Maryline Beurg, Dakota Elle Konrad, Robert Fettiplace
Transmembrane channel-like protein 1 (TMC1), a pore-forming component of the mechano-electrical transducer (MET) channel in cochlear outer hair cells, is subject to numerous mutations causing deafness and hair cell death. We studied mice harboring semidominant mutations Tmc1 p.T416K, p.M412K, and p.D569N, which all display functional MET channels at postnatal day (P)6 but become deaf by P21. Early signs of concomitant hair cell apoptosis were assayed in neonatal Tmc1 mutants by labeling with Calcein-acetomethyl ester (AM), MitoTracker, and Annexin V, the latter labeling scramblase externalization of phosphatidyl serine. Reduced labeling with Calcein-AM was correlated with reduced MitoTracker, the targeting of mitochondria being confirmed with the uncoupling agent carbonylcyanide p -trifluoromethoxyphenylhydrazone, and use of MitoLight to monitor mitochondrial membrane potential. These markers demonstrated mitochondrial dysfunction in Tmc1 mutants, even at P6 when MET currents were still present. Acoustic brainstem responses established that Tmc1 p.D569N and Tmc1 p.M412K mice were deaf by P15 and Tmc1 p.T416K by P21. Two methods of blocking the stereociliary PMCA2 Ca 2+ pump both elicited scramblase activity, suggesting that apoptosis is promoted by elevation of hair bundle [Ca 2+ ]. Reduced PMCA2 density was found in the stereocilia of Tmc1 mutants and was correlated with a decrease in MET channel Ca 2+ permeability. Cre-Lox excision of the mutant M412K exon at P1 fully preserved hearing across all frequencies by P19 and promoted recovery to wild type of PMCA2 density. These results demonstrate that hair cells in Tmc1 mutants have embarked on apoptosis at P6 and argue for connections between stereociliary PMCA2 density, hair cell apoptosis, and deafness.
{"title":"Hair cell apoptosis and deafness in Tmc1 mutations","authors":"Maryline Beurg, Dakota Elle Konrad, Robert Fettiplace","doi":"10.1073/pnas.2425215122","DOIUrl":"https://doi.org/10.1073/pnas.2425215122","url":null,"abstract":"Transmembrane channel-like protein 1 (TMC1), a pore-forming component of the mechano-electrical transducer (MET) channel in cochlear outer hair cells, is subject to numerous mutations causing deafness and hair cell death. We studied mice harboring semidominant mutations <jats:italic>Tmc1</jats:italic> p.T416K, p.M412K, and p.D569N, which all display functional MET channels at postnatal day (P)6 but become deaf by P21. Early signs of concomitant hair cell apoptosis were assayed in neonatal <jats:italic>Tmc1</jats:italic> mutants by labeling with Calcein-acetomethyl ester (AM), MitoTracker, and Annexin V, the latter labeling scramblase externalization of phosphatidyl serine. Reduced labeling with Calcein-AM was correlated with reduced MitoTracker, the targeting of mitochondria being confirmed with the uncoupling agent carbonylcyanide <jats:italic>p</jats:italic> -trifluoromethoxyphenylhydrazone, and use of MitoLight to monitor mitochondrial membrane potential. These markers demonstrated mitochondrial dysfunction in <jats:italic>Tmc1</jats:italic> mutants, even at P6 when MET currents were still present. Acoustic brainstem responses established that <jats:italic>Tmc1</jats:italic> p.D569N and <jats:italic>Tmc1</jats:italic> p.M412K mice were deaf by P15 and <jats:italic>Tmc1</jats:italic> p.T416K by P21. Two methods of blocking the stereociliary PMCA2 Ca <jats:sup>2+</jats:sup> pump both elicited scramblase activity, suggesting that apoptosis is promoted by elevation of hair bundle [Ca <jats:sup>2+</jats:sup> ]. Reduced PMCA2 density was found in the stereocilia of <jats:italic>Tmc1</jats:italic> mutants and was correlated with a decrease in MET channel Ca <jats:sup>2+</jats:sup> permeability. Cre-Lox excision of the mutant M412K exon at P1 fully preserved hearing across all frequencies by P19 and promoted recovery to wild type of PMCA2 density. These results demonstrate that hair cells in <jats:italic>Tmc1</jats:italic> mutants have embarked on apoptosis at P6 and argue for connections between stereociliary PMCA2 density, hair cell apoptosis, and deafness.","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"33 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143653414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-18Epub Date: 2025-03-10DOI: 10.1073/pnas.2501153122
Valerian V Dolja
{"title":"How nidoviruses evolved the largest known RNA genomes.","authors":"Valerian V Dolja","doi":"10.1073/pnas.2501153122","DOIUrl":"https://doi.org/10.1073/pnas.2501153122","url":null,"abstract":"","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"122 11","pages":"e2501153122"},"PeriodicalIF":9.4,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kairui Feng, Ning Lin, Robert E. Kopp, Siyuan Xian, Michael Oppenheimer
Conventional computational models of climate adaptation frameworks inadequately consider decision-makers’ capacity to learn, update, and improve decisions. Here, we investigate the potential of reinforcement learning (RL), a machine learning technique that efficaciously acquires knowledge from the environment and systematically optimizes dynamic decisions, in modeling and informing adaptive climate decision-making. We consider coastal flood risk mitigations for Manhattan, New York City, USA (NYC), illustrating the benefit of continuously incorporating observations of sea-level rise into systematic designs of adaptive strategies. We find that when designing adaptive seawalls to protect NYC, the RL-derived strategy significantly reduces the expected net cost by 6 to 36% under the moderate emissions scenario SSP2-4.5 (9 to 77% under the high emissions scenario SSP5-8.5), compared to conventional methods. When considering multiple adaptive policies, including accomodation and retreat as well as protection, the RL approach leads to a further 5% (15%) cost reduction, showing RL’s flexibility in coordinatively addressing complex policy design problems. RL also outperforms conventional methods in controlling tail risk (i.e., low probability, high impact outcomes) and in avoiding losses induced by misinformation about the climate state (e.g., deep uncertainty), demonstrating the importance of systematic learning and updating in addressing extremes and uncertainties related to climate adaptation.
{"title":"Reinforcement learning–based adaptive strategies for climate change adaptation: An application for coastal flood risk management","authors":"Kairui Feng, Ning Lin, Robert E. Kopp, Siyuan Xian, Michael Oppenheimer","doi":"10.1073/pnas.2402826122","DOIUrl":"https://doi.org/10.1073/pnas.2402826122","url":null,"abstract":"Conventional computational models of climate adaptation frameworks inadequately consider decision-makers’ capacity to learn, update, and improve decisions. Here, we investigate the potential of reinforcement learning (RL), a machine learning technique that efficaciously acquires knowledge from the environment and systematically optimizes dynamic decisions, in modeling and informing adaptive climate decision-making. We consider coastal flood risk mitigations for Manhattan, New York City, USA (NYC), illustrating the benefit of continuously incorporating observations of sea-level rise into systematic designs of adaptive strategies. We find that when designing adaptive seawalls to protect NYC, the RL-derived strategy significantly reduces the expected net cost by 6 to 36% under the moderate emissions scenario SSP2-4.5 (9 to 77% under the high emissions scenario SSP5-8.5), compared to conventional methods. When considering multiple adaptive policies, including accomodation and retreat as well as protection, the RL approach leads to a further 5% (15%) cost reduction, showing RL’s flexibility in coordinatively addressing complex policy design problems. RL also outperforms conventional methods in controlling tail risk (i.e., low probability, high impact outcomes) and in avoiding losses induced by misinformation about the climate state (e.g., deep uncertainty), demonstrating the importance of systematic learning and updating in addressing extremes and uncertainties related to climate adaptation.","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"55 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143653411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-18Epub Date: 2025-02-27DOI: 10.1073/pnas.2502585122
{"title":"Correction for Chae et al., Vulnerability to natural disasters and sustainable consumption: Unraveling political and regional differences.","authors":"","doi":"10.1073/pnas.2502585122","DOIUrl":"https://doi.org/10.1073/pnas.2502585122","url":null,"abstract":"","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"122 11","pages":"e2502585122"},"PeriodicalIF":9.4,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143524217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-18Epub Date: 2025-02-28DOI: 10.1073/pnas.2502598122
{"title":"Correction for Hogan et al., The genetic regulatory architecture and epigenomic basis for age-related changes in rattlesnake venom.","authors":"","doi":"10.1073/pnas.2502598122","DOIUrl":"https://doi.org/10.1073/pnas.2502598122","url":null,"abstract":"","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"122 11","pages":"e2502598122"},"PeriodicalIF":9.4,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143527987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-18Epub Date: 2025-03-06DOI: 10.1073/pnas.2424291122
Ethan L Grossman, Bryce B Barney, Zeyang Sun, Gregory A Henkes, Yang Gao, Michael M Joachimski
{"title":"Cold low-latitude Ordovician paleotemperatures may be in hot water.","authors":"Ethan L Grossman, Bryce B Barney, Zeyang Sun, Gregory A Henkes, Yang Gao, Michael M Joachimski","doi":"10.1073/pnas.2424291122","DOIUrl":"https://doi.org/10.1073/pnas.2424291122","url":null,"abstract":"","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"122 11","pages":"e2424291122"},"PeriodicalIF":9.4,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-18Epub Date: 2025-03-10DOI: 10.1073/pnas.2501246122
Harald Schwalbe, Ines Burkhart
{"title":"G-quadruplexes and their unexpected ability to fold proteins.","authors":"Harald Schwalbe, Ines Burkhart","doi":"10.1073/pnas.2501246122","DOIUrl":"https://doi.org/10.1073/pnas.2501246122","url":null,"abstract":"","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"122 11","pages":"e2501246122"},"PeriodicalIF":9.4,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ziwei Yang, Li Zhang, Samantha Ottavi, Jacob B. Geri, Andrew Perkowski, Xiuju Jiang, Daniel Pfau, Ruslana Bryk, Jeffrey Aubé, Matthew Zimmerman, Véronique Dartois, Carl Nathan
Mycobacterium tuberculosis (Mtb) primarily infects macrophages. In vitro without antibiotics, wild-type Mtb hastens death of the macrophages, but the processes leading to rapid cell death are not well understood. Our earlier work indicated that the death of Mtb-infected mouse macrophages in vitro is markedly exacerbated by induction of interferon-β (IFN-β) [L. Zhang et al., J. Exp. Med. 18 , e20200887 (2021)]. Here, we identified a key downstream response to IFN-β in the context of Mtb infection as the massive induction of cis-aconitate decarboxylase (ACOD1), not only in its canonical subcellular localization in mitochondria but also in the cytosol, where it bound to the lysosome-stabilizing protein HSP70. ACOD1’s product, itaconate, protected Mtb-infected macrophages. However, the contrasting and predominant effect of high-level ACOD1 expression was to act in a noncatalytic manner to promote HSP70’s degradation, leading to lysosomal membrane permeabilization (LMP). Mtb-induced macrophage death was markedly diminished by inhibitors of cysteine proteases, consistent with lysosome-mediated cell death. Neither ACOD1 inhibitors nor cysteine protease inhibitors are suitable for potential host-directed therapy (HDT) of tuberculosis. Instead, this work directs attention to how ACOD1 acts nonenzymatically to promote the degradation of HSP70.
{"title":"ACOD1-mediated lysosomal membrane permeabilization contributes to Mycobacterium tuberculosis –induced macrophage death","authors":"Ziwei Yang, Li Zhang, Samantha Ottavi, Jacob B. Geri, Andrew Perkowski, Xiuju Jiang, Daniel Pfau, Ruslana Bryk, Jeffrey Aubé, Matthew Zimmerman, Véronique Dartois, Carl Nathan","doi":"10.1073/pnas.2425309122","DOIUrl":"https://doi.org/10.1073/pnas.2425309122","url":null,"abstract":"<jats:italic>Mycobacterium tuberculosis</jats:italic> (Mtb) primarily infects macrophages. In vitro without antibiotics, wild-type Mtb hastens death of the macrophages, but the processes leading to rapid cell death are not well understood. Our earlier work indicated that the death of Mtb-infected mouse macrophages in vitro is markedly exacerbated by induction of interferon-β (IFN-β) [L. Zhang et al., <jats:italic>J. Exp. Med.</jats:italic> 18 , e20200887 (2021)]. Here, we identified a key downstream response to IFN-β in the context of Mtb infection as the massive induction of cis-aconitate decarboxylase (ACOD1), not only in its canonical subcellular localization in mitochondria but also in the cytosol, where it bound to the lysosome-stabilizing protein HSP70. ACOD1’s product, itaconate, protected Mtb-infected macrophages. However, the contrasting and predominant effect of high-level ACOD1 expression was to act in a noncatalytic manner to promote HSP70’s degradation, leading to lysosomal membrane permeabilization (LMP). Mtb-induced macrophage death was markedly diminished by inhibitors of cysteine proteases, consistent with lysosome-mediated cell death. Neither ACOD1 inhibitors nor cysteine protease inhibitors are suitable for potential host-directed therapy (HDT) of tuberculosis. Instead, this work directs attention to how ACOD1 acts nonenzymatically to promote the degradation of HSP70.","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"91 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143653400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lukas Rimle, Ben P. Phillips, Isabela M. Codo Costa Barra, Noëlle Arnold, Charlie Hennebert, Thomas Meier, Christoph von Ballmoos
Mitochondrial respiratory complexes I to IV and the F 1 F o -ATP synthase (complex V) are large protein assemblies producing the universal cellular energy currency adenosine triphosphate (ATP). Individual complexes have been extensively studied in vitro, but functional co-reconstitution of several mammalian complexes into proteoliposomes, in particular, the combination of a primary pump with the ATP synthase, is less well understood. Here, we present a generic and scalable strategy to purify mammalian respiratory complexes I, III and the ATP synthase from enriched mitochondria in enzymatically fully active form, and procedures to reassemble the complexes into liposomes. A robust functionality can be shown by in situ monitoring of ATP synthesis rates and by using selected inhibitors of the respiratory chain complexes. By inclusion of cytochrome c oxidase, our procedures allowed us to reconstruct the entire mitochondrial respiratory chain (complexes I, III, IV, and V) in ubiquinone Q 10 containing liposomes, demonstrating oxidative phosphorylation by nicotinamide adenine dinucleotide hydrogen driven ATP synthesis. The system was fully coupled at all levels and was used to probe cardiolipin as an essential component to activate the mammalian respiratory chain. Structural characterization using electron cryomicroscopy allowed us to resolve apo-state complex III and complex V at high and medium resolution, respectively, using in silico particle sorting, confirming the presence of all protein subunits and cofactors in native stoichiometry and conformation. The reported findings will facilitate future endeavors to characterize or modulate these key bioenergetic processes.
{"title":"A splendid molecular factory: De- and reconstruction of the mammalian respiratory chain","authors":"Lukas Rimle, Ben P. Phillips, Isabela M. Codo Costa Barra, Noëlle Arnold, Charlie Hennebert, Thomas Meier, Christoph von Ballmoos","doi":"10.1073/pnas.2416162122","DOIUrl":"https://doi.org/10.1073/pnas.2416162122","url":null,"abstract":"Mitochondrial respiratory complexes I to IV and the F <jats:sub>1</jats:sub> F <jats:sub>o</jats:sub> -ATP synthase (complex V) are large protein assemblies producing the universal cellular energy currency adenosine triphosphate (ATP). Individual complexes have been extensively studied in vitro, but functional co-reconstitution of several mammalian complexes into proteoliposomes, in particular, the combination of a primary pump with the ATP synthase, is less well understood. Here, we present a generic and scalable strategy to purify mammalian respiratory complexes I, III and the ATP synthase from enriched mitochondria in enzymatically fully active form, and procedures to reassemble the complexes into liposomes. A robust functionality can be shown by in situ monitoring of ATP synthesis rates and by using selected inhibitors of the respiratory chain complexes. By inclusion of cytochrome <jats:italic>c</jats:italic> oxidase, our procedures allowed us to reconstruct the entire mitochondrial respiratory chain (complexes I, III, IV, and V) in ubiquinone Q <jats:sub>10</jats:sub> containing liposomes, demonstrating oxidative phosphorylation by nicotinamide adenine dinucleotide hydrogen driven ATP synthesis. The system was fully coupled at all levels and was used to probe cardiolipin as an essential component to activate the mammalian respiratory chain. Structural characterization using electron cryomicroscopy allowed us to resolve apo-state complex III and complex V at high and medium resolution, respectively, using in silico particle sorting, confirming the presence of all protein subunits and cofactors in native stoichiometry and conformation. The reported findings will facilitate future endeavors to characterize or modulate these key bioenergetic processes.","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"47 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143653406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Karen Grace Bondoc-Naumovitz, Emanuele Crosato, Kirsty Y. Wan
Diatoms, a highly successful group of photosynthetic algae, contribute to a quarter of global primary production. Many species are motile, despite having no appendages and a completely rigid cell body. Cells move to seek out nutrients, locate mating partners, and undergo vertical migration. To explore the natural diversity of diatom motility, we perform a comparative study across five common biofilm-forming species. Combining morphological measurements with high-resolution cell tracking, we establish how gliding movements relate to the morphology of the raphe—a specialized slit in the cell wall responsible for motility generation. Our detailed analyses reveal that cells exhibit a rich but species-dependent phenotype, switching stochastically between four stereotyped motility states. We model this behavior and use stochastic simulations to predict how heterogeneity in microscale navigation patterns leads to differences in long-time diffusivity and dispersal. In a representative species, we extend these findings to quantify diatom gliding in complex, naturalistic 3D environments, suggesting that cells may exploit these distinct motility signatures to achieve niche segregation in nature.
{"title":"Functional morphology of gliding motility in benthic diatoms","authors":"Karen Grace Bondoc-Naumovitz, Emanuele Crosato, Kirsty Y. Wan","doi":"10.1073/pnas.2426910122","DOIUrl":"https://doi.org/10.1073/pnas.2426910122","url":null,"abstract":"Diatoms, a highly successful group of photosynthetic algae, contribute to a quarter of global primary production. Many species are motile, despite having no appendages and a completely rigid cell body. Cells move to seek out nutrients, locate mating partners, and undergo vertical migration. To explore the natural diversity of diatom motility, we perform a comparative study across five common biofilm-forming species. Combining morphological measurements with high-resolution cell tracking, we establish how gliding movements relate to the morphology of the raphe—a specialized slit in the cell wall responsible for motility generation. Our detailed analyses reveal that cells exhibit a rich but species-dependent phenotype, switching stochastically between four stereotyped motility states. We model this behavior and use stochastic simulations to predict how heterogeneity in microscale navigation patterns leads to differences in long-time diffusivity and dispersal. In a representative species, we extend these findings to quantify diatom gliding in complex, naturalistic 3D environments, suggesting that cells may exploit these distinct motility signatures to achieve niche segregation in nature.","PeriodicalId":20548,"journal":{"name":"Proceedings of the National Academy of Sciences of the United States of America","volume":"91 1","pages":""},"PeriodicalIF":11.1,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143653409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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