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Figure 11. Model for unconventional cilia targeting of P/rds. A, The summarized localizations of P/rds and the CT truncations in photoreceptor cells and mammalian cells. ++, +, +/−, and − indicate that the transgenes' signals were strong, weak, very weak, and undetectable, respectively. Note: When overexpressed in mammalian cells, P/rds can also be detected in Golgi and other intracellular compartments. B, In both mammalian cells (left) and X. laevis rods (right), P/rds bypasses the Golgi apparatus, either the later portions or altogether, to reach the cilia, thus taking an unconventional secretory pathway (green arrow, P/rds). The Golgi retention signal prevents conventional secretion of P/rds1-312 or P/rds1-316 (red arrow, P/rds1-312 or P/rds1-316), but does not block unconventional cilia targeting in rods (red dash-dotted arrow), likely due to trafficking driven by oligomerization with endogenous P/rds. After release from Golgi (left, blue dotted arrow, P/rds1-288), P/rds1-288 is incapable of taking the secretory pathway in mammalian cells (left, blue arrow). Routes labeled 1 and 2 are the estimated routes explaining the cell-line-dependent variability observed between hTERT-RPE1 and IMCD3 cells. Neither 1 or 2 is a complete secretory pathway and cannot deliver P/rds1-288 to the cell surface. P/rds1-288 can reach the cilium through unconventional secretion in rods (right, blue dotted and dash-dotted arrows).

Image published in: Tian G et al. (2014)

Copyright © 2014. This image is reproduced with permission of the publisher and the copyright holder. This is an Open Access article distributed under the terms of the Creative Commons Attribution License.

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