期刊
ELIFE
卷 10, 期 -, 页码 -出版社
eLIFE SCIENCES PUBL LTD
DOI: 10.7554/eLife.65910
关键词
CapZ; F-actin; endosome; RAB5; endosomal trafficking; Rabaptin-5; Arp2; 3; Rabex-5; Human
类别
资金
- Research Grants Council, University Grants Committee [11101717, 11103620]
- National Natural Science Foundation of China [21778045, 2070702]
- Science, Technology and Innovation Commission of Shenzhen Municipality [JCYJ20160229165235739, JCYJ20170413141331470]
The study reveals that CapZ regulates endosomal trafficking by controlling the density of F-actin around early endosomes and recruiting RAB5 effectors.
Actin filaments (F-actin) have been implicated in various steps of endosomal trafficking, and the length of F-actin is controlled by actin capping proteins, such as CapZ, which is a stable heterodimeric protein complex consisting of alpha and beta subunits. However, the role of these capping proteins in endosomal trafficking remains elusive. Here, we found that CapZ docks to endocytic vesicles via its C-terminal actin-binding motif. CapZ knockout significantly increases the F-actin density around immature early endosomes, and this impedes fusion between these vesicles, manifested by the accumulation of small endocytic vesicles in CapZ-knockout cells. CapZ also recruits several RAB5 effectors, such as Rabaptin-5 and Rabex-5, to RAB5-positive early endosomes via its N-terminal domain, and this further activates RAB5. Collectively, our results indicate that CapZ regulates endosomal trafficking by controlling actin density around early endosomes and recruiting RAB5 effectors.
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