RalA-exocyst-dependent Recycling Endosome Trafficking Is Required for the Completion of Cytokinesis

In eukaryotic cells, recycling endosome-mediated trafficking contributes to the completion of cytokinesis, in a manner under the control of the centrosome. We report that the exocyst complex and its interacting GTPase RalA play a critical role in this polarized trafficking process. RalA resides in t...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of biological chemistry 2006-12, Vol.281 (50), p.38609-38616
Main Authors: Chen, Xiao-Wei, Inoue, Mayumi, Hsu, Shu C., Saltiel, Alan R.
Format: Article
Language:English
Subjects:
3T3 Cells
Animals
Base Sequence
Cytokinesis
Endosomes - metabolism
Fluorescent Antibody Technique
Mice
Protein Transport
ral GTP-Binding Proteins - metabolism
RNA, Small Interfering
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:In eukaryotic cells, recycling endosome-mediated trafficking contributes to the completion of cytokinesis, in a manner under the control of the centrosome. We report that the exocyst complex and its interacting GTPase RalA play a critical role in this polarized trafficking process. RalA resides in the recycling endosome and relocates from the pericentrosomal region to key cytokinetic structures including the cleavage furrow, and later, the abscission site. This event is coupled to the dynamic redistribution of the exocyst proteins. These associate with the centrosome in interphase and concentrate on the central spindle/midbody during cytokinesis. Disruption of RalA-exocyst function leads to cytokinesis failure in late stages, particularly abscission, resembling the cytokinesis defects induced by loss of centrosome function. These data suggest that RalA and the exocyst may regulate vesicle delivery to the centrosome-related abscission site during the terminal stage of cytokinesis, implicating RalA as a critical regulator of cell cycle progression.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.M512847200