ArticleNature communications2021
Mechanism of actin-dependent activation of nucleotidyl cyclase toxins from bacterial human pathogens.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- Interplay between T3SS effectors, ExoY activation, and cGMP signaling in Pseudomonas aeruginosa infection.Nature communications · 2025Article
- Cryo-EM structure revealed a novel F-actin binding motif in abioRxiv : the preprint server for biology · 2025Article
- Biofilm Formation ofMicroorganisms · 2025Review
- Structure of the F-tractin-F-actin complex.The Journal of cell biology · 2025Article
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
- Structure and activation mechanism of the Makes caterpillars floppy 1 toxin.Nature communications · 2023Article
- Molecular mechanisms of inorganic-phosphate release from the core and barbed end of actin filaments.Nature structural & molecular biology · 2023Article
- Functional and structural insights into the multi-step activation and catalytic mechanism of bacterial ExoY nucleotidyl cyclase toxins bound to actin-profilin.PLoS pathogens · 2023Article
- Actin dynamics in protein homeostasis.Bioscience reports · 2022Review
- Mechanism of threonine ADP-ribosylation of F-actin by a Tc toxin.Nature communications · 2022Article
- Bacterial Nucleotidyl Cyclases Activated by Calmodulin or Actin in Host Cells: Enzyme Specificities and Cytotoxicity Mechanisms Identified to Date.International journal of molecular sciences · 2022Review
- Molecular Mechanisms Involved in Pseudomonas aeruginosa Bacteremia.Advances in experimental medicine and biology · 2022Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial human pathogens secrete initially inactive nucleotidyl cyclases that become potent enzymes by binding to actin inside eukaryotic host cells. The underlying molecular mechanism of this activation is, however, unclear. Here, we report structures of ExoY from Pseudomonas aeruginosa and Vibrio vulnificus bound to their corresponding activators F-actin and profilin-G-actin. The structures reveal that in contrast to the apo-state, two flexible regions become ordered and interact strongly with actin. The specific stabilization of these regions results in an allosteric stabilization of the nucleotide binding pocket and thereby to an activation of the enzyme. Differences in the sequence and conformation of the actin-binding regions are responsible for the selective binding to either F- or G-actin. Other nucleotidyl cyclase toxins that bind to calmodulin rather than actin undergo a similar disordered-to-ordered transition during activation, suggesting that the allosteric activation-by-stabilization mechanism of ExoY is conserved in these enzymes, albeit the different activator.
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