Vimentin supports cell polarization by enhancing centrosome function and microtubule acetylation
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Abstract
Cell polarity is important for controlling cell shape, motility, and cell division processes. Vimentin intermediate filaments are necessary for proper polarization of migrating fibroblasts and assembly of vimentin and microtubule networks is dynamically coordinated, but the precise details of how vimentin mediates cell polarity remain unclear. Here, we characterize the effects of vimentin on the structure and function of the centrosome and the stability of microtubule filaments in wild-type and vimentin-null mouse embryonic fibroblasts (mEFs). We find that vimentin mediates the structure of the pericentrosomal material, promotes centrosome-mediated microtubule regrowth, and increases the level of stable acetylated microtubules in the cell. Loss of vimentin also impairs centrosome repositioning during cell polarization and migration processes that occur during wound closure. Our results suggest that vimentin modulates centrosome structure and function as well as microtubule network stability, which has important implications for how cells establish proper cell polarization and persistent migration.
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Abstract
Re: figure 4 and the associated claim, is acetylated alpha-tubulin normalized by the total alpha tubulin intensity less? Or is it proportional to reduced microtubes generally in vim-/- MEFs? Given PCM defects and impaired re-assembly of mictotubules after nocodazole treatment, basal turnover and the total mictotubule network may also be affected in vim-/- MEFs, but if I’m not mistaken, that’s never quantified here. Depending on the normalized outcome, the reduced acetylation rates may be independently reliant upon vimentin or be a consequence of globally reduced microtubules.
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Abstract
Re: figure 4 and the associated claim, is acetylated alpha-tubulin normalized by the total alpha tubulin intensity less? Or is it proportional to reduced microtubes generally in vim-/- MEFs? Given PCM defects and impaired re-assembly of mictotubules after nocodazole treatment, basal turnover and the total mictotubule network may also be affected in vim-/- MEFs, but if I’m not mistaken, that’s never quantified here. Depending on the normalized outcome, the reduced acetylation rates may be independently reliant upon vimentin or be a consequence of globally reduced microtubules.
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