ArticleCurrent biology : CB2017
Profilin Directly Promotes Microtubule Growth through Residues Mutated in Amyotrophic Lateral Sclerosis.
Article in Current biology : CB, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 75 citations in OpenAlex.
- Profilin-1 Deficiency Activates STING to Drive T Cell-Mediated Anti-Tumor Immunity in Breast Cancer.bioRxiv : the preprint server for biology · 2026Article
- Profilin and Its Isoforms: Unravelling the Functional Diversity Across Life Forms.Current protein & peptide science · 2026Review
- OsBRK1-mediated phosphorylation of OsPFN2 regulates meiotic spindle-actin assembly and rice fertility.Plant communications · 2025Article
- Viral-mediated knockdown of Atxn2 attenuates TDP-43 pathology and muscle dysfunction in the PFN1Acta neuropathologica communications · 2025Article
- Using ALS to understand profilin 1's diverse roles in cellular physiology.Cytoskeleton (Hoboken, N.J.) · 2025Review
- Mechanical confinement prevents ectopic platelet release.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Prolonged depletion of profilin 1 or F-actin causes an adaptive response in microtubules.The Journal of cell biology · 2024Article
- Profilin affects microtubule dynamics via actin.The Journal of cell biology · 2024Article
- Article
- Expression of ALS-PFN1 impairs vesicular degradation in iPSC-derived microglia.Nature communications · 2024Article
- Transcriptome analysis of the cerebral cortex of acrylamide-exposed wild-type and IL-1β-knockout mice.Archives of toxicology · 2024Article
- Proximity Proteomics Revealed Aberrant mRNA Splicing Elicited by ALS-Linked Profilin-1 Mutants.Analytical chemistry · 2023Article
- Vascular endothelial cell-specific disruption of thePNAS nexus · 2023Article
- Changes in cell surface excess are coordinated with protrusion dynamics during 3D motility.Biophysical journal · 2023Article
- Cytoskeletal adaptation following long-term dysregulation of actomyosin in neuronal processes.bioRxiv : the preprint server for biology · 2023Article
- Novel variant c.92T > G (p.Val31Gly) in theFrontiers in neurology · 2023Article
- How neurons maintain their axons long-term: an integrated view of axon biology and pathology.Frontiers in neuroscience · 2023Review
- Fine-grained, nonlinear registration of live cell movies reveals spatiotemporal organization of diffuse molecular processes.PLoS computational biology · 2022Article
- Structure of the Monkeypox virus profilin-like protein A42R reveals potential functional differences from cellular profilins.Acta crystallographica. Section F, Structural biology communications · 2022Article
- Multiple roles for the cytoskeleton in ALS.Experimental neurology · 2022Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Profilin is an abundant actin monomer-binding protein with critical actin regulatory roles in vivo [1, 2]. However, profilin also influences microtubule dynamics in cells, which may be mediated in part through its interactions with formins that in turn bind microtubules [3, 4]. Specific residues on human profilin-1 (PFN1) are mutated in patients with amyotrophic lateral sclerosis (ALS) [5, 6]. However, the observation that some ALS-linked PFN1 mutants fail to alter cellular actin organization or dynamics [5-8] or in vitro actin-monomer affinity [9] has been perplexing, given that profilin is best understood as an actin regulator. Here, we investigated direct effects of profilin on microtubule dynamics and whether ALS-linked mutations in PFN1 disrupt such functions. We found that human, fly, and yeast profilin homologs all directly enhance microtubule growth rate by several-fold in vitro. Microtubule stimulatory effects were unaffected by mutations in the canonical actin- or poly-proline-binding sites of profilin. Instead, microtubule activities depended on specific surface residues on profilin mutated in ALS patients. Furthermore, microtubule effects were attenuated by increasing concentrations of actin monomers, suggesting competition between actin and microtubules for binding profilin. Consistent with these biochemical observations, a 2-fold increase in the expression level of wild-type PFN1, but not the ALS-linked PFN1 mutants, increased microtubule growth rates in cells. Together, these results demonstrate that profilin directly enhances the growth rate of microtubules. They further suggest that ALS-linked mutations in PFN1 may perturb cellular microtubule dynamics and/or the coordination between the actin and microtubule cytoskeletons, leading to motor neuron degeneration.
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