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J. Cell Biol.,
Volume 142, Number 3, August 10, 1998 697-710
* Margaret M. Dyson Vision Research Institute, Department of Ophthalmology and Department of Cell Biology and Anatomy,
Cornell University Medical College, New York 10021; and Retinal pigment epithelial (RPE) cells apically polarize proteins that are basolateral in other
epithelia. This reversal may be generated by the association of RPE with photoreceptors and the interphotoreceptor matrix, postnatal expansion of the RPE apical
surface, and/or changes in RPE sorting machinery. We
compared two proteins exhibiting reversed, apical polarities in RPE cells, neural cell adhesion molecule
(N-CAM; 140-kD isoform) and extracellular matrix
metalloproteinase inducer (EMMPRIN), with the
cognate apical marker, p75-neurotrophin receptor
(p75-NTR). N-CAM and p75-NTR were apically localized from birth to adulthood, contrasting with a basolateral to apical switch of EMMPRIN in developing
postnatal rat RPE. Morphometric analysis demonstrated that this switch cannot be attributed to expansion of the apical surface of maturing RPE because the
basolateral membrane expanded proportionally, maintaining a 3:1 apical/basolateral ratio. Kinetic analysis of
polarized surface delivery in MDCK and RPE-J cells
showed that EMMPRIN has a basolateral signal in its
cytoplasmic tail recognized by both cell lines. In contrast, the basolateral signal of N-CAM is recognized by
MDCK cells but not RPE-J cells. Deletion of N-CAM's
basolateral signal did not prevent its apical localization
in vivo. The data demonstrate that the apical polarity of
EMMPRIN and N-CAM in mature RPE results from
suppressed decoding of specific basolateral signals resulting in randomized delivery to the cell surface.
Laboratory of Immunology, National Eye Institute, Bethesda,
Maryland 20892
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