(r) N-terminal fragment of N-cadherin as well as a number of secreted proteases. Both of these components are also shown to be present in vivo in the vitreous humor. Northern blot analysis indicates a single mRNA encoding N-cadherin in the retina and no evidence for a second message that could encode the 90 x 10(3) M(r) fragment. However, the amount of N-cadherin mRNA detectable on northern blots decreases during development. The results reported here suggest that the down-regulation of N-cadherin that occurs during retinal development is possibly mediated by multiple mechanisms, which include turnover at the cell surface mediated by endogenous proteolysis, reduced levels of N-cadherin mRNA and modulation by growth factors.     

Contrasting Effects of the Cotton Defoliant Thidiazuron and Aminoethoxyvinylglycine,an Inhibitor of Ethylene Formation,on Stomatal Aperture and on Ethylene Formation in Bean (Phaseolus vulgaris) Leaves

The cotton defoliant, thidiazuron, 1-phenyl-3-(1,2,3-thiadiazol-5-yl)-urea stimulated ethylene formation in primary leaves of Phaseolus vulgaris var. Favorit, three to eight days after spraying. Aminoethoxyvinylglycine (AVG), an inhibitor of ethylene formation, delayed this ethylene outburst by two to three days when sprayed together with the defoliant. Under conditions of dryness, thidiazuron inhibited the stomatal closure of bean leaves. Spraying with AVG counteracted this effect of thidiazuron on the stomates and caused a partial and reversible closure ca 1 day after spraying.