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Vol. 10, Issue 5, 1445-1462, May 1999
Department of Biological Sciences, Carnegie Mellon University,
Pittsburgh, Pennsylvania 15213
Physiological conditions that impinge on constitutive traffic
and affect organelle structure are not known. We report that osmotically induced cell volume changes, which are known to occur under
a variety of conditions, rapidly inhibited endoplasmic reticulum (ER)-to-Golgi transport in mammalian cells. Both ER export and ER Golgi
intermediate compartment (ERGIC)-to-Golgi trafficking steps were
blocked, but retrograde transport was active, and it mediated ERGIC and
Golgi collapse into the ER. Extensive tubulation and relatively rapid
Golgi resident redistribution were observed under hypo-osmotic
conditions, whereas a slower redistribution of the same markers,
without apparent tubulation, was observed under hyperosmotic
conditions. The osmotic stress response correlated with the
perturbation of COPI function, because both hypo- and hyperosmotic
conditions slowed brefeldin A-induced dissociation of 
COP from Golgi
membranes. Remarkably, Golgi residents reemerged after several hours of
sustained incubation in hypotonic or hypertonic medium. Reemergence was
independent of new protein synthesis but required PKC, an
activity known to mediate cell volume recovery. Taken together these
results indicate the existence of a coupling between cell volume and
constitutive traffic that impacts organelle structure through
independent effects on anterograde and retrograde flow and that
involves, in part, modulation of COPI function.
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