GRIP1 is involved in the interaction of vimentin filaments with focal adhesions in endothelial cells

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Vimentin intermediate filaments are dynamic structures that are able to move in cytoplasm due to activity of the motor proteins, kinesin-1 and cytoplasmic dynein. How exactly motors interact with vimentin filaments remains unclear. In this work, I show that Glutamate Receptor Interacting Protein (GRIP1) known as adapter for kinesin-1 on neuronal cargoes is also a mediator for kinesin-1 interaction with vimentin filaments, and this interaction provides crosstalk between vimentin filaments and focal adhesions. GRIP1 associates with vimentin filaments in various cells and co-immunoprecipitates with vimentin from cell lysate. Human endothelial cells knockout by GRIP1 gene lose focal adhesions and dramatically change their adhesive properties. Hypothetically, kinesin-1 engages GRIP1 to deliver vimentin filaments to the cell periphery so that they make contact with focal adhesions and stabilize them.

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作者简介

F. Gyoeva

Institute of Protein Research, Russian Academy of Sciences

编辑信件的主要联系方式.
Email: fgyoeva@gmail.com
俄罗斯联邦, Pouschino, Moscow Region, 142290

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2. Fig. 1. Characterization of anti-GRIP1 antibodies using immunoblotting and immunofluorescence staining. a – Schematic diagram of the GRIP1 molecule structure. б – Result of immunoblotting of REF52 rat fibroblast homogenate with anti-GRIP1 antibodies. в – REF52 cells treated simultaneously with anti-GRIP1 and anti-vimentin antibodies. г – The same staining of REF52 cells pre-treated with colcemid until complete depolymerization of microtubules. Scale bar is 10 μm in all images.

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3. Fig. 2. Antibodies to GRIP1 do not interact with vimentin, but precipitate it from the cell extract. a – Two identical immunoblots with a homogenate of CAD cells treated in parallel with antibodies to GRIP1 and vimentin. б – GRIP1 was precipitated from the extract (1) of REF52 cells; the anti-GRIP1 precipitate (2) contained vimentin, in contrast to the control (3) obtained by incubating the same portion of the cell extract with pure agarose beads with bound protein A.

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4. Fig. 3. Dominant-negative inhibition of GRIP1 interaction with kinesin affects the entry of intermediate filaments (IF) into CAD cell neurites. a – Schematic representation of the position of GBD (GRIP1 Binding Domain) on the kinesin heavy chain. б – Effect of the presence of GBD on IF distribution in CAD cells. Cells in complete medium were transfected with a plasmid encoding GFP-GBD, GFP (as a control), or GFP-GBD-short and after 20–24 h were transferred to serum-free medium to induce process formation for the next 48 h. Cells were then fixed and subjected to immunofluorescence staining with anti-mouse vimentin 3c8 (б), anti-GRIP1 (в, images inverted for clarity), anti-α-tubulin DM1α (г), and anti-neurofilament protein NF-M N2912 (д). Scale bar is 10 μm in all images.

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5. Fig. 4. Knockout of the GRIP1 gene alters the adhesive properties of CAD cells but does not prevent the filling of processes with vimentin. a – Immunoblotting of control and GRIP1 knockout CAD cell homogenates with anti-GRIP1 antibodies. б – Comparison of immunofluorescence staining of control and GRIP1 knockout CAD cells with anti-GRIP1 antibodies. в – Phase-contrast image of control and GRIP1 knockout CAD cells in complete and serum-free medium. г – Immunofluorescence staining of control and GRIP1 knockout CAD cells incubated in serum-free medium with anti-vimentin antibodies. Panels б and г – scale bar 10 μm.

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6. Fig. 5. Knockout of the GRIP1 gene in EA.hy926 endothelial cells. a – Comparison of homogenates of EA.hy926 cells – control and with knockout of the GRIP1 protein gene, in immunoblotting with anti-GRIP1 antibodies. б – Comparison of EA.hy926 cells – control and with knockout of the GRIP1 protein gene – by double immunofluorescence staining with anti-GRIP1 antibodies and antibodies to vimentin.

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7. Fig. 6. GRIP1-depleted EA.hy926 endothelial cells lack FC and have altered HF locations. a – Phase-contrast image of EA.hy926 cells – control and with GRIP1 gene knockout. б – Distribution of vimentin (V9 antibody) in EA.hy926 cells – control and with GRIP1 gene knockout, on plain glass and glass coated with poly-L-lysine. в – Immunofluorescence staining of EA.hy926 cells (control and with GRIP1 gene knockout) with antibodies to vinculin, a FC marker. FC are indicated by arrows. Scale bars (б and в) are 10 μm, (a) – 50 μm.

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8. Fig. 7. GRIP1 and focal adhesions (FA) colocalize at the fibroblast periphery. Relative positions of filaments decorated with anti-GRIP1 antibodies (a) and FA (б) in REF52 fibroblast. FA are visualized by the expression of a plasmid encoding human zyxin fused with the fluorescent protein mKate. The last image (г) is an enlarged region highlighted in the merged image (в).

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