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Rab22A recruits BLOC ‐1 and BLOC ‐2 to promote the biogenesis of recycling endosomes
Author(s) -
Shakya Saurabh,
Sharma Prerna,
Bhatt Anshul Milap,
Jani Riddhi Atul,
Delevoye Cédric,
Gangi Setty Subba Rao
Publication year - 2018
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201845918
Subject(s) - endosome , microbiology and biotechnology , biogenesis , biology , rab , escrt , organelle , lysosome , intracellular , biochemistry , gtpase , enzyme , gene
Abstract Recycling endosomes ( RE s) are transient endosomal tubular intermediates of early/sorting endosomes (E/ SE s) 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 RNA i 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/ SE s or lysosomes. Rab22A forms a complex with BLOC ‐1, BLOC ‐2 and the kinesin‐3 family motor KIF 13A 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‐ KIF 13A complex on E/ SE s to generate RE s that maintain cellular and organelle homeostasis.