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PLoS Genet. 2016 Jun 6;12(6):e1006093. doi: 10.1371/journal.pgen.1006093. eCollection 2016 Jun.

RAB-10 Promotes EHBP-1 Bridging of Filamentous Actin and Tubular Recycling Endosomes.

Author information

1
Department of Medical Genetics, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
2
Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, New Jersey, United States of America.
3
Institute for Brain Research, Huazhong University of Science and Technology, Wuhan, Hubei, China.
4
Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Abstract

EHBP-1 (Ehbp1) is a conserved regulator of endocytic recycling, acting as an effector of small GTPases including RAB-10 (Rab10). Here we present evidence that EHBP-1 associates with tubular endosomal phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2] enriched membranes through an N-terminal C2-like (NT-C2) domain, and define residues within the NT-C2 domain that mediate membrane interaction. Furthermore, our results indicate that the EHBP-1 central calponin homology (CH) domain binds to actin microfilaments in a reaction that is stimulated by RAB-10(GTP). Loss of any aspect of this RAB-10/EHBP-1 system in the C. elegans intestinal epithelium leads to retention of basolateral recycling cargo in endosomes that have lost their normal tubular endosomal network (TEN) organization. We propose a mechanism whereby RAB-10 promotes the ability of endosome-bound EHBP-1 to also bind to the actin cytoskeleton, thereby promoting endosomal tubulation.

PMID:
27272733
PMCID:
PMC4894640
DOI:
10.1371/journal.pgen.1006093
[Indexed for MEDLINE]
Free PMC Article

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