--- _id: '7776' abstract: - lang: eng text: We present an analysis of finite-size effects in jammed packings of N soft, frictionless spheres at zero temperature. There is a 1/N correction to the discrete jump in the contact number at the transition so that jammed packings exist only above isostaticity. As a result, the canonical power-law scalings of the contact number and elastic moduli break down at low pressure. These quantities exhibit scaling collapse with a nontrivial scaling function, demonstrating that the jamming transition can be considered a phase transition. Scaling is achieved as a function of N in both two and three dimensions, indicating an upper critical dimension of 2. article_number: '095704' article_processing_charge: No article_type: original author: - first_name: Carl Peter full_name: Goodrich, Carl Peter id: EB352CD2-F68A-11E9-89C5-A432E6697425 last_name: Goodrich orcid: 0000-0002-1307-5074 - first_name: Andrea J. full_name: Liu, Andrea J. last_name: Liu - first_name: Sidney R. full_name: Nagel, Sidney R. last_name: Nagel citation: ama: Goodrich CP, Liu AJ, Nagel SR. Finite-size scaling at the jamming transition. Physical Review Letters. 2012;109(9). doi:10.1103/physrevlett.109.095704 apa: Goodrich, C. P., Liu, A. J., & Nagel, S. R. (2012). Finite-size scaling at the jamming transition. Physical Review Letters. American Physical Society. https://doi.org/10.1103/physrevlett.109.095704 chicago: Goodrich, Carl Peter, Andrea J. Liu, and Sidney R. Nagel. “Finite-Size Scaling at the Jamming Transition.” Physical Review Letters. American Physical Society, 2012. https://doi.org/10.1103/physrevlett.109.095704. ieee: C. P. Goodrich, A. J. Liu, and S. R. Nagel, “Finite-size scaling at the jamming transition,” Physical Review Letters, vol. 109, no. 9. American Physical Society, 2012. ista: Goodrich CP, Liu AJ, Nagel SR. 2012. Finite-size scaling at the jamming transition. Physical Review Letters. 109(9), 095704. mla: Goodrich, Carl Peter, et al. “Finite-Size Scaling at the Jamming Transition.” Physical Review Letters, vol. 109, no. 9, 095704, American Physical Society, 2012, doi:10.1103/physrevlett.109.095704. short: C.P. Goodrich, A.J. Liu, S.R. Nagel, Physical Review Letters 109 (2012). date_created: 2020-04-30T11:44:12Z date_published: 2012-08-27T00:00:00Z date_updated: 2021-01-12T08:15:27Z day: '27' doi: 10.1103/physrevlett.109.095704 extern: '1' intvolume: ' 109' issue: '9' language: - iso: eng month: '08' oa_version: None publication: Physical Review Letters publication_identifier: issn: - 0031-9007 - 1079-7114 publication_status: published publisher: American Physical Society quality_controlled: '1' status: public title: Finite-size scaling at the jamming transition type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 109 year: '2012' ... --- _id: '801' abstract: - lang: eng text: Fungal cell walls frequently contain a polymer of mannose and galactose called galactomannan. In the pathogenic filamentous fungus Aspergillus fumigatus, this polysaccharide is made of a linear mannan backbone with side chains of galactofuran and is anchored to the plasma membrane via a glycosylphosphatidylinositol or is covalently linked to the cell wall. To date, the biosynthesis and significance of this polysaccharide are unknown. The present data demonstrate that deletion of the Golgi UDP-galactofuranose transporter GlfB or the GDP-mannose transporter GmtA leads to the absence of galactofuran or galactomannan, respectively. This indicates that the biosynthesis of galactomannan probably occurs in the lumen of the Golgi apparatus and thus contrasts with the biosynthesis of other fungal cell wall polysaccharides studied to date that takes place at the plasma membrane. Transglycosylation of galactomannan from the membrane to the cell wall is hypothesized because both the cell wall-bound and membrane-bound polysaccharide forms are affected in the generated mutants. Considering the severe growth defect of the A. fumigatus GmtA-deficient mutant, proving this paradigm might provide new targets for antifungal therapy. acknowledgement: This work was supported by the Deutsche Forschungsgemeinschaft. article_processing_charge: No article_type: original author: - first_name: Jakob full_name: Engel, Jakob last_name: Engel - first_name: Philipp S full_name: Schmalhorst, Philipp S id: 309D50DA-F248-11E8-B48F-1D18A9856A87 last_name: Schmalhorst orcid: 0000-0002-5795-0133 - first_name: Françoise full_name: Routier, Françoise last_name: Routier citation: ama: Engel J, Schmalhorst PS, Routier F. Biosynthesis of the fungal cell wall polysaccharide galactomannan requires intraluminal GDP-mannose. Journal of Biological Chemistry. 2012;287(53):44418-44424. doi:10.1074/jbc.M112.398321 apa: Engel, J., Schmalhorst, P. S., & Routier, F. (2012). Biosynthesis of the fungal cell wall polysaccharide galactomannan requires intraluminal GDP-mannose. Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology. https://doi.org/10.1074/jbc.M112.398321 chicago: Engel, Jakob, Philipp S Schmalhorst, and Françoise Routier. “Biosynthesis of the Fungal Cell Wall Polysaccharide Galactomannan Requires Intraluminal GDP-Mannose.” Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology, 2012. https://doi.org/10.1074/jbc.M112.398321. ieee: J. Engel, P. S. Schmalhorst, and F. Routier, “Biosynthesis of the fungal cell wall polysaccharide galactomannan requires intraluminal GDP-mannose,” Journal of Biological Chemistry, vol. 287, no. 53. American Society for Biochemistry and Molecular Biology, pp. 44418–44424, 2012. ista: Engel J, Schmalhorst PS, Routier F. 2012. Biosynthesis of the fungal cell wall polysaccharide galactomannan requires intraluminal GDP-mannose. Journal of Biological Chemistry. 287(53), 44418–44424. mla: Engel, Jakob, et al. “Biosynthesis of the Fungal Cell Wall Polysaccharide Galactomannan Requires Intraluminal GDP-Mannose.” Journal of Biological Chemistry, vol. 287, no. 53, American Society for Biochemistry and Molecular Biology, 2012, pp. 44418–24, doi:10.1074/jbc.M112.398321. short: J. Engel, P.S. Schmalhorst, F. Routier, Journal of Biological Chemistry 287 (2012) 44418–44424. date_created: 2018-12-11T11:48:34Z date_published: 2012-12-28T00:00:00Z date_updated: 2022-03-21T07:57:14Z day: '28' doi: 10.1074/jbc.M112.398321 extern: '1' external_id: pmid: - '23139423' intvolume: ' 287' issue: '53' language: - iso: eng month: '12' oa_version: None page: 44418 - 44424 pmid: 1 publication: Journal of Biological Chemistry publication_status: published publisher: American Society for Biochemistry and Molecular Biology publist_id: '6852' quality_controlled: '1' scopus_import: '1' status: public title: Biosynthesis of the fungal cell wall polysaccharide galactomannan requires intraluminal GDP-mannose type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 287 year: '2012' ... --- _id: '8024' abstract: - lang: eng text: In dynamical models of cortical networks, the recurrent connectivity can amplify the input given to the network in two distinct ways. One is induced by the presence of near-critical eigenvalues in the connectivity matrix W, producing large but slow activity fluctuations along the corresponding eigenvectors (dynamical slowing). The other relies on W not being normal, which allows the network activity to make large but fast excursions along specific directions. Here we investigate the trade-off between non-normal amplification and dynamical slowing in the spontaneous activity of large random neuronal networks composed of excitatory and inhibitory neurons. We use a Schur decomposition of W to separate the two amplification mechanisms. Assuming linear stochastic dynamics, we derive an exact expression for the expected amount of purely non-normal amplification. We find that amplification is very limited if dynamical slowing must be kept weak. We conclude that, to achieve strong transient amplification with little slowing, the connectivity must be structured. We show that unidirectional connections between neurons of the same type together with reciprocal connections between neurons of different types, allow for amplification already in the fast dynamical regime. Finally, our results also shed light on the differences between balanced networks in which inhibition exactly cancels excitation and those where inhibition dominates. article_number: '011909' article_processing_charge: No article_type: original author: - first_name: Guillaume full_name: Hennequin, Guillaume last_name: Hennequin - first_name: Tim P full_name: Vogels, Tim P id: CB6FF8D2-008F-11EA-8E08-2637E6697425 last_name: Vogels orcid: 0000-0003-3295-6181 - first_name: Wulfram full_name: Gerstner, Wulfram last_name: Gerstner citation: ama: Hennequin G, Vogels TP, Gerstner W. Non-normal amplification in random balanced neuronal networks. Physical Review E. 2012;86(1). doi:10.1103/physreve.86.011909 apa: Hennequin, G., Vogels, T. P., & Gerstner, W. (2012). Non-normal amplification in random balanced neuronal networks. Physical Review E. American Physical Society. https://doi.org/10.1103/physreve.86.011909 chicago: Hennequin, Guillaume, Tim P Vogels, and Wulfram Gerstner. “Non-Normal Amplification in Random Balanced Neuronal Networks.” Physical Review E. American Physical Society, 2012. https://doi.org/10.1103/physreve.86.011909. ieee: G. Hennequin, T. P. Vogels, and W. Gerstner, “Non-normal amplification in random balanced neuronal networks,” Physical Review E, vol. 86, no. 1. American Physical Society, 2012. ista: Hennequin G, Vogels TP, Gerstner W. 2012. Non-normal amplification in random balanced neuronal networks. Physical Review E. 86(1), 011909. mla: Hennequin, Guillaume, et al. “Non-Normal Amplification in Random Balanced Neuronal Networks.” Physical Review E, vol. 86, no. 1, 011909, American Physical Society, 2012, doi:10.1103/physreve.86.011909. short: G. Hennequin, T.P. Vogels, W. Gerstner, Physical Review E 86 (2012). date_created: 2020-06-25T13:09:06Z date_published: 2012-06-11T00:00:00Z date_updated: 2021-01-12T08:16:35Z day: '11' doi: 10.1103/physreve.86.011909 extern: '1' external_id: pmid: - '23005454' intvolume: ' 86' issue: '1' language: - iso: eng month: '06' oa_version: None pmid: 1 publication: Physical Review E publication_identifier: eisbn: - 1550-2376 issn: - 1539-3755 publication_status: published publisher: American Physical Society quality_controlled: '1' status: public title: Non-normal amplification in random balanced neuronal networks type: journal_article user_id: D865714E-FA4E-11E9-B85B-F5C5E5697425 volume: 86 year: '2012' ... --- _id: '808' abstract: - lang: eng text: Using correlated live-cell imaging and electron tomography we found that actin branch junctions in protruding and treadmilling lamellipodia are not concentrated at the front as previously supposed, but link actin filament subsets in which there is a continuum of distances from a junction to the filament plus ends, for up to at least 1 mm. When branch sites were observed closely spaced on the same filament their separation was commonly a multiple of the actin helical repeat of 36 nm. Image averaging of branch junctions in the tomograms yielded a model for the in vivo branch at 2.9 nm resolution, which was comparable with that derived for the in vitro actin- Arp2/3 complex. Lamellipodium initiation was monitored in an intracellular wound-healing model and was found to involve branching from the sides of actin filaments oriented parallel to the plasmalemma. Many filament plus ends, presumably capped, terminated behind the lamellipodium tip and localized on the dorsal and ventral surfaces of the actin network. These findings reveal how branching events initiate and maintain a network of actin filaments of variable length, and provide the first structural model of the branch junction in vivo. A possible role of filament capping in generating the lamellipodium leaflet is discussed and a mathematical model of protrusion is also presented. acknowledgement: This work was supported by the Austrian Science Fund [projects FWF I516-B09 and FWF P21292-B09 to J.V.S.]; the Vienna Science and Technology Fund [WWTF-grant numbers MA 09-004 to J.V.S. and C.S], ZIT - The Technology Agency of the City of Vienna [VSOE, CMCN to J.V.S. and G.P.R.]; the Deutsche Forschungsgemeinschaft [grant number RO 2414/1-2 to K.R.]; the Daiko research foundation [grant number 9134 to A.N.]; and a Grant-in-Aid for Scientific Research [S, grant number 20227008 to Y.M.] and a Grant-in-Aid for Young Scientists [B, grant number 22770145 to A.N.] (B) from The Ministry of Education, Culture, Sports, Science and Technology of the Japanese Government. Deposited in PMC for immediate release. We thank Tibor Kulcsar for assistance with graphics. author: - first_name: Marlene full_name: Vinzenz, Marlene last_name: Vinzenz - first_name: Maria full_name: Nemethova, Maria id: 34E27F1C-F248-11E8-B48F-1D18A9856A87 last_name: Nemethova - first_name: Florian full_name: Schur, Florian id: 48AD8942-F248-11E8-B48F-1D18A9856A87 last_name: Schur orcid: 0000-0003-4790-8078 - first_name: Jan full_name: Mueller, Jan last_name: Mueller - first_name: Akihiro full_name: Narita, Akihiro last_name: Narita - first_name: Edit full_name: Urban, Edit last_name: Urban - first_name: Christoph full_name: Winkler, Christoph last_name: Winkler - first_name: Christian full_name: Schmeiser, Christian last_name: Schmeiser - first_name: Stefan full_name: Koestler, Stefan last_name: Koestler - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Guenter full_name: Resch, Guenter last_name: Resch - first_name: Yuichiro full_name: Maéda, Yuichiro last_name: Maéda - first_name: John full_name: Small, John last_name: Small citation: ama: Vinzenz M, Nemethova M, Schur FK, et al. Actin branching in the initiation and maintenance of lamellipodia. Journal of Cell Science. 2012;125(11):2775-2785. doi:10.1242/jcs.107623 apa: Vinzenz, M., Nemethova, M., Schur, F. K., Mueller, J., Narita, A., Urban, E., … Small, J. (2012). Actin branching in the initiation and maintenance of lamellipodia. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.107623 chicago: Vinzenz, Marlene, Maria Nemethova, Florian KM Schur, Jan Mueller, Akihiro Narita, Edit Urban, Christoph Winkler, et al. “Actin Branching in the Initiation and Maintenance of Lamellipodia.” Journal of Cell Science. Company of Biologists, 2012. https://doi.org/10.1242/jcs.107623. ieee: M. Vinzenz et al., “Actin branching in the initiation and maintenance of lamellipodia,” Journal of Cell Science, vol. 125, no. 11. Company of Biologists, pp. 2775–2785, 2012. ista: Vinzenz M, Nemethova M, Schur FK, Mueller J, Narita A, Urban E, Winkler C, Schmeiser C, Koestler S, Rottner K, Resch G, Maéda Y, Small J. 2012. Actin branching in the initiation and maintenance of lamellipodia. Journal of Cell Science. 125(11), 2775–2785. mla: Vinzenz, Marlene, et al. “Actin Branching in the Initiation and Maintenance of Lamellipodia.” Journal of Cell Science, vol. 125, no. 11, Company of Biologists, 2012, pp. 2775–85, doi:10.1242/jcs.107623. short: M. Vinzenz, M. Nemethova, F.K. Schur, J. Mueller, A. Narita, E. Urban, C. Winkler, C. Schmeiser, S. Koestler, K. Rottner, G. Resch, Y. Maéda, J. Small, Journal of Cell Science 125 (2012) 2775–2785. date_created: 2018-12-11T11:48:37Z date_published: 2012-06-01T00:00:00Z date_updated: 2021-01-12T08:16:47Z day: '01' ddc: - '570' doi: 10.1242/jcs.107623 extern: '1' file: - access_level: open_access checksum: 2f59e15cc3a85bb500a9887cef2aab67 content_type: application/pdf creator: kschuh date_created: 2019-02-12T08:54:51Z date_updated: 2020-07-14T12:48:09Z file_id: '5956' file_name: 2012_Biologists_Vinzenz.pdf file_size: 3326073 relation: main_file file_date_updated: 2020-07-14T12:48:09Z has_accepted_license: '1' intvolume: ' 125' issue: '11' language: - iso: eng month: '06' oa: 1 oa_version: None page: 2775 - 2785 publication: Journal of Cell Science publication_status: published publisher: Company of Biologists publist_id: '6842' quality_controlled: '1' status: public title: Actin branching in the initiation and maintenance of lamellipodia tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 125 year: '2012' ... --- _id: '8246' abstract: - lang: eng text: The Staphylococcus aureus cell wall stress stimulon (CWSS) is activated by cell envelope-targeting antibiotics or depletion of essential cell wall biosynthesis enzymes. The functionally uncharacterized S. aureus LytR-CpsA-Psr (LCP) proteins, MsrR, SA0908 and SA2103, all belong to the CWSS. Although not essential, deletion of all three LCP proteins severely impairs cell division. We show here that VraSR-dependent CWSS expression was up to 250-fold higher in single, double and triple LCP mutants than in wild type S. aureus in the absence of external stress. The LCP triple mutant was virtually depleted of wall teichoic acids (WTA), which could be restored to different degrees by any of the single LCP proteins. Subinhibitory concentrations of tunicamycin, which inhibits the first WTA synthesis enzyme TarO (TagO), could partially complement the severe growth defect of the LCP triple mutant. Both of the latter findings support a role for S. aureus LCP proteins in late WTA synthesis, as in Bacillus subtilis where LCP proteins were recently proposed to transfer WTA from lipid carriers to the cell wall peptidoglycan. Intrinsic activation of the CWSS upon LCP deletion and the fact that LCP proteins were essential for WTA-loading of the cell wall, highlight their important role(s) in S. aureus cell envelope biogenesis. article_processing_charge: No article_type: original author: - first_name: Vanina full_name: Dengler, Vanina last_name: Dengler - first_name: Patricia Stutzmann full_name: Meier, Patricia Stutzmann last_name: Meier - first_name: Ronald full_name: Heusser, Ronald last_name: Heusser - first_name: Peter full_name: Kupferschmied, Peter last_name: Kupferschmied - first_name: Judit full_name: Fazekas, Judit id: 36432834-F248-11E8-B48F-1D18A9856A87 last_name: Fazekas orcid: 0000-0002-8777-3502 - first_name: Sarah full_name: Friebe, Sarah last_name: Friebe - first_name: Sibylle Burger full_name: Staufer, Sibylle Burger last_name: Staufer - first_name: Paul A. full_name: Majcherczyk, Paul A. last_name: Majcherczyk - first_name: Philippe full_name: Moreillon, Philippe last_name: Moreillon - first_name: Brigitte full_name: Berger-Bächi, Brigitte last_name: Berger-Bächi - first_name: Nadine full_name: McCallum, Nadine last_name: McCallum citation: ama: Dengler V, Meier PS, Heusser R, et al. Deletion of hypothetical wall teichoic acid ligases in Staphylococcus aureus activates the cell wall stress response. FEMS Microbiology Letters. 2012;333(2):109-120. doi:10.1111/j.1574-6968.2012.02603.x apa: Dengler, V., Meier, P. S., Heusser, R., Kupferschmied, P., Singer, J., Friebe, S., … McCallum, N. (2012). Deletion of hypothetical wall teichoic acid ligases in Staphylococcus aureus activates the cell wall stress response. FEMS Microbiology Letters. Oxford University Press. https://doi.org/10.1111/j.1574-6968.2012.02603.x chicago: Dengler, Vanina, Patricia Stutzmann Meier, Ronald Heusser, Peter Kupferschmied, Judit Singer, Sarah Friebe, Sibylle Burger Staufer, et al. “Deletion of Hypothetical Wall Teichoic Acid Ligases in Staphylococcus Aureus Activates the Cell Wall Stress Response.” FEMS Microbiology Letters. Oxford University Press, 2012. https://doi.org/10.1111/j.1574-6968.2012.02603.x. ieee: V. Dengler et al., “Deletion of hypothetical wall teichoic acid ligases in Staphylococcus aureus activates the cell wall stress response,” FEMS Microbiology Letters, vol. 333, no. 2. Oxford University Press, pp. 109–120, 2012. ista: Dengler V, Meier PS, Heusser R, Kupferschmied P, Singer J, Friebe S, Staufer SB, Majcherczyk PA, Moreillon P, Berger-Bächi B, McCallum N. 2012. Deletion of hypothetical wall teichoic acid ligases in Staphylococcus aureus activates the cell wall stress response. FEMS Microbiology Letters. 333(2), 109–120. mla: Dengler, Vanina, et al. “Deletion of Hypothetical Wall Teichoic Acid Ligases in Staphylococcus Aureus Activates the Cell Wall Stress Response.” FEMS Microbiology Letters, vol. 333, no. 2, Oxford University Press, 2012, pp. 109–20, doi:10.1111/j.1574-6968.2012.02603.x. short: V. Dengler, P.S. Meier, R. Heusser, P. Kupferschmied, J. Singer, S. Friebe, S.B. Staufer, P.A. Majcherczyk, P. Moreillon, B. Berger-Bächi, N. McCallum, FEMS Microbiology Letters 333 (2012) 109–120. date_created: 2020-08-10T11:54:47Z date_published: 2012-08-01T00:00:00Z date_updated: 2021-01-12T08:17:43Z day: '01' doi: 10.1111/j.1574-6968.2012.02603.x extern: '1' external_id: pmid: - '22640011' intvolume: ' 333' issue: '2' language: - iso: eng month: '08' oa_version: None page: 109-120 pmid: 1 publication: FEMS Microbiology Letters publication_identifier: issn: - 0378-1097 publication_status: published publisher: Oxford University Press quality_controlled: '1' status: public title: Deletion of hypothetical wall teichoic acid ligases in Staphylococcus aureus activates the cell wall stress response type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 333 year: '2012' ...