Rab11 Regulates Recycling through the Pericentriolar Recycling Endosome

Rab11 Regulates Recycling through the Pericentriolar Recycling Endosome

November 1996 | Oliver Ullrich, Sigrid Reinsch, Sylvie Urbé, Marino Zerial, Robert G. Parton
Rab11 regulates recycling through the pericentriolar recycling endosome. Rab11 is a small GTPase that plays a key role in the regulation of membrane traffic. In this study, it was shown that Rab11 colocalizes with internalized transferrin in the pericentriolar recycling compartment of CHO and BHK cells. Expression of Rab11 mutants that are preferentially in the GTP- or GDP-bound state caused opposite effects on the distribution of transferrin-containing elements. Rab11-GTP caused accumulation of labeled elements in the perinuclear area of the cell, whereas Rab11-GDP caused a dispersion of the transferrin labeling. Functional studies showed that the early steps of uptake and recycling for transferrin were not affected by overexpression of Rab11 proteins. However, recycling from the later recycling endosome was inhibited in cells overexpressing the Rab11-GDP mutant. Rab5, which regulates early endocytic trafficking, acted before Rab11 in the transferrin-recycling pathway as expression of Rab5-GTP prevented transport to the Rab11-positive recycling endosome. These results suggest a novel role for Rab11 in controlling traffic through the recycling endosome. Rab11 is associated with the pericentriolar recycling endosome and regulates the "slow cycle" of transferrin recycling through this compartment. Rab11 is also present on the Golgi complex and the recycling endosome. Rab11 shows partial colocalization with overexpressed WT Rab5, but not with mutant GTP-bound Rab5. Rab11 mutants have opposite effects on the recycling endosomes, comparable to the effects of Rab5 mutants on the sorting endosomes. The effect of Rab11 mutants on transferrin recycling was studied, and it was found that Rab11 controls the traffic through the recycling endosome. The study also shows that Rab11 is a good candidate for a component of the molecular machinery involved in the traffic through the recycling endosome. The results suggest that Rab11 is involved in the transport from the sorting endosome to the recycling endosome. The study also highlights the complexity of the endocytic and recycling pathways and the need for more molecular markers to understand these pathways.Rab11 regulates recycling through the pericentriolar recycling endosome. Rab11 is a small GTPase that plays a key role in the regulation of membrane traffic. In this study, it was shown that Rab11 colocalizes with internalized transferrin in the pericentriolar recycling compartment of CHO and BHK cells. Expression of Rab11 mutants that are preferentially in the GTP- or GDP-bound state caused opposite effects on the distribution of transferrin-containing elements. Rab11-GTP caused accumulation of labeled elements in the perinuclear area of the cell, whereas Rab11-GDP caused a dispersion of the transferrin labeling. Functional studies showed that the early steps of uptake and recycling for transferrin were not affected by overexpression of Rab11 proteins. However, recycling from the later recycling endosome was inhibited in cells overexpressing the Rab11-GDP mutant. Rab5, which regulates early endocytic trafficking, acted before Rab11 in the transferrin-recycling pathway as expression of Rab5-GTP prevented transport to the Rab11-positive recycling endosome. These results suggest a novel role for Rab11 in controlling traffic through the recycling endosome. Rab11 is associated with the pericentriolar recycling endosome and regulates the "slow cycle" of transferrin recycling through this compartment. Rab11 is also present on the Golgi complex and the recycling endosome. Rab11 shows partial colocalization with overexpressed WT Rab5, but not with mutant GTP-bound Rab5. Rab11 mutants have opposite effects on the recycling endosomes, comparable to the effects of Rab5 mutants on the sorting endosomes. The effect of Rab11 mutants on transferrin recycling was studied, and it was found that Rab11 controls the traffic through the recycling endosome. The study also shows that Rab11 is a good candidate for a component of the molecular machinery involved in the traffic through the recycling endosome. The results suggest that Rab11 is involved in the transport from the sorting endosome to the recycling endosome. The study also highlights the complexity of the endocytic and recycling pathways and the need for more molecular markers to understand these pathways.
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