ArticleCytoskeleton (Hoboken, N.J.)2015
Combinatorial genetic analysis of a network of actin disassembly-promoting factors.
Article in Cytoskeleton (Hoboken, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Direct observation of cortactin protecting Arp2/3-actin filament branch junctions from GMF-mediated destabilization.European journal of cell biology · 2024Article
- Mechanisms of actin disassembly and turnover.The Journal of cell biology · 2023Review
- Cytosolic concentrations of actin binding proteins and the implications for in vivo F-actin turnover.The Journal of cell biology · 2023Article
- HIV Infection: Shaping the Complex, Dynamic, and Interconnected Network of the Cytoskeleton.International journal of molecular sciences · 2023Review
- Coro1B and Coro1C regulate lamellipodia dynamics and cell motility by tuning branched actin turnover.The Journal of cell biology · 2022Article
- Long non-coding RNA FGD5-AS1 contributes to cisplatin resistance in hepatocellular carcinoma via sponging microRNA-153-3p by upregulating Twinfilin Actin Binding Protein 1 (TWF1).Bioengineered · 2021Article
- The Actin-Disassembly Protein Glia Maturation Factor γ Enhances Actin Remodeling and B Cell Antigen Receptor Signaling at the Immune Synapse.Frontiers in cell and developmental biology · 2021Article
- Genetically inspired in vitro reconstitution ofMolecular biology of the cell · 2020Article
- The discovery of actin: "to see what everyone else has seen, and to think what nobody has thought".Journal of muscle research and cell motility · 2020Review
- MicroRNA-30c inhibits pancreatic cancer cell proliferation by targeting twinfilin 1 and indicates a poor prognosis.World journal of gastroenterology · 2019Article
- Species-Specific Functions of Twinfilin in Actin Filament Depolymerization.Journal of molecular biology · 2018Article
- GMF as an Actin Network Remodeling Factor.Trends in cell biology · 2018Review
- ADF/Cofilin Accelerates Actin Dynamics by Severing Filaments and Promoting Their Depolymerization at Both Ends.Current biology : CB · 2017Article
- Global treadmilling coordinates actin turnover and controls the size of actin networks.Nature reviews. Molecular cell biology · 2017Review
- The C-terminal dimerization motif of cyclase-associated protein is essential for actin monomer regulation.The Biochemical journal · 2016Article
- Ssp1 CaMKK: A Sensor of Actin Polarization That Controls Mitotic Commitment through Srk1 in Schizosaccharomyces pombe.PloS one · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The patterning of actin cytoskeleton structures in vivo is a product of spatially and temporally regulated polymer assembly balanced by polymer disassembly. While in recent years our understanding of actin assembly mechanisms has grown immensely, our knowledge of actin disassembly machinery and mechanisms has remained comparatively sparse. Saccharomyces cerevisiae is an ideal system to tackle this problem, both because of its amenabilities to genetic manipulation and live-cell imaging and because only a single gene encodes each of the core disassembly factors: cofilin (COF1), Srv2/CAP (SRV2), Aip1 (AIP1), GMF (GMF1/AIM7), coronin (CRN1), and twinfilin (TWF1). Among these six factors, only the functions of cofilin are essential and have been well defined. Here, we investigated the functions of the nonessential actin disassembly factors by performing genetic and live-cell imaging analyses on a combinatorial set of isogenic single, double, triple, and quadruple mutants in S. cerevisiae. Our results show that each disassembly factor makes an important contribution to cell viability, actin organization, and endocytosis. Further, our data reveal new relationships among these factors, providing insights into how they work together to orchestrate actin turnover. Finally, we observe specific combinations of mutations that are lethal, e.g., srv2Δ aip1Δ and srv2Δ crn1Δ twf1Δ, demonstrating that while cofilin is essential, it is not sufficient in vivo, and that combinations of the other disassembly factors perform vital functions.
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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.