Rab22A recruits BLOC-1 and BLOC-2 to promote the biogenesis of recycling endosomes.

Autor: Shakya S; Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India., Sharma P; Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India., Bhatt AM; Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India., Jani RA; Structure and Membrane Compartments, CNRS, UMR 144, Institut Curie, PSL Research University, Paris, France., Delevoye C; Structure and Membrane Compartments, CNRS, UMR 144, Institut Curie, PSL Research University, Paris, France.; Cell and Tissue Imaging Facility (PICT-IBiSA), CNRS, UMR 144, Institut Curie, PSL Research University, Paris, France., Setty SR; Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India subba@iisc.ac.in.
Jazyk: angličtina
Zdroj: EMBO reports [EMBO Rep] 2018 Dec; Vol. 19 (12). Date of Electronic Publication: 2018 Nov 07.
DOI: 10.15252/embr.201845918
Abstrakt: Recycling endosomes (REs) are transient endosomal tubular intermediates of early/sorting endosomes (E/SEs) that function in cargo recycling to the cell surface and deliver the cell type-specific cargo to lysosome-related organelles such as melanosomes in melanocytes. However, the mechanism of RE biogenesis is largely unknown. In this study, by using an endosomal Rab-specific RNAi screen, we identified Rab22A as a critical player during RE biogenesis. Rab22A-knockdown results in reduced RE dynamics and concurrent cargo accumulation in the E/SEs or lysosomes. Rab22A forms a complex with BLOC-1, BLOC-2 and the kinesin-3 family motor KIF13A on endosomes. Consistently, the RE-dependent transport defects observed in Rab22A-depleted cells phenocopy those in BLOC-1-/BLOC-2-deficient cells. Further, Rab22A depletion reduced the membrane association of BLOC-1/BLOC-2. Taken together, these findings suggest that Rab22A promotes the assembly of a BLOC-1-BLOC-2-KIF13A complex on E/SEs to generate REs that maintain cellular and organelle homeostasis.
(© 2018 The Authors. Published under the terms of the CC BY 4.0 license.)
Databáze: MEDLINE
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