ArticleBiophysical journal1999
Myosin I contributes to the generation of resting cortical tension.
Article in Biophysical journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 177 citations in OpenAlex.
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- Self-organization of PIP3 waves is controlled by the topology and curvature of cell membranes.Biophysical journal · 2024Article
- A conserved pressure-driven mechanism for regulating cytosolic osmolarity.Current biology : CB · 2023Article
- A conserved pressure-driven mechanism for regulating cytosolic osmolarity.bioRxiv : the preprint server for biology · 2023Article
- MYO1H is a novel candidate gene for autosomal dominant pure hereditary spastic paraplegia.Molecular genetics and genomics : MGG · 2022Article
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- Single-cell mechanical analysis and tension quantification via electrodeformation relaxation.Physical review. E · 2021Article
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- Unite to divide - how models and biological experimentation have come together to reveal mechanisms of cytokinesis.Journal of cell science · 2018Review
- Getting in shape and swimming: the role of cortical forces and membrane heterogeneity in eukaryotic cells.Journal of mathematical biology · 2018Article
- The actin cortex at a glance.Journal of cell science · 2018Review
- In pursuit of the mechanics that shape cell surfaces.Nature physics · 2018Article
- Myosin-1c promotes E-cadherin tension and force-dependent recruitment of α-actinin to the epithelial cell junction.Journal of cell science · 2018Article
- Method to study cell migration under uniaxial compression.Molecular biology of the cell · 2017Article
- Mechanochemical Signaling Directs Cell-Shape Change.Biophysical journal · 2017Review
- The biomechanical properties of an epithelial tissue determine the location of its vasculature.Nature communications · 2016Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The amoeboid myosin I's are required for cellular cortical functions such as pseudopod formation and macropinocytosis, as demonstrated by the finding that Dictyostelium cells overexpressing or lacking one or more of these actin-based motors are defective in these processes. Defects in these processes are concomitant with changes in the actin-filled cortex of various Dictyostelium myosin I mutants. Given that the amoeboid myosin I's possess both actin- and membrane-binding domains, the mutant phenotypes could be due to alterations in the generation and/or regulation of cell cortical tension. This has been directly tested by analyzing mutant Dictyostelium that either lacks or overexpresses various myosin I's, using micropipette aspiration techniques. Dictyostelium cells lacking only one myosin I have normal levels of cortical tension. However, myosin I double mutants have significantly reduced (50%) cortical tension, and those that mildly overexpress an amoeboid myosin I exhibit increased cortical tension. Treatment of either type of mutant with the lectin concanavalin A (ConA) that cross-links surface receptors results in significant increases in cortical tension, suggesting that the contractile activity of these myosin I's is not controlled by this stimulus. These results demonstrate that myosin I's work cooperatively to contribute substantially to the generation of resting cortical tension that is required for efficient cell migration and macropinocytosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.