High impact information on Rab11

• In pIIb, Delta passes through the recycling endosome which is marked by Rab 11 [1].
• In pIIa, however, the recycling endosome does not form because the centrosome fails to recruit Nuclear fallout, a Rab 11 binding partner that is essential for recycling endosome formation [1].
• Actin cytoskeleton remodeling during early Drosophila furrow formation requires recycling endosomal components Nuclear-fallout and Rab11 [2].
• Nuf is a homologue of arfophilin-2, an ADP ribosylation factor effector that binds Rab11 and influences recycling endosome (RE) organization [2].
• Taken together, these data identify Bchs as an antagonist of Rab11 during development and uncover a role for these regulators of vesicle trafficking in synaptic morphogenesis [3].

Biological context of Rab11

• Bchs, a BEACH domain protein, antagonizes Rab11 in synapse morphogenesis and other developmental events [3].
• Trafficking through Rab11 endosomes is required for cellularization during Drosophila embryogenesis [4].
• We identify Rab11 endosomes as key trafficking intermediates that control vesicle exocytosis and membrane growth during cellularization [4].
• Decreased levels of Rab11 protein and increased cell death in Rab11mo third-instar larval eye-antennal discs suggest that the retinal defects originate during larval development [5].
• In an effort to identify the role of Rab11, a small GTP binding protein, during Drosophila differentiation, phenotypic manifestations associated with different alleles of Rab11 were studied [5].

Anatomical context of Rab11

• Such analyses also reveal a requirement for Rab11 in the organization of microtubule plus ends and osk mRNA localization and translation [6].
• Specifically, we show that alpha-adaptin and Rab11, which function critically in the endocytic pathways of all previously examined animal cells, are localized to neighboring compartments at the posterior pole of stage 8-10 oocytes [6].
• We also provide evidence that in fly photoreceptors Sec15 colocalizes with Rab11 and that loss of Sec15 affects rhabdomere morphology [7].
• Furthermore, new work reveals that vesicles derived from the Rab11 recycling endosome (RE) promote actin remodeling at the furrow [8].
• Rab11, a small GTPase implicated in membrane traffic, immunolocalizes to the trans-Golgi network, cytoplasmic vesicles and tubules, and the base of rhabdomeres [9].

Physical interactions of Rab11

• These results establish a role for Rab11 in the post-Golgi transport of rhodopsin and of other proteins to the rhabdomeric membranes of photoreceptors, and in analogous transport processes in other cells [9].
• Furthermore, Rab11 is required for transport of TRP, another rhabdomeric protein, and for development of specialized membrane structures within Garland cells [9].

Co-localisations of Rab11

• One hour after release from the endoplasmic reticulum, rhodopsin colocalizes with Rab11 in vesicles at the base of the rhabdomere [9].

Regulatory relationships of Rab11

• In addition, shibire controls vesicular trafficking through Rab11-positive endosomes [4].

Other interactions of Rab11

• This C-terminal domain was found to bind a subset of Rab GTPases, especially Rab11, in a GTP-dependent manner [7].
• Rab11 mediates post-Golgi trafficking of rhodopsin to the photosensitive apical membrane of Drosophila photoreceptors [9].
• Consistent with a direct role of shibire in vesicular trafficking through Rab11 endosomes, Shibire is enriched in this compartment [4].
• During the process, individual cell boundaries grow and shrink, resulting in local neighbor exchanges, and Cadherin is actively endocytosed and recycled through Rab11 endosomes [10].

References