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The ESCRT Complexes: from Lysosome Biogenesis to Viral Budding
Author(s) -
Hurley James H
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.433.1
Subject(s) - escrt , cytokinesis , midbody , budding , biogenesis , microbiology and biotechnology , tsg101 , biology , ingression , abscission , septin , organelle biogenesis , chemistry , endosome , cell division , biochemistry , cell , genetics , microvesicles , intracellular , microrna , gene
The ESCRT machinery consists of five complexes conserved from yeast through humans, ESCRT 0‐III and VPS4‐VTA1, and the ALIX protein. These complexes carry out a conserved membrane scission reaction in HIV‐1 budding, the biogenesis of multivesicular bodies, and the membrane abscission step in cytokinesis. I first address how ESCRT complexes assemble on membranes. With respect to cytokinesis, ESCRT‐I and ALIX are recruited to the midbody, the site of the membrane abscission step in the final separation of daughter cells, by interactions between GPPXY motifs and a non‐canonical coiled‐coil in CEP55. The ESCRT complexes and spastin coordinate membrane abscission with the cleavage of microtubules in the central spindle. ESCRT‐I and ALIX are targeted to the site of HIV‐1 budding by direct interactions with PTAP and YPXL motifs, respectively, in HIV‐1 Gag p6. In MVB biogenesis, HIV‐1 budding, and cytokinesis, ESCRT‐I and ALIX either directly or indirectly, recruit ESCRT‐III. ESCRT‐III is thought to be responsible for the membrane scission. A model for the recruitment and action of the ESCRTs and ALIX to their sites of action in HIV‐1 budding, cytokinesis, and MVB biogenesis has been formulated.