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Arl4D modulates microtubule dynamics via its interaction with EB1
Author(s) -
Lee FangJen Scott,
Lin ShinJin,
Huang Chunfang,
Wu TsungSheng,
Li ChunChun
Publication year - 2018
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.2018.32.1_supplement.lb139
Subject(s) - centrosome , microtubule , microbiology and biotechnology , microtubule associated protein , dynactin , microtubule nucleation , biology , tubulin , cytoskeleton , guanine nucleotide exchange factor , dynein , gtpase , chemistry , cell , genetics , cell cycle
ADP‐ribosylation factor (Arf)‐like 4D (Arl4D), one of Arf small GTPases, functions in cell morphology, cell migration, and actin cytoskeleton remodelling. EB1 is a microtubule plus end– tracking proteins that preferentially localized at the tips of growing microtubule plus ends and centrosome. Depletion of EB1 is known to result in many centrosome‐related defect. Here, we report that Arl4D binding to EB1 modulates microtubule plus‐end dynamics at the centrosome. In vivo and in vitro binding assay showed that Arl4D interacts with EB1 in a GTP‐dependent manner and C‐terminal EBH region of EB1 is both required and sufficient for this interaction. We found that Arl4D co‐localizes with γ‐tubulin in centrosomes and depletion of Arl4D resulted in centrosomal microtubule regrowth defect in COS‐7 cell. Arl4D knockout mouse embryonic fibroblasts (MEF) cells were also observed microtubule regrowth defect, which can be rescued by expressing human Arl4D. We also show that Arl4D‐EB1 interaction is essential for microtubule regrowth at the centrosome. In addition, we demonstrate that Arl4D binding to EB1 increases the association of the p150 Glued subunit of dynactin to EB1, which is important for microtubule stabilization. Together, our results indicate that Arl4D modulates microtubule dynamics through regulating EB1‐p150 association at the centrosome. Support or Funding Information National Health Research Institutes, Taiwan (NHRI‐EX106‐10601B1) This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

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