Targeting and transport: How microtubules control focal adhesion dynamics
Open accessAbstract
Directional cell migration requires force generation that relies on the coordinated remodeling of interactions with the extracellular matrix (ECM), which is mediated by integrin-based focal adhesions (FAs). Normal FA turnover requires dynamic microtubules, and three members of the diverse group of microtubule plus-end-tracking proteins are principally involved in mediating microtubule interactions with FAs. Microtubules also alter the assembly state of FAs by modulating Rho GTPase signaling, and recent evidence suggests that microtubule-mediated clathrin-dependent and -independent endocytosis regulates FA dynamics. In addition, FA-associated microtubules may provide a polarized microtubule track for localized secretion of matrix metalloproteases (MMPs). Thus, different aspects of the molecular mechanisms by which microtubules control FA turnover in migrating cells are beginning to emerge.
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Local stabilization and expansion of microtubules near focal adhesions can potentially trigger GEF-H1 release and RhoA-dependent focal adhesion disassembly during cell movement.
“Furthermore, local stabilization and expansion of microtubules in the vicinity of focal adhesions 32,74 can potentially trigger GEF-H1 release and RhoA-dependent focal adhesion disassembly during cell movement.”
From Taxane-induced conformational changes in the microtubule lattice activate GEF-H1-dependent RhoA signalling (2026) · cites this paper as [74]
In “Microtubules modulate Rho GTPase signaling,” the paper says growing microtubules would be expected to sequester GEF-H1, decreasing rather than triggering RhoA activity; it also says a direct link between GEF-H1 and local microtubule-induced focal adhesion disassembly has not been established. In “Microtubule-mediated transport from and to FAs,” it reports that disassembly induced by microtubule regrowth is independent of RhoA activity. (LLM, conf=0.88)
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- Authors
- Stehbens, S., & Wittmann, T.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- Wittmann, Torsten
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2012-08-20
- Volume
- 198
- Issue
- 4
- Pages
- 481-489
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC3514042
- OpenAlex
- W2102283558
- Cited by
- 244
- References
- 111
- Citations by year
- 2026: 8 · 2025: 9 · 2024: 9 · 2023: 12 · 2022: 12 · 2021: 15 · 2020: 19 · 2019: 25 · 2018: 21 · 2017: 16 · 2016: 30 · 2015: 20 · 2014: 28 · 2013: 18 · 2012: 2
- FWCI
- 2.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Cell Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM079139)
- National Center for Research Resources (C06RR16490, C06RR016490, S10RR026758)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Keywords
- microtubules, focal adhesions, cell migration, integrins, extracellular matrix, microtubule plus-end tracking proteins, Rho GTPase signaling, endocytosis, clathrin, matrix metalloproteinases, focal adhesion turnover, cell polarity
- MeSH terms
- Animals, Endocytosis, Extracellular Matrix, Humans, Microtubules, Signal Transduction, Focal Adhesions
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