ArticleProceedings of the National Academy of Sciences of the United States of America2020
Regulation of INF2-mediated actin polymerization through site-specific lysine acetylation of actin itself.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 56 citations in OpenAlex.
- ERM Inhibition Confers Ferroptosis Resistance through ROS-Induced NRF2 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Regulation of the formin INF2 by actin monomers and calcium/calmodulin.The Journal of cell biology · 2026Article
- Structural and functional dissection of the WH2/DAD motif of INF2, a formin linked to human inherited degenerative disorders.The FEBS journal · 2026Article
- Structural and functional mechanisms of actin isoforms.The FEBS journal · 2025Review
- HDAC11-Mediated Deacetylation of Triosephosphate Isomerase 1 Promotes Idiopathic Pulmonary Fibrosis.Research (Washington, D.C.) · 2025Article
- Regulation of formin INF2 and its alteration in INF2-linked inherited disorders.Cellular and molecular life sciences : CMLS · 2024Review
- INF2 mutations cause kidney disease through a gain-of-function mechanism.Science advances · 2024Article
- Cyclase-associated protein (CAP) inhibits inverted formin 2 (INF2) to induce dendritic spine maturation.Cellular and molecular life sciences : CMLS · 2024Article
- INF2 formin variants linked to human inherited kidney disease reprogram the transcriptome, causing mitotic chaos and cell death.Cellular and molecular life sciences : CMLS · 2024Article
- The DNA-dependent protein kinase catalytic subunit promotes sepsis-induced cardiac dysfunction through disrupting INF-2-dependent mitochondrial dynamics.International journal of medical sciences · 2024Article
- Activated Drp1 Initiates the Formation of Endoplasmic Reticulum-Mitochondrial Contacts via Shrm4-Mediated Actin Bundling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Purification of modified mammalian actin isoforms for in vitro reconstitution assays.European journal of cell biology · 2023Review
- Actin Isoform Composition and Binding Factors Fine-Tune Regulatory Impact of Mical Enzymes.International journal of molecular sciences · 2023Article
- Acetylation-dependent coupling between G6PD activity and apoptotic signaling.Nature communications · 2023Article
- Characterization of cytoskeletal and structural effects of INF2 variants causing glomerulopathy and neuropathy.Scientific reports · 2023Article
- Purification of human β- and γ-actin from budding yeast.Journal of cell science · 2023Article
- INF2-mediated actin filament reorganization confers intrinsic resilience to neuronal ischemic injury.Nature communications · 2022Article
- A solution to the long-standing problem of actin expression and purification.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Myosin II proteins are required for organization of calcium-induced actin networks upstream of mitochondrial division.Molecular biology of the cell · 2022Article
- Role of formin INF2 in human diseases.Molecular biology reports · 2022Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
INF2 is a formin protein that accelerates actin polymerization. A common mechanism for formin regulation is autoinhibition, through interaction between the N-terminal diaphanous inhibitory domain (DID) and C-terminal diaphanous autoregulatory domain (DAD). We recently showed that INF2 uses a variant of this mechanism that we term "facilitated autoinhibition," whereby a complex consisting of cyclase-associated protein (CAP) bound to lysine-acetylated actin (KAc-actin) is required for INF2 inhibition, in a manner requiring INF2-DID. Deacetylation of actin in the CAP/KAc-actin complex activates INF2. Here we use lysine-to-glutamine mutations as acetylmimetics to map the relevant lysines on actin for INF2 regulation, focusing on K50, K61, and K328. Biochemically, K50Q- and K61Q-actin, when bound to CAP2, inhibit full-length INF2 but not INF2 lacking DID. When not bound to CAP, these mutant actins polymerize similarly to WT-actin in the presence or absence of INF2, suggesting that the effect of the mutation is directly on INF2 regulation. In U2OS cells, K50Q- and K61Q-actin inhibit INF2-mediated actin polymerization when expressed at low levels. Direct-binding studies show that the CAP WH2 domain binds INF2-DID with submicromolar affinity but has weak affinity for actin monomers, while INF2-DAD binds CAP/K50Q-actin 5-fold better than CAP/WT-actin. Actin in complex with full-length CAP2 is predominately ATP-bound. These interactions suggest an inhibition model whereby CAP/KAc-actin serves as a bridge between INF2 DID and DAD. In U2OS cells, INF2 is 90-fold and 5-fold less abundant than CAP1 and CAP2, respectively, suggesting that there is sufficient CAP for full INF2 inhibition.
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