ArticleMolecular & cellular proteomics : MCP2012
Cells lacking β-actin are genetically reprogrammed and maintain conditional migratory capacity.
Article in Molecular & cellular proteomics : MCP, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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54 citing papers in PubMed, 91 citations in OpenAlex.
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- Nuclear actin-dependent Meg3 expression suppresses metabolic genes by affecting the chromatin architecture at sites of elevated H3K27 acetylation levels.Nucleic acids research · 2025Article
- Reference genes for qPCR expression in black tiger shrimp, Penaeus monodon.Molecular biology reports · 2024Article
- Mechanistic toxicology in light of genetic compensation.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Actin Polymerization Defects Induce Mitochondrial Dysfunction in Cellular Models of Nemaline Myopathies.Antioxidants (Basel, Switzerland) · 2023Article
- A defective mechanosensing pathway affects fibroblast-to-myofibroblast transition in the old male mouse heart.iScience · 2023Article
- Structural insights into actin isoforms.eLife · 2023Article
- Silencing of Nesprin-2 inhibits the differentiation of myofibroblasts from fibroblasts induced by mechanical stretch.International wound journal · 2022Article
- The association betweenFrontiers in cardiovascular medicine · 2022Article
- The Cytoplasmic Actins in the Regulation of Endothelial Cell Function.International journal of molecular sciences · 2021Review
- The remodelling of actin composition as a hallmark of cancer.Translational oncology · 2021Review
- High-content siRNA 3D co-cultures to identify myoepithelial cell-derived breast cancer suppressor proteins.Scientific data · 2021Article
- The regulation of actin dynamics during cell division and malignancy.American journal of cancer research · 2021Review
- Emerging roles of cytoskeletal proteins in regulating gene expression and genome organization during differentiation.Nucleus (Austin, Tex.) · 2020Review
- Knockout ofInternational journal of molecular sciences · 2020Article
- Biological approaches for hypertrophic scars.International wound journal · 2020Review
- Transcriptional adaptation ineLife · 2020Article
- T-type, but not L-type, voltage-gated calcium channels are dispensable for lymphatic pacemaking and spontaneous contractions.Scientific reports · 2020Article
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Authors and funding
18 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vertebrate nonmuscle cells express two actin isoforms: cytoplasmic β- and γ-actin. Because of the presence and localized translation of β-actin at the leading edge, this isoform is generally accepted to specifically generate protrusive forces for cell migration. Recent evidence also implicates β-actin in gene regulation. Cell migration without β-actin has remained unstudied until recently and it is unclear whether other actin isoforms can compensate for this cytoplasmic function and/or for its nuclear role. Primary mouse embryonic fibroblasts lacking β-actin display compensatory expression of other actin isoforms. Consistent with this preservation of polymerization capacity, β-actin knockout cells have unchanged lamellipodial protrusion rates despite a severe migration defect. To solve this paradox we applied quantitative proteomics revealing a broad genetic reprogramming of β-actin knockout cells. This also explains why reintroducing β-actin in knockout cells does not restore the affected cell migration. Pathway analysis suggested increased Rho-ROCK signaling, consistent with observed phenotypic changes. We therefore developed and tested a model explaining the phenotypes in β-actin knockout cells based on increased Rho-ROCK signaling and increased TGFβ production resulting in increased adhesion and contractility in the knockout cells. Inhibiting ROCK or myosin restores migration of β-actin knockout cells indicating that other actins compensate for β-actin in this process. Consequently, isoactins act redundantly in providing propulsive forces for cell migration, but β-actin has a unique nuclear function, regulating expression on transcriptional and post-translational levels, thereby preventing myogenic differentiation.
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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.