Fig. 7. A functional secretory pathway is maintained in GBF1-depleted cells. (A) GBF1 depletion inhibits COPI recruitment to membranes and leads to an increased frequency of tubular connections between the ERGIC and the cis-Golgi. Despite the block in COPI recruitment, a functional pathway capable of trafficking soluble cargo proteins is maintained in GBF1-depleted cells. However, trafficking of transmembrane cargo proteins is inhibited without COPI-mediated events. (B) In control cells, tubular connections between the ERGIC and the cis-Golgi facilitate trafficking of soluble proteins by a COPI-independent mechanism. The tubules might also transit transmembrane proteins by a COPI-requiring mechanism.