--- _id: '653' abstract: - lang: eng text: The extent of heterogeneity among driver gene mutations present in naturally occurring metastases - that is, treatment-naive metastatic disease - is largely unknown. To address this issue, we carried out 60× whole-genome sequencing of 26 metastases from four patients with pancreatic cancer. We found that identical mutations in known driver genes were present in every metastatic lesion for each patient studied. Passenger gene mutations, which do not have known or predicted functional consequences, accounted for all intratumoral heterogeneity. Even with respect to these passenger mutations, our analysis suggests that the genetic similarity among the founding cells of metastases was higher than that expected for any two cells randomly taken from a normal tissue. The uniformity of known driver gene mutations among metastases in the same patient has critical and encouraging implications for the success of future targeted therapies in advanced-stage disease. acknowledgement: 'We thank the Memorial Sloan Kettering Cancer Center Molecular Cytology core facility for immunohistochemistry staining. This work was supported by Office of Naval Research grant N00014-16-1-2914, the Bill and Melinda Gates Foundation (OPP1148627), and a gift from B. Wu and E. Larson (M.A.N.), National Institutes of Health grants CA179991 (C.A.I.-D. and I.B.), F31 CA180682 (A.P.M.-M.), CA43460 (B.V.), and P50 CA62924, the Monastra Foundation, the Virginia and D.K. Ludwig Fund for Cancer Research, the Lustgarten Foundation for Pancreatic Cancer Research, the Sol Goldman Center for Pancreatic Cancer Research, the Sol Goldman Sequencing Center, ERC Start grant 279307: Graph Games (J.G.R., D.K., and C.K.), Austrian Science Fund (FWF) grant P23499-N23 (J.G.R., D.K., and C.K.), and FWF NFN grant S11407-N23 RiSE/SHiNE (J.G.R., D.K., and C.K.).' article_processing_charge: No article_type: original author: - first_name: Alvin full_name: Makohon Moore, Alvin last_name: Makohon Moore - first_name: Ming full_name: Zhang, Ming last_name: Zhang - first_name: Johannes full_name: Reiter, Johannes id: 4A918E98-F248-11E8-B48F-1D18A9856A87 last_name: Reiter orcid: 0000-0002-0170-7353 - first_name: Ivana full_name: Božić, Ivana last_name: Božić - first_name: Benjamin full_name: Allen, Benjamin last_name: Allen - first_name: Deepanjan full_name: Kundu, Deepanjan id: 1d4c0f4f-e8a3-11ec-a351-e36772758c45 last_name: Kundu - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Fay full_name: Wong, Fay last_name: Wong - first_name: Yuchen full_name: Jiao, Yuchen last_name: Jiao - first_name: Zachary full_name: Kohutek, Zachary last_name: Kohutek - first_name: Jungeui full_name: Hong, Jungeui last_name: Hong - first_name: Marc full_name: Attiyeh, Marc last_name: Attiyeh - first_name: Breanna full_name: Javier, Breanna last_name: Javier - first_name: Laura full_name: Wood, Laura last_name: Wood - first_name: Ralph full_name: Hruban, Ralph last_name: Hruban - first_name: Martin full_name: Nowak, Martin last_name: Nowak - first_name: Nickolas full_name: Papadopoulos, Nickolas last_name: Papadopoulos - first_name: Kenneth full_name: Kinzler, Kenneth last_name: Kinzler - first_name: Bert full_name: Vogelstein, Bert last_name: Vogelstein - first_name: Christine full_name: Iacobuzio Donahue, Christine last_name: Iacobuzio Donahue citation: ama: Makohon Moore A, Zhang M, Reiter J, et al. Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer. Nature Genetics. 2017;49(3):358-366. doi:10.1038/ng.3764 apa: Makohon Moore, A., Zhang, M., Reiter, J., Božić, I., Allen, B., Kundu, D., … Iacobuzio Donahue, C. (2017). Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer. Nature Genetics. Nature Publishing Group. https://doi.org/10.1038/ng.3764 chicago: Makohon Moore, Alvin, Ming Zhang, Johannes Reiter, Ivana Božić, Benjamin Allen, Deepanjan Kundu, Krishnendu Chatterjee, et al. “Limited Heterogeneity of Known Driver Gene Mutations among the Metastases of Individual Patients with Pancreatic Cancer.” Nature Genetics. Nature Publishing Group, 2017. https://doi.org/10.1038/ng.3764. ieee: A. Makohon Moore et al., “Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer,” Nature Genetics, vol. 49, no. 3. Nature Publishing Group, pp. 358–366, 2017. ista: Makohon Moore A, Zhang M, Reiter J, Božić I, Allen B, Kundu D, Chatterjee K, Wong F, Jiao Y, Kohutek Z, Hong J, Attiyeh M, Javier B, Wood L, Hruban R, Nowak M, Papadopoulos N, Kinzler K, Vogelstein B, Iacobuzio Donahue C. 2017. Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer. Nature Genetics. 49(3), 358–366. mla: Makohon Moore, Alvin, et al. “Limited Heterogeneity of Known Driver Gene Mutations among the Metastases of Individual Patients with Pancreatic Cancer.” Nature Genetics, vol. 49, no. 3, Nature Publishing Group, 2017, pp. 358–66, doi:10.1038/ng.3764. short: A. Makohon Moore, M. Zhang, J. Reiter, I. Božić, B. Allen, D. Kundu, K. Chatterjee, F. Wong, Y. Jiao, Z. Kohutek, J. Hong, M. Attiyeh, B. Javier, L. Wood, R. Hruban, M. Nowak, N. Papadopoulos, K. Kinzler, B. Vogelstein, C. Iacobuzio Donahue, Nature Genetics 49 (2017) 358–366. date_created: 2018-12-11T11:47:43Z date_published: 2017-03-01T00:00:00Z date_updated: 2022-06-10T09:55:08Z day: '01' ddc: - '000' department: - _id: KrCh doi: 10.1038/ng.3764 ec_funded: 1 external_id: pmid: - '28092682' file: - access_level: open_access checksum: e442dc3b7420a36ec805e9bb45cc1a2e content_type: application/pdf creator: dernst date_created: 2019-11-19T08:13:50Z date_updated: 2020-07-14T12:47:33Z file_id: '7050' file_name: 2017_NatureGenetics_Makohon.pdf file_size: 908099 relation: main_file file_date_updated: 2020-07-14T12:47:33Z has_accepted_license: '1' intvolume: ' 49' issue: '3' language: - iso: eng month: '03' oa: 1 oa_version: Submitted Version page: 358 - 366 pmid: 1 project: - _id: 2581B60A-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '279307' name: 'Quantitative Graph Games: Theory and Applications' - _id: 2584A770-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P 23499-N23 name: Modern Graph Algorithmic Techniques in Formal Verification - _id: 25863FF4-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S11407 name: Game Theory publication: Nature Genetics publication_identifier: issn: - '10614036' publication_status: published publisher: Nature Publishing Group publist_id: '7092' quality_controlled: '1' scopus_import: '1' status: public title: Limited heterogeneity of known driver gene mutations among the metastases of individual patients with pancreatic cancer type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 49 year: '2017' ... --- _id: '6527' abstract: - lang: eng text: "A memory-hard function (MHF) ƒn with parameter n can be computed in sequential time and space n. Simultaneously, a high amortized parallel area-time complexity (aAT) is incurred per evaluation. In practice, MHFs are used to limit the rate at which an adversary (using a custom computational device) can evaluate a security sensitive function that still occasionally needs to be evaluated by honest users (using an off-the-shelf general purpose device). The most prevalent examples of such sensitive functions are Key Derivation Functions (KDFs) and password hashing algorithms where rate limits help mitigate off-line dictionary attacks. As the honest users' inputs to these functions are often (low-entropy) passwords special attention is given to a class of side-channel resistant MHFs called iMHFs.\r\n\r\nEssentially all iMHFs can be viewed as some mode of operation (making n calls to some round function) given by a directed acyclic graph (DAG) with very low indegree. Recently, a combinatorial property of a DAG has been identified (called \"depth-robustness\") which results in good provable security for an iMHF based on that DAG. Depth-robust DAGs have also proven useful in other cryptographic applications. Unfortunately, up till now, all known very depth-robust DAGs are impractically complicated and little is known about their exact (i.e. non-asymptotic) depth-robustness both in theory and in practice.\r\n\r\nIn this work we build and analyze (both formally and empirically) several exceedingly simple and efficient to navigate practical DAGs for use in iMHFs and other applications. For each DAG we:\r\n*Prove that their depth-robustness is asymptotically maximal.\r\n*Prove bounds of at least 3 orders of magnitude better on their exact depth-robustness compared to known bounds for other practical iMHF.\r\n*Implement and empirically evaluate their depth-robustness and aAT against a variety of state-of-the art (and several new) depth-reduction and low aAT attacks. \r\nWe find that, against all attacks, the new DAGs perform significantly better in practice than Argon2i, the most widely deployed iMHF in practice.\r\n\r\nAlong the way we also improve the best known empirical attacks on the aAT of Argon2i by implementing and testing several heuristic versions of a (hitherto purely theoretical) depth-reduction attack. Finally, we demonstrate practicality of our constructions by modifying the Argon2i code base to use one of the new high aAT DAGs. Experimental benchmarks on a standard off-the-shelf CPU show that the new modifications do not adversely affect the impressive throughput of Argon2i (despite seemingly enjoying significantly higher aAT).\r\n" author: - first_name: Joel F full_name: Alwen, Joel F id: 2A8DFA8C-F248-11E8-B48F-1D18A9856A87 last_name: Alwen - first_name: Jeremiah full_name: Blocki, Jeremiah last_name: Blocki - first_name: Ben full_name: Harsha, Ben last_name: Harsha citation: ama: 'Alwen JF, Blocki J, Harsha B. Practical graphs for optimal side-channel resistant memory-hard functions. In: Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security. ACM Press; 2017:1001-1017. doi:10.1145/3133956.3134031' apa: 'Alwen, J. F., Blocki, J., & Harsha, B. (2017). Practical graphs for optimal side-channel resistant memory-hard functions. In Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security (pp. 1001–1017). Dallas, TX, USA: ACM Press. https://doi.org/10.1145/3133956.3134031' chicago: Alwen, Joel F, Jeremiah Blocki, and Ben Harsha. “Practical Graphs for Optimal Side-Channel Resistant Memory-Hard Functions.” In Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security, 1001–17. ACM Press, 2017. https://doi.org/10.1145/3133956.3134031. ieee: J. F. Alwen, J. Blocki, and B. Harsha, “Practical graphs for optimal side-channel resistant memory-hard functions,” in Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security, Dallas, TX, USA, 2017, pp. 1001–1017. ista: 'Alwen JF, Blocki J, Harsha B. 2017. Practical graphs for optimal side-channel resistant memory-hard functions. Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security. CCS: Conference on Computer and Communications Security, 1001–1017.' mla: Alwen, Joel F., et al. “Practical Graphs for Optimal Side-Channel Resistant Memory-Hard Functions.” Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security, ACM Press, 2017, pp. 1001–17, doi:10.1145/3133956.3134031. short: J.F. Alwen, J. Blocki, B. Harsha, in:, Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security, ACM Press, 2017, pp. 1001–1017. conference: end_date: 2017-11-03 location: Dallas, TX, USA name: 'CCS: Conference on Computer and Communications Security' start_date: 2017-10-30 date_created: 2019-06-06T13:21:29Z date_published: 2017-10-30T00:00:00Z date_updated: 2021-01-12T08:07:53Z day: '30' department: - _id: KrPi doi: 10.1145/3133956.3134031 ec_funded: 1 language: - iso: eng main_file_link: - open_access: '1' url: https://eprint.iacr.org/2017/443 month: '10' oa: 1 oa_version: Submitted Version page: 1001-1017 project: - _id: 258AA5B2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '682815' name: Teaching Old Crypto New Tricks publication: Proceedings of the 2017 ACM SIGSAC Conference on Computer and Communications Security publication_identifier: isbn: - '9781450349468' publication_status: published publisher: ACM Press quality_controlled: '1' scopus_import: 1 status: public title: Practical graphs for optimal side-channel resistant memory-hard functions type: conference user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2017' ... --- _id: '654' abstract: - lang: eng text: In November 2016, developmental biologists, synthetic biologists and engineers gathered in Paris for a meeting called ‘Engineering the embryo’. The participants shared an interest in exploring how synthetic systems can reveal new principles of embryonic development, and how the in vitro manipulation and modeling of development using stem cells can be used to integrate ideas and expertise from physics, developmental biology and tissue engineering. As we review here, the conference pinpointed some of the challenges arising at the intersection of these fields, along with great enthusiasm for finding new approaches and collaborations. author: - first_name: Anna full_name: Kicheva, Anna id: 3959A2A0-F248-11E8-B48F-1D18A9856A87 last_name: Kicheva orcid: 0000-0003-4509-4998 - first_name: Nicolas full_name: Rivron, Nicolas last_name: Rivron citation: ama: Kicheva A, Rivron N. Creating to understand – developmental biology meets engineering in Paris. Development. 2017;144(5):733-736. doi:10.1242/dev.144915 apa: Kicheva, A., & Rivron, N. (2017). Creating to understand – developmental biology meets engineering in Paris. Development. Company of Biologists. https://doi.org/10.1242/dev.144915 chicago: Kicheva, Anna, and Nicolas Rivron. “Creating to Understand – Developmental Biology Meets Engineering in Paris.” Development. Company of Biologists, 2017. https://doi.org/10.1242/dev.144915. ieee: A. Kicheva and N. Rivron, “Creating to understand – developmental biology meets engineering in Paris,” Development, vol. 144, no. 5. Company of Biologists, pp. 733–736, 2017. ista: Kicheva A, Rivron N. 2017. Creating to understand – developmental biology meets engineering in Paris. Development. 144(5), 733–736. mla: Kicheva, Anna, and Nicolas Rivron. “Creating to Understand – Developmental Biology Meets Engineering in Paris.” Development, vol. 144, no. 5, Company of Biologists, 2017, pp. 733–36, doi:10.1242/dev.144915. short: A. Kicheva, N. Rivron, Development 144 (2017) 733–736. date_created: 2018-12-11T11:47:44Z date_published: 2017-03-01T00:00:00Z date_updated: 2021-01-12T08:07:54Z day: '01' ddc: - '571' department: - _id: AnKi doi: 10.1242/dev.144915 ec_funded: 1 file: - access_level: open_access checksum: eef22a0f42a55b232cb2d1188a2322cb content_type: application/pdf creator: system date_created: 2018-12-12T10:15:20Z date_updated: 2020-07-14T12:47:33Z file_id: '5139' file_name: IST-2018-987-v1+1_2017_KichevaRivron__Creating_to.pdf file_size: 228206 relation: main_file file_date_updated: 2020-07-14T12:47:33Z has_accepted_license: '1' intvolume: ' 144' issue: '5' language: - iso: eng month: '03' oa: 1 oa_version: Submitted Version page: 733 - 736 project: - _id: B6FC0238-B512-11E9-945C-1524E6697425 call_identifier: H2020 grant_number: '680037' name: Coordination of Patterning And Growth In the Spinal Cord publication: Development publication_identifier: issn: - '09501991' publication_status: published publisher: Company of Biologists publist_id: '7089' pubrep_id: '987' quality_controlled: '1' scopus_import: 1 status: public title: Creating to understand – developmental biology meets engineering in Paris type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 144 year: '2017' ... --- _id: '6526' abstract: - lang: eng text: 'This paper studies the complexity of estimating Rényi divergences of discrete distributions: p observed from samples and the baseline distribution q known a priori. Extending the results of Acharya et al. (SODA''15) on estimating Rényi entropy, we present improved estimation techniques together with upper and lower bounds on the sample complexity. We show that, contrarily to estimating Rényi entropy where a sublinear (in the alphabet size) number of samples suffices, the sample complexity is heavily dependent on events occurring unlikely in q, and is unbounded in general (no matter what an estimation technique is used). For any divergence of integer order bigger than 1, we provide upper and lower bounds on the number of samples dependent on probabilities of p and q (the lower bounds hold for non-integer orders as well). We conclude that the worst-case sample complexity is polynomial in the alphabet size if and only if the probabilities of q are non-negligible. This gives theoretical insights into heuristics used in the applied literature to handle numerical instability, which occurs for small probabilities of q. Our result shows that they should be handled with care not only because of numerical issues, but also because of a blow up in the sample complexity.' article_number: '8006529' author: - first_name: Maciej full_name: Skórski, Maciej id: EC09FA6A-02D0-11E9-8223-86B7C91467DD last_name: Skórski citation: ama: 'Skórski M. On the complexity of estimating Rènyi divergences. In: 2017 IEEE International Symposium on Information Theory (ISIT). IEEE; 2017. doi:10.1109/isit.2017.8006529' apa: 'Skórski, M. (2017). On the complexity of estimating Rènyi divergences. In 2017 IEEE International Symposium on Information Theory (ISIT). Aachen, Germany: IEEE. https://doi.org/10.1109/isit.2017.8006529' chicago: Skórski, Maciej. “On the Complexity of Estimating Rènyi Divergences.” In 2017 IEEE International Symposium on Information Theory (ISIT). IEEE, 2017. https://doi.org/10.1109/isit.2017.8006529. ieee: M. Skórski, “On the complexity of estimating Rènyi divergences,” in 2017 IEEE International Symposium on Information Theory (ISIT), Aachen, Germany, 2017. ista: 'Skórski M. 2017. On the complexity of estimating Rènyi divergences. 2017 IEEE International Symposium on Information Theory (ISIT). ISIT: International Symposium on Information Theory, 8006529.' mla: Skórski, Maciej. “On the Complexity of Estimating Rènyi Divergences.” 2017 IEEE International Symposium on Information Theory (ISIT), 8006529, IEEE, 2017, doi:10.1109/isit.2017.8006529. short: M. Skórski, in:, 2017 IEEE International Symposium on Information Theory (ISIT), IEEE, 2017. conference: end_date: 2017-06-30 location: Aachen, Germany name: 'ISIT: International Symposium on Information Theory' start_date: 2017-06-25 date_created: 2019-06-06T12:53:09Z date_published: 2017-08-09T00:00:00Z date_updated: 2021-01-12T08:07:53Z day: '09' department: - _id: KrPi doi: 10.1109/isit.2017.8006529 ec_funded: 1 external_id: arxiv: - '1702.01666' language: - iso: eng main_file_link: - open_access: '1' url: https://arxiv.org/abs/1702.01666 month: '08' oa: 1 oa_version: Preprint project: - _id: 258AA5B2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '682815' name: Teaching Old Crypto New Tricks publication: 2017 IEEE International Symposium on Information Theory (ISIT) publication_identifier: isbn: - '9781509040964' publication_status: published publisher: IEEE quality_controlled: '1' scopus_import: 1 status: public title: On the complexity of estimating Rènyi divergences type: conference user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 year: '2017' ... --- _id: '655' abstract: - lang: eng text: 'The bacterial flagellum is a self-assembling nanomachine. The external flagellar filament, several times longer than a bacterial cell body, is made of a few tens of thousands subunits of a single protein: flagellin. A fundamental problem concerns the molecular mechanism of how the flagellum grows outside the cell, where no discernible energy source is available. Here, we monitored the dynamic assembly of individual flagella using in situ labelling and real-time immunostaining of elongating flagellar filaments. We report that the rate of flagellum growth, initially ~1,700 amino acids per second, decreases with length and that the previously proposed chain mechanism does not contribute to the filament elongation dynamics. Inhibition of the proton motive force-dependent export apparatus revealed a major contribution of substrate injection in driving filament elongation. The combination of experimental and mathematical evidence demonstrates that a simple, injection-diffusion mechanism controls bacterial flagella growth outside the cell.' article_number: e23136 author: - first_name: Thibaud full_name: Renault, Thibaud last_name: Renault - first_name: Anthony full_name: Abraham, Anthony last_name: Abraham - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Guillaume full_name: Paradis, Guillaume last_name: Paradis - first_name: Simon full_name: Rainville, Simon last_name: Rainville - first_name: Emmanuelle full_name: Charpentier, Emmanuelle last_name: Charpentier - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 - first_name: Yuhai full_name: Tu, Yuhai last_name: Tu - first_name: Keiichi full_name: Namba, Keiichi last_name: Namba - first_name: James full_name: Keener, James last_name: Keener - first_name: Tohru full_name: Minamino, Tohru last_name: Minamino - first_name: Marc full_name: Erhardt, Marc last_name: Erhardt citation: ama: Renault T, Abraham A, Bergmiller T, et al. Bacterial flagella grow through an injection diffusion mechanism. eLife. 2017;6. doi:10.7554/eLife.23136 apa: Renault, T., Abraham, A., Bergmiller, T., Paradis, G., Rainville, S., Charpentier, E., … Erhardt, M. (2017). Bacterial flagella grow through an injection diffusion mechanism. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.23136 chicago: Renault, Thibaud, Anthony Abraham, Tobias Bergmiller, Guillaume Paradis, Simon Rainville, Emmanuelle Charpentier, Calin C Guet, et al. “Bacterial Flagella Grow through an Injection Diffusion Mechanism.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.23136. ieee: T. Renault et al., “Bacterial flagella grow through an injection diffusion mechanism,” eLife, vol. 6. eLife Sciences Publications, 2017. ista: Renault T, Abraham A, Bergmiller T, Paradis G, Rainville S, Charpentier E, Guet CC, Tu Y, Namba K, Keener J, Minamino T, Erhardt M. 2017. Bacterial flagella grow through an injection diffusion mechanism. eLife. 6, e23136. mla: Renault, Thibaud, et al. “Bacterial Flagella Grow through an Injection Diffusion Mechanism.” ELife, vol. 6, e23136, eLife Sciences Publications, 2017, doi:10.7554/eLife.23136. short: T. Renault, A. Abraham, T. Bergmiller, G. Paradis, S. Rainville, E. Charpentier, C.C. Guet, Y. Tu, K. Namba, J. Keener, T. Minamino, M. Erhardt, ELife 6 (2017). date_created: 2018-12-11T11:47:44Z date_published: 2017-03-06T00:00:00Z date_updated: 2021-01-12T08:07:55Z day: '06' ddc: - '579' department: - _id: CaGu doi: 10.7554/eLife.23136 file: - access_level: open_access checksum: 39e1c3e82ddac83a30422fa72fa1a383 content_type: application/pdf creator: system date_created: 2018-12-12T10:08:53Z date_updated: 2020-07-14T12:47:33Z file_id: '4716' file_name: IST-2017-904-v1+1_elife-23136-v2.pdf file_size: 5520359 relation: main_file - access_level: open_access checksum: a6d542253028f52e00aa29739ddffe8f content_type: application/pdf creator: system date_created: 2018-12-12T10:08:54Z date_updated: 2020-07-14T12:47:33Z file_id: '4717' file_name: IST-2017-904-v1+2_elife-23136-figures-v2.pdf file_size: 11242920 relation: main_file file_date_updated: 2020-07-14T12:47:33Z has_accepted_license: '1' intvolume: ' 6' language: - iso: eng month: '03' oa: 1 oa_version: Published Version publication: eLife publication_identifier: issn: - 2050084X publication_status: published publisher: eLife Sciences Publications publist_id: '7082' pubrep_id: '904' quality_controlled: '1' scopus_import: 1 status: public title: Bacterial flagella grow through an injection diffusion mechanism tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 6 year: '2017' ... --- _id: '657' abstract: - lang: eng text: Plant organs are typically organized into three main tissue layers. The middle ground tissue layer comprises the majority of the plant body and serves a wide range of functions, including photosynthesis, selective nutrient uptake and storage, and gravity sensing. Ground tissue patterning and maintenance in Arabidopsis are controlled by a well-established gene network revolving around the key regulator SHORT-ROOT (SHR). In contrast, it is completely unknown how ground tissue identity is first specified from totipotent precursor cells in the embryo. The plant signaling molecule auxin, acting through AUXIN RESPONSE FACTOR (ARF) transcription factors, is critical for embryo patterning. The auxin effector ARF5/MONOPTEROS (MP) acts both cell-autonomously and noncell-autonomously to control embryonic vascular tissue formation and root initiation, respectively. Here we show that auxin response and ARF activity cell-autonomously control the asymmetric division of the first ground tissue cells. By identifying embryonic target genes, we show that MP transcriptionally initiates the ground tissue lineage and acts upstream of the regulatory network that controls ground tissue patterning and maintenance. Strikingly, whereas the SHR network depends on MP, this MP function is, at least in part, SHR independent. Our study therefore identifies auxin response as a regulator of ground tissue specification in the embryonic root, and reveals that ground tissue initiation and maintenance use different regulators and mechanisms. Moreover, our data provide a framework for the simultaneous formation of multiple cell types by the same transcriptional regulator. author: - first_name: Barbara full_name: Möller, Barbara last_name: Möller - first_name: Colette full_name: Ten Hove, Colette last_name: Ten Hove - first_name: Daoquan full_name: Xiang, Daoquan last_name: Xiang - first_name: Nerys full_name: Williams, Nerys last_name: Williams - first_name: Lorena full_name: López, Lorena last_name: López - first_name: Saiko full_name: Yoshida, Saiko id: 2E46069C-F248-11E8-B48F-1D18A9856A87 last_name: Yoshida - first_name: Margot full_name: Smit, Margot last_name: Smit - first_name: Raju full_name: Datla, Raju last_name: Datla - first_name: Dolf full_name: Weijers, Dolf last_name: Weijers citation: ama: Möller B, Ten Hove C, Xiang D, et al. Auxin response cell autonomously controls ground tissue initiation in the early arabidopsis embryo. PNAS. 2017;114(12):E2533-E2539. doi:10.1073/pnas.1616493114 apa: Möller, B., Ten Hove, C., Xiang, D., Williams, N., López, L., Yoshida, S., … Weijers, D. (2017). Auxin response cell autonomously controls ground tissue initiation in the early arabidopsis embryo. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1616493114 chicago: Möller, Barbara, Colette Ten Hove, Daoquan Xiang, Nerys Williams, Lorena López, Saiko Yoshida, Margot Smit, Raju Datla, and Dolf Weijers. “Auxin Response Cell Autonomously Controls Ground Tissue Initiation in the Early Arabidopsis Embryo.” PNAS. National Academy of Sciences, 2017. https://doi.org/10.1073/pnas.1616493114. ieee: B. Möller et al., “Auxin response cell autonomously controls ground tissue initiation in the early arabidopsis embryo,” PNAS, vol. 114, no. 12. National Academy of Sciences, pp. E2533–E2539, 2017. ista: Möller B, Ten Hove C, Xiang D, Williams N, López L, Yoshida S, Smit M, Datla R, Weijers D. 2017. Auxin response cell autonomously controls ground tissue initiation in the early arabidopsis embryo. PNAS. 114(12), E2533–E2539. mla: Möller, Barbara, et al. “Auxin Response Cell Autonomously Controls Ground Tissue Initiation in the Early Arabidopsis Embryo.” PNAS, vol. 114, no. 12, National Academy of Sciences, 2017, pp. E2533–39, doi:10.1073/pnas.1616493114. short: B. Möller, C. Ten Hove, D. Xiang, N. Williams, L. López, S. Yoshida, M. Smit, R. Datla, D. Weijers, PNAS 114 (2017) E2533–E2539. date_created: 2018-12-11T11:47:45Z date_published: 2017-03-21T00:00:00Z date_updated: 2021-01-12T08:08:02Z day: '21' department: - _id: JiFr doi: 10.1073/pnas.1616493114 external_id: pmid: - '28265057' intvolume: ' 114' issue: '12' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5373392/ month: '03' oa: 1 oa_version: Submitted Version page: E2533 - E2539 pmid: 1 publication: PNAS publication_identifier: issn: - '00278424' publication_status: published publisher: National Academy of Sciences publist_id: '7076' quality_controlled: '1' scopus_import: 1 status: public title: Auxin response cell autonomously controls ground tissue initiation in the early arabidopsis embryo type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 114 year: '2017' ... --- _id: '656' abstract: - lang: eng text: Human neurons transplanted into a mouse model for Alzheimer’s disease show human-specific vulnerability to β-amyloid plaques and may help to identify new therapeutic targets. article_number: eaam9867 author: - first_name: Gaia full_name: Novarino, Gaia id: 3E57A680-F248-11E8-B48F-1D18A9856A87 last_name: Novarino orcid: 0000-0002-7673-7178 citation: ama: Novarino G. Modeling Alzheimer’s disease in mice with human neurons. Science Translational Medicine. 2017;9(381). doi:10.1126/scitranslmed.aam9867 apa: Novarino, G. (2017). Modeling Alzheimer’s disease in mice with human neurons. Science Translational Medicine. American Association for the Advancement of Science. https://doi.org/10.1126/scitranslmed.aam9867 chicago: Novarino, Gaia. “Modeling Alzheimer’s Disease in Mice with Human Neurons.” Science Translational Medicine. American Association for the Advancement of Science, 2017. https://doi.org/10.1126/scitranslmed.aam9867. ieee: G. Novarino, “Modeling Alzheimer’s disease in mice with human neurons,” Science Translational Medicine, vol. 9, no. 381. American Association for the Advancement of Science, 2017. ista: Novarino G. 2017. Modeling Alzheimer’s disease in mice with human neurons. Science Translational Medicine. 9(381), eaam9867. mla: Novarino, Gaia. “Modeling Alzheimer’s Disease in Mice with Human Neurons.” Science Translational Medicine, vol. 9, no. 381, eaam9867, American Association for the Advancement of Science, 2017, doi:10.1126/scitranslmed.aam9867. short: G. Novarino, Science Translational Medicine 9 (2017). date_created: 2018-12-11T11:47:45Z date_published: 2017-03-15T00:00:00Z date_updated: 2021-01-12T08:07:59Z day: '15' department: - _id: GaNo doi: 10.1126/scitranslmed.aam9867 intvolume: ' 9' issue: '381' language: - iso: eng month: '03' oa_version: None publication: Science Translational Medicine publication_identifier: issn: - '19466234' publication_status: published publisher: American Association for the Advancement of Science publist_id: '7079' quality_controlled: '1' scopus_import: 1 status: public title: Modeling Alzheimer's disease in mice with human neurons type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 9 year: '2017' ... --- _id: '658' abstract: - lang: eng text: 'With the accelerated development of robot technologies, control becomes one of the central themes of research. In traditional approaches, the controller, by its internal functionality, finds appropriate actions on the basis of specific objectives for the task at hand. While very successful in many applications, self-organized control schemes seem to be favored in large complex systems with unknown dynamics or which are difficult to model. Reasons are the expected scalability, robustness, and resilience of self-organizing systems. The paper presents a self-learning neurocontroller based on extrinsic differential plasticity introduced recently, applying it to an anthropomorphic musculoskeletal robot arm with attached objects of unknown physical dynamics. The central finding of the paper is the following effect: by the mere feedback through the internal dynamics of the object, the robot is learning to relate each of the objects with a very specific sensorimotor pattern. Specifically, an attached pendulum pilots the arm into a circular motion, a half-filled bottle produces axis oriented shaking behavior, a wheel is getting rotated, and wiping patterns emerge automatically in a table-plus-brush setting. By these object-specific dynamical patterns, the robot may be said to recognize the object''s identity, or in other words, it discovers dynamical affordances of objects. Furthermore, when including hand coordinates obtained from a camera, a dedicated hand-eye coordination self-organizes spontaneously. These phenomena are discussed from a specific dynamical system perspective. Central is the dedicated working regime at the border to instability with its potentially infinite reservoir of (limit cycle) attractors "waiting" to be excited. Besides converging toward one of these attractors, variate behavior is also arising from a self-induced attractor morphing driven by the learning rule. We claim that experimental investigations with this anthropomorphic, self-learning robot not only generate interesting and potentially useful behaviors, but may also help to better understand what subjective human muscle feelings are, how they can be rooted in sensorimotor patterns, and how these concepts may feed back on robotics.' article_number: '00008' article_processing_charge: Yes author: - first_name: Ralf full_name: Der, Ralf last_name: Der - first_name: Georg S full_name: Martius, Georg S id: 3A276B68-F248-11E8-B48F-1D18A9856A87 last_name: Martius citation: ama: Der R, Martius GS. Self organized behavior generation for musculoskeletal robots. Frontiers in Neurorobotics. 2017;11(MAR). doi:10.3389/fnbot.2017.00008 apa: Der, R., & Martius, G. S. (2017). Self organized behavior generation for musculoskeletal robots. Frontiers in Neurorobotics. Frontiers Research Foundation. https://doi.org/10.3389/fnbot.2017.00008 chicago: Der, Ralf, and Georg S Martius. “Self Organized Behavior Generation for Musculoskeletal Robots.” Frontiers in Neurorobotics. Frontiers Research Foundation, 2017. https://doi.org/10.3389/fnbot.2017.00008. ieee: R. Der and G. S. Martius, “Self organized behavior generation for musculoskeletal robots,” Frontiers in Neurorobotics, vol. 11, no. MAR. Frontiers Research Foundation, 2017. ista: Der R, Martius GS. 2017. Self organized behavior generation for musculoskeletal robots. Frontiers in Neurorobotics. 11(MAR), 00008. mla: Der, Ralf, and Georg S. Martius. “Self Organized Behavior Generation for Musculoskeletal Robots.” Frontiers in Neurorobotics, vol. 11, no. MAR, 00008, Frontiers Research Foundation, 2017, doi:10.3389/fnbot.2017.00008. short: R. Der, G.S. Martius, Frontiers in Neurorobotics 11 (2017). date_created: 2018-12-11T11:47:45Z date_published: 2017-03-16T00:00:00Z date_updated: 2021-01-12T08:08:04Z day: '16' ddc: - '006' department: - _id: ChLa - _id: GaTk doi: 10.3389/fnbot.2017.00008 ec_funded: 1 file: - access_level: open_access checksum: b1bc43f96d1df3313c03032c2a46388d content_type: application/pdf creator: system date_created: 2018-12-12T10:18:49Z date_updated: 2020-07-14T12:47:33Z file_id: '5371' file_name: IST-2017-903-v1+1_fnbot-11-00008.pdf file_size: 8439566 relation: main_file file_date_updated: 2020-07-14T12:47:33Z has_accepted_license: '1' intvolume: ' 11' issue: MAR language: - iso: eng month: '03' oa: 1 oa_version: Published Version project: - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme publication: Frontiers in Neurorobotics publication_identifier: issn: - '16625218' publication_status: published publisher: Frontiers Research Foundation publist_id: '7078' pubrep_id: '903' quality_controlled: '1' scopus_import: 1 status: public title: Self organized behavior generation for musculoskeletal robots tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2EBD1598-F248-11E8-B48F-1D18A9856A87 volume: 11 year: '2017' ... --- _id: '659' abstract: - lang: eng text: Migration frequently involves Rac-mediated protrusion of lamellipodia, formed by Arp2/3 complex-dependent branching thought to be crucial for force generation and stability of these networks. The formins FMNL2 and FMNL3 are Cdc42 effectors targeting to the lamellipodium tip and shown here to nucleate and elongate actin filaments with complementary activities in vitro. In migrating B16-F1 melanoma cells, both formins contribute to the velocity of lamellipodium protrusion. Loss of FMNL2/3 function in melanoma cells and fibroblasts reduces lamellipodial width, actin filament density and -bundling, without changing patterns of Arp2/3 complex incorporation. Strikingly, in melanoma cells, FMNL2/3 gene inactivation almost completely abolishes protrusion forces exerted by lamellipodia and modifies their ultrastructural organization. Consistently, CRISPR/Cas-mediated depletion of FMNL2/3 in fibroblasts reduces both migration and capability of cells to move against viscous media. Together, we conclude that force generation in lamellipodia strongly depends on FMNL formin activity, operating in addition to Arp2/3 complex-dependent filament branching. article_number: '14832' article_processing_charge: No author: - first_name: Frieda full_name: Kage, Frieda last_name: Kage - first_name: Moritz full_name: Winterhoff, Moritz last_name: Winterhoff - first_name: Vanessa full_name: Dimchev, Vanessa last_name: Dimchev - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Tobias full_name: Thalheim, Tobias last_name: Thalheim - first_name: Anika full_name: Freise, Anika last_name: Freise - first_name: Stefan full_name: Brühmann, Stefan last_name: Brühmann - first_name: Jana full_name: Kollasser, Jana last_name: Kollasser - first_name: Jennifer full_name: Block, Jennifer last_name: Block - first_name: Georgi A full_name: Dimchev, Georgi A last_name: Dimchev - first_name: Matthias full_name: Geyer, Matthias last_name: Geyer - first_name: Hams full_name: Schnittler, Hams last_name: Schnittler - first_name: Cord full_name: Brakebusch, Cord last_name: Brakebusch - first_name: Theresia full_name: Stradal, Theresia last_name: Stradal - first_name: Marie full_name: Carlier, Marie last_name: Carlier - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Josef full_name: Käs, Josef last_name: Käs - first_name: Jan full_name: Faix, Jan last_name: Faix - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner citation: ama: Kage F, Winterhoff M, Dimchev V, et al. FMNL formins boost lamellipodial force generation. Nature Communications. 2017;8. doi:10.1038/ncomms14832 apa: Kage, F., Winterhoff, M., Dimchev, V., Müller, J., Thalheim, T., Freise, A., … Rottner, K. (2017). FMNL formins boost lamellipodial force generation. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms14832 chicago: Kage, Frieda, Moritz Winterhoff, Vanessa Dimchev, Jan Müller, Tobias Thalheim, Anika Freise, Stefan Brühmann, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/ncomms14832. ieee: F. Kage et al., “FMNL formins boost lamellipodial force generation,” Nature Communications, vol. 8. Nature Publishing Group, 2017. ista: Kage F, Winterhoff M, Dimchev V, Müller J, Thalheim T, Freise A, Brühmann S, Kollasser J, Block J, Dimchev GA, Geyer M, Schnittler H, Brakebusch C, Stradal T, Carlier M, Sixt MK, Käs J, Faix J, Rottner K. 2017. FMNL formins boost lamellipodial force generation. Nature Communications. 8, 14832. mla: Kage, Frieda, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature Communications, vol. 8, 14832, Nature Publishing Group, 2017, doi:10.1038/ncomms14832. short: F. Kage, M. Winterhoff, V. Dimchev, J. Müller, T. Thalheim, A. Freise, S. Brühmann, J. Kollasser, J. Block, G.A. Dimchev, M. Geyer, H. Schnittler, C. Brakebusch, T. Stradal, M. Carlier, M.K. Sixt, J. Käs, J. Faix, K. Rottner, Nature Communications 8 (2017). date_created: 2018-12-11T11:47:46Z date_published: 2017-03-22T00:00:00Z date_updated: 2021-01-12T08:08:06Z day: '22' ddc: - '570' department: - _id: MiSi doi: 10.1038/ncomms14832 file: - access_level: open_access checksum: dae30190291c3630e8102d8714a8d23e content_type: application/pdf creator: system date_created: 2018-12-12T10:14:21Z date_updated: 2020-07-14T12:47:34Z file_id: '5072' file_name: IST-2017-902-v1+1_Kage_et_al-2017-Nature_Communications.pdf file_size: 9523746 relation: main_file file_date_updated: 2020-07-14T12:47:34Z has_accepted_license: '1' intvolume: ' 8' language: - iso: eng month: '03' oa: 1 oa_version: Published Version publication: Nature Communications publication_identifier: issn: - '20411723' publication_status: published publisher: Nature Publishing Group publist_id: '7075' pubrep_id: '902' quality_controlled: '1' scopus_import: 1 status: public title: FMNL formins boost lamellipodial force generation tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2017' ... --- _id: '660' abstract: - lang: eng text: Growing microtubules are protected from depolymerization by the presence of a GTP or GDP/Pi cap. End-binding proteins of the EB1 family bind to the stabilizing cap, allowing monitoring of its size in real time. The cap size has been shown to correlate with instantaneous microtubule stability. Here we have quantitatively characterized the properties of cap size fluctuations during steadystate growth and have developed a theory predicting their timescale and amplitude from the kinetics of microtubule growth and cap maturation. In contrast to growth speed fluctuations, cap size fluctuations show a characteristic timescale, which is defined by the lifetime of the cap sites. Growth fluctuations affect the amplitude of cap size fluctuations; however, cap size does not affect growth speed, indicating that microtubules are far from instability during most of their time of growth. Our theory provides the basis for a quantitative understanding of microtubule stability fluctuations during steady-state growth. acknowledgement: We thank Philippe Cluzel for helpful discussions and Gunnar Pruessner for data analysis advice. This work was supported by the Francis Crick Institute, which receives its core funding from Cancer Research UK Grant FC001163, Medical Research Council Grant FC001163, and Wellcome Trust Grant FC001163. This work was also supported by European Research Council Advanced Grant Project 323042 (to C.D. and T.S.). author: - first_name: Jamie full_name: Rickman, Jamie last_name: Rickman - first_name: Christian F full_name: Düllberg, Christian F id: 459064DC-F248-11E8-B48F-1D18A9856A87 last_name: Düllberg orcid: 0000-0001-6335-9748 - first_name: Nicholas full_name: Cade, Nicholas last_name: Cade - first_name: Lewis full_name: Griffin, Lewis last_name: Griffin - first_name: Thomas full_name: Surrey, Thomas last_name: Surrey citation: ama: Rickman J, Düllberg CF, Cade N, Griffin L, Surrey T. Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation. PNAS. 2017;114(13):3427-3432. doi:10.1073/pnas.1620274114 apa: Rickman, J., Düllberg, C. F., Cade, N., Griffin, L., & Surrey, T. (2017). Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1620274114 chicago: Rickman, Jamie, Christian F Düllberg, Nicholas Cade, Lewis Griffin, and Thomas Surrey. “Steady State EB Cap Size Fluctuations Are Determined by Stochastic Microtubule Growth and Maturation.” PNAS. National Academy of Sciences, 2017. https://doi.org/10.1073/pnas.1620274114. ieee: J. Rickman, C. F. Düllberg, N. Cade, L. Griffin, and T. Surrey, “Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation,” PNAS, vol. 114, no. 13. National Academy of Sciences, pp. 3427–3432, 2017. ista: Rickman J, Düllberg CF, Cade N, Griffin L, Surrey T. 2017. Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation. PNAS. 114(13), 3427–3432. mla: Rickman, Jamie, et al. “Steady State EB Cap Size Fluctuations Are Determined by Stochastic Microtubule Growth and Maturation.” PNAS, vol. 114, no. 13, National Academy of Sciences, 2017, pp. 3427–32, doi:10.1073/pnas.1620274114. short: J. Rickman, C.F. Düllberg, N. Cade, L. Griffin, T. Surrey, PNAS 114 (2017) 3427–3432. date_created: 2018-12-11T11:47:46Z date_published: 2017-03-28T00:00:00Z date_updated: 2021-01-12T08:08:09Z day: '28' department: - _id: MaLo doi: 10.1073/pnas.1620274114 external_id: pmid: - '28280102' intvolume: ' 114' issue: '13' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380103/ month: '03' oa: 1 oa_version: Submitted Version page: 3427 - 3432 pmid: 1 publication: PNAS publication_identifier: issn: - '00278424' publication_status: published publisher: National Academy of Sciences publist_id: '7073' quality_controlled: '1' scopus_import: 1 status: public title: Steady state EB cap size fluctuations are determined by stochastic microtubule growth and maturation type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 114 year: '2017' ... --- _id: '662' abstract: - lang: eng text: 'We report a direct-numerical-simulation study of the Taylor-Couette flow in the quasi-Keplerian regime at shear Reynolds numbers up to (105). Quasi-Keplerian rotating flow has been investigated for decades as a simplified model system to study the origin of turbulence in accretion disks that is not fully understood. The flow in this study is axially periodic and thus the experimental end-wall effects on the stability of the flow are avoided. Using optimal linear perturbations as initial conditions, our simulations find no sustained turbulence: the strong initial perturbations distort the velocity profile and trigger turbulence that eventually decays.' article_number: '044107' author: - first_name: Liang full_name: Shi, Liang last_name: Shi - first_name: Björn full_name: Hof, Björn id: 3A374330-F248-11E8-B48F-1D18A9856A87 last_name: Hof orcid: 0000-0003-2057-2754 - first_name: Markus full_name: Rampp, Markus last_name: Rampp - first_name: Marc full_name: Avila, Marc last_name: Avila citation: ama: Shi L, Hof B, Rampp M, Avila M. Hydrodynamic turbulence in quasi Keplerian rotating flows. Physics of Fluids. 2017;29(4). doi:10.1063/1.4981525 apa: Shi, L., Hof, B., Rampp, M., & Avila, M. (2017). Hydrodynamic turbulence in quasi Keplerian rotating flows. Physics of Fluids. American Institute of Physics. https://doi.org/10.1063/1.4981525 chicago: Shi, Liang, Björn Hof, Markus Rampp, and Marc Avila. “Hydrodynamic Turbulence in Quasi Keplerian Rotating Flows.” Physics of Fluids. American Institute of Physics, 2017. https://doi.org/10.1063/1.4981525. ieee: L. Shi, B. Hof, M. Rampp, and M. Avila, “Hydrodynamic turbulence in quasi Keplerian rotating flows,” Physics of Fluids, vol. 29, no. 4. American Institute of Physics, 2017. ista: Shi L, Hof B, Rampp M, Avila M. 2017. Hydrodynamic turbulence in quasi Keplerian rotating flows. Physics of Fluids. 29(4), 044107. mla: Shi, Liang, et al. “Hydrodynamic Turbulence in Quasi Keplerian Rotating Flows.” Physics of Fluids, vol. 29, no. 4, 044107, American Institute of Physics, 2017, doi:10.1063/1.4981525. short: L. Shi, B. Hof, M. Rampp, M. Avila, Physics of Fluids 29 (2017). date_created: 2018-12-11T11:47:47Z date_published: 2017-04-01T00:00:00Z date_updated: 2021-01-12T08:08:15Z day: '01' department: - _id: BjHo doi: 10.1063/1.4981525 intvolume: ' 29' issue: '4' language: - iso: eng main_file_link: - open_access: '1' url: https://arxiv.org/abs/1703.01714 month: '04' oa: 1 oa_version: Submitted Version project: - _id: 2511D90C-B435-11E9-9278-68D0E5697425 grant_number: SFB 963 TP A8 name: Astrophysical instability of currents and turbulences publication: Physics of Fluids publication_identifier: issn: - '10706631' publication_status: published publisher: American Institute of Physics publist_id: '7072' quality_controlled: '1' scopus_import: 1 status: public title: Hydrodynamic turbulence in quasi Keplerian rotating flows type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 29 year: '2017' ... --- _id: '663' abstract: - lang: eng text: 'In this paper, we propose an approach to automatically compute invariant clusters for nonlinear semialgebraic hybrid systems. An invariant cluster for an ordinary differential equation (ODE) is a multivariate polynomial invariant g(u→, x→) = 0, parametric in u→, which can yield an infinite number of concrete invariants by assigning different values to u→ so that every trajectory of the system can be overapproximated precisely by the intersection of a group of concrete invariants. For semialgebraic systems, which involve ODEs with multivariate polynomial right-hand sides, given a template multivariate polynomial g(u→, x→), an invariant cluster can be obtained by first computing the remainder of the Lie derivative of g(u→, x→) divided by g(u→, x→) and then solving the system of polynomial equations obtained from the coefficients of the remainder. Based on invariant clusters and sum-of-squares (SOS) programming, we present a new method for the safety verification of hybrid systems. Experiments on nonlinear benchmark systems from biology and control theory show that our approach is efficient. ' author: - first_name: Hui full_name: Kong, Hui id: 3BDE25AA-F248-11E8-B48F-1D18A9856A87 last_name: Kong orcid: 0000-0002-3066-6941 - first_name: Sergiy full_name: Bogomolov, Sergiy last_name: Bogomolov orcid: 0000-0002-0686-0365 - first_name: Christian full_name: Schilling, Christian last_name: Schilling - first_name: Yu full_name: Jiang, Yu last_name: Jiang - first_name: Thomas A full_name: Henzinger, Thomas A id: 40876CD8-F248-11E8-B48F-1D18A9856A87 last_name: Henzinger orcid: 0000−0002−2985−7724 citation: ama: 'Kong H, Bogomolov S, Schilling C, Jiang Y, Henzinger TA. Safety verification of nonlinear hybrid systems based on invariant clusters. In: Proceedings of the 20th International Conference on Hybrid Systems. ACM; 2017:163-172. doi:10.1145/3049797.3049814' apa: 'Kong, H., Bogomolov, S., Schilling, C., Jiang, Y., & Henzinger, T. A. (2017). Safety verification of nonlinear hybrid systems based on invariant clusters. In Proceedings of the 20th International Conference on Hybrid Systems (pp. 163–172). Pittsburgh, PA, United States: ACM. https://doi.org/10.1145/3049797.3049814' chicago: Kong, Hui, Sergiy Bogomolov, Christian Schilling, Yu Jiang, and Thomas A Henzinger. “Safety Verification of Nonlinear Hybrid Systems Based on Invariant Clusters.” In Proceedings of the 20th International Conference on Hybrid Systems, 163–72. ACM, 2017. https://doi.org/10.1145/3049797.3049814. ieee: H. Kong, S. Bogomolov, C. Schilling, Y. Jiang, and T. A. Henzinger, “Safety verification of nonlinear hybrid systems based on invariant clusters,” in Proceedings of the 20th International Conference on Hybrid Systems, Pittsburgh, PA, United States, 2017, pp. 163–172. ista: 'Kong H, Bogomolov S, Schilling C, Jiang Y, Henzinger TA. 2017. Safety verification of nonlinear hybrid systems based on invariant clusters. Proceedings of the 20th International Conference on Hybrid Systems. HSCC: Hybrid Systems Computation and Control , 163–172.' mla: Kong, Hui, et al. “Safety Verification of Nonlinear Hybrid Systems Based on Invariant Clusters.” Proceedings of the 20th International Conference on Hybrid Systems, ACM, 2017, pp. 163–72, doi:10.1145/3049797.3049814. short: H. Kong, S. Bogomolov, C. Schilling, Y. Jiang, T.A. Henzinger, in:, Proceedings of the 20th International Conference on Hybrid Systems, ACM, 2017, pp. 163–172. conference: end_date: 2017-04-20 location: Pittsburgh, PA, United States name: 'HSCC: Hybrid Systems Computation and Control ' start_date: 2017-04-18 date_created: 2018-12-11T11:47:47Z date_published: 2017-04-01T00:00:00Z date_updated: 2021-01-12T08:08:17Z day: '01' ddc: - '000' department: - _id: ToHe doi: 10.1145/3049797.3049814 file: - access_level: open_access checksum: b7667434cbf5b5f0ade3bea1dbe5bf63 content_type: application/pdf creator: system date_created: 2018-12-12T10:11:20Z date_updated: 2020-07-14T12:47:34Z file_id: '4873' file_name: IST-2017-817-v1+1_p163-kong.pdf file_size: 1650530 relation: main_file file_date_updated: 2020-07-14T12:47:34Z has_accepted_license: '1' language: - iso: eng month: '04' oa: 1 oa_version: Submitted Version page: 163 - 172 publication: Proceedings of the 20th International Conference on Hybrid Systems publication_identifier: isbn: - 978-145034590-3 publication_status: published publisher: ACM publist_id: '7067' pubrep_id: '817' quality_controlled: '1' scopus_import: 1 status: public title: Safety verification of nonlinear hybrid systems based on invariant clusters type: conference user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2017' ... --- _id: '667' abstract: - lang: eng text: Perinatal exposure to penicillin may result in longlasting gut and behavioral changes. article_number: '2786' author: - first_name: Gaia full_name: Novarino, Gaia id: 3E57A680-F248-11E8-B48F-1D18A9856A87 last_name: Novarino orcid: 0000-0002-7673-7178 citation: ama: Novarino G. The antisocial side of antibiotics. Science Translational Medicine. 2017;9(387). doi:10.1126/scitranslmed.aan2786 apa: Novarino, G. (2017). The antisocial side of antibiotics. Science Translational Medicine. American Association for the Advancement of Science. https://doi.org/10.1126/scitranslmed.aan2786 chicago: Novarino, Gaia. “The Antisocial Side of Antibiotics.” Science Translational Medicine. American Association for the Advancement of Science, 2017. https://doi.org/10.1126/scitranslmed.aan2786. ieee: G. Novarino, “The antisocial side of antibiotics,” Science Translational Medicine, vol. 9, no. 387. American Association for the Advancement of Science, 2017. ista: Novarino G. 2017. The antisocial side of antibiotics. Science Translational Medicine. 9(387), 2786. mla: Novarino, Gaia. “The Antisocial Side of Antibiotics.” Science Translational Medicine, vol. 9, no. 387, 2786, American Association for the Advancement of Science, 2017, doi:10.1126/scitranslmed.aan2786. short: G. Novarino, Science Translational Medicine 9 (2017). date_created: 2018-12-11T11:47:48Z date_published: 2017-04-26T00:00:00Z date_updated: 2021-01-12T08:08:30Z day: '26' department: - _id: GaNo doi: 10.1126/scitranslmed.aan2786 intvolume: ' 9' issue: '387' language: - iso: eng month: '04' oa_version: None publication: Science Translational Medicine publication_identifier: issn: - '19466234' publication_status: published publisher: American Association for the Advancement of Science publist_id: '7060' quality_controlled: '1' scopus_import: 1 status: public title: The antisocial side of antibiotics type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 9 year: '2017' ... --- _id: '668' abstract: - lang: eng text: Macrophage filopodia, finger-like membrane protrusions, were first implicated in phagocytosis more than 100 years ago, but little is still known about the involvement of these actin-dependent structures in particle clearance. Using spinning disk confocal microscopy to image filopodial dynamics in mouse resident Lifeact-EGFP macrophages, we show that filopodia, or filopodia-like structures, support pathogen clearance by multiple means. Filopodia supported the phagocytic uptake of bacterial (Escherichia coli) particles by (i) capturing along the filopodial shaft and surfing toward the cell body, the most common mode of capture; (ii) capturing via the tip followed by retraction; (iii) combinations of surfing and retraction; or (iv) sweeping actions. In addition, filopodia supported the uptake of zymosan (Saccharomyces cerevisiae) particles by (i) providing fixation, (ii) capturing at the tip and filopodia-guided actin anterograde flow with phagocytic cup formation, and (iii) the rapid growth of new protrusions. To explore the role of filopodia-inducing Cdc42, we generated myeloid-restricted Cdc42 knock-out mice. Cdc42-deficient macrophages exhibited rapid phagocytic cup kinetics, but reduced particle clearance, which could be explained by the marked rounded-up morphology of these cells. Macrophages lacking Myo10, thought to act downstream of Cdc42, had normal morphology, motility, and phagocytic cup formation, but displayed markedly reduced filopodia formation. In conclusion, live-cell imaging revealed multiple mechanisms involving macrophage filopodia in particle capture and engulfment. Cdc42 is not critical for filopodia or phagocytic cup formation, but plays a key role in driving macrophage lamellipodial spreading. article_type: original author: - first_name: Markus full_name: Horsthemke, Markus last_name: Horsthemke - first_name: Anne full_name: Bachg, Anne last_name: Bachg - first_name: Katharina full_name: Groll, Katharina last_name: Groll - first_name: Sven full_name: Moyzio, Sven last_name: Moyzio - first_name: Barbara full_name: Müther, Barbara last_name: Müther - first_name: Sandra full_name: Hemkemeyer, Sandra last_name: Hemkemeyer - first_name: Roland full_name: Wedlich Söldner, Roland last_name: Wedlich Söldner - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Sebastian full_name: Tacke, Sebastian last_name: Tacke - first_name: Martin full_name: Bähler, Martin last_name: Bähler - first_name: Peter full_name: Hanley, Peter last_name: Hanley citation: ama: Horsthemke M, Bachg A, Groll K, et al. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 2017;292(17):7258-7273. doi:10.1074/jbc.M116.766923 apa: Horsthemke, M., Bachg, A., Groll, K., Moyzio, S., Müther, B., Hemkemeyer, S., … Hanley, P. (2017). Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology. https://doi.org/10.1074/jbc.M116.766923 chicago: Horsthemke, Markus, Anne Bachg, Katharina Groll, Sven Moyzio, Barbara Müther, Sandra Hemkemeyer, Roland Wedlich Söldner, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology, 2017. https://doi.org/10.1074/jbc.M116.766923. ieee: M. Horsthemke et al., “Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion,” Journal of Biological Chemistry, vol. 292, no. 17. American Society for Biochemistry and Molecular Biology, pp. 7258–7273, 2017. ista: Horsthemke M, Bachg A, Groll K, Moyzio S, Müther B, Hemkemeyer S, Wedlich Söldner R, Sixt MK, Tacke S, Bähler M, Hanley P. 2017. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 292(17), 7258–7273. mla: Horsthemke, Markus, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal of Biological Chemistry, vol. 292, no. 17, American Society for Biochemistry and Molecular Biology, 2017, pp. 7258–73, doi:10.1074/jbc.M116.766923. short: M. Horsthemke, A. Bachg, K. Groll, S. Moyzio, B. Müther, S. Hemkemeyer, R. Wedlich Söldner, M.K. Sixt, S. Tacke, M. Bähler, P. Hanley, Journal of Biological Chemistry 292 (2017) 7258–7273. date_created: 2018-12-11T11:47:49Z date_published: 2017-04-28T00:00:00Z date_updated: 2021-01-12T08:08:34Z day: '28' ddc: - '570' department: - _id: MiSi doi: 10.1074/jbc.M116.766923 file: - access_level: open_access checksum: d488162874326a4bb056065fa549dc4a content_type: application/pdf creator: dernst date_created: 2019-10-24T15:25:42Z date_updated: 2020-07-14T12:47:37Z file_id: '6971' file_name: 2017_JBC_Horsthemke.pdf file_size: 5647880 relation: main_file file_date_updated: 2020-07-14T12:47:37Z has_accepted_license: '1' intvolume: ' 292' issue: '17' language: - iso: eng month: '04' oa: 1 oa_version: Published Version page: 7258 - 7273 publication: Journal of Biological Chemistry publication_identifier: issn: - '00219258' publication_status: published publisher: American Society for Biochemistry and Molecular Biology publist_id: '7059' quality_controlled: '1' scopus_import: 1 status: public title: Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 292 year: '2017' ... --- _id: '669' abstract: - lang: eng text: 'The exocyst, a eukaryotic tethering complex, coregulates targeted exocytosis as an effector of small GTPases in polarized cell growth. In land plants, several exocyst subunits are encoded by double or triple paralogs, culminating in tens of EXO70 paralogs. Out of 23 Arabidopsis thaliana EXO70 isoforms, we analyzed seven isoforms expressed in pollen. Genetic and microscopic analyses of single mutants in EXO70A2, EXO70C1, EXO70C2, EXO70F1, EXO70H3, EXO70H5, and EXO70H6 genes revealed that only a loss-of-function EXO70C2 allele resulted in a significant male-specific transmission defect (segregation 40%:51%:9%) due to aberrant pollen tube growth. Mutant pollen tubes grown in vitro exhibited an enhanced growth rate and a decreased thickness of the tip cell wall, causing tip bursts. However, exo70C2 pollen tubes could frequently recover and restart their speedy elongation, resulting in a repetitive stop-and-go growth dynamics. A pollenspecific depletion of the closest paralog, EXO70C1, using artificial microRNA in the exo70C2 mutant background, resulted in a complete pollen-specific transmission defect, suggesting redundant functions of EXO70C1 and EXO70C2. Both EXO70C1 and EXO70C2, GFP tagged and expressed under the control of their native promoters, localized in the cytoplasm of pollen grains, pollen tubes, and also root trichoblast cells. The expression of EXO70C2-GFP complemented the aberrant growth of exo70C2 pollen tubes. The absent EXO70C2 interactions with core exocyst subunits in the yeast two-hybrid assay, cytoplasmic localization, and genetic effect suggest an unconventional EXO70 function possibly as a regulator of exocytosis outside the exocyst complex. In conclusion, EXO70C2 is a novel factor contributing to the regulation of optimal tip growth of Arabidopsis pollen tubes. ' article_processing_charge: No article_type: original author: - first_name: Lukáš full_name: Synek, Lukáš last_name: Synek - first_name: Nemanja full_name: Vukašinović, Nemanja last_name: Vukašinović - first_name: Ivan full_name: Kulich, Ivan last_name: Kulich - first_name: Michal full_name: Hála, Michal last_name: Hála - first_name: Klára full_name: Aldorfová, Klára last_name: Aldorfová - first_name: Matyas full_name: Fendrych, Matyas id: 43905548-F248-11E8-B48F-1D18A9856A87 last_name: Fendrych orcid: 0000-0002-9767-8699 - first_name: Viktor full_name: Žárský, Viktor last_name: Žárský citation: ama: Synek L, Vukašinović N, Kulich I, et al. EXO70C2 is a key regulatory factor for optimal tip growth of pollen. Plant Physiology. 2017;174(1):223-240. doi:10.1104/pp.16.01282 apa: Synek, L., Vukašinović, N., Kulich, I., Hála, M., Aldorfová, K., Fendrych, M., & Žárský, V. (2017). EXO70C2 is a key regulatory factor for optimal tip growth of pollen. Plant Physiology. American Society of Plant Biologists. https://doi.org/10.1104/pp.16.01282 chicago: Synek, Lukáš, Nemanja Vukašinović, Ivan Kulich, Michal Hála, Klára Aldorfová, Matyas Fendrych, and Viktor Žárský. “EXO70C2 Is a Key Regulatory Factor for Optimal Tip Growth of Pollen.” Plant Physiology. American Society of Plant Biologists, 2017. https://doi.org/10.1104/pp.16.01282. ieee: L. Synek et al., “EXO70C2 is a key regulatory factor for optimal tip growth of pollen,” Plant Physiology, vol. 174, no. 1. American Society of Plant Biologists, pp. 223–240, 2017. ista: Synek L, Vukašinović N, Kulich I, Hála M, Aldorfová K, Fendrych M, Žárský V. 2017. EXO70C2 is a key regulatory factor for optimal tip growth of pollen. Plant Physiology. 174(1), 223–240. mla: Synek, Lukáš, et al. “EXO70C2 Is a Key Regulatory Factor for Optimal Tip Growth of Pollen.” Plant Physiology, vol. 174, no. 1, American Society of Plant Biologists, 2017, pp. 223–40, doi:10.1104/pp.16.01282. short: L. Synek, N. Vukašinović, I. Kulich, M. Hála, K. Aldorfová, M. Fendrych, V. Žárský, Plant Physiology 174 (2017) 223–240. date_created: 2018-12-11T11:47:49Z date_published: 2017-05-01T00:00:00Z date_updated: 2021-01-12T08:08:35Z day: '01' ddc: - '580' department: - _id: JiFr doi: 10.1104/pp.16.01282 external_id: pmid: - '28356503' file: - access_level: open_access checksum: 97155acc6aa5f0d0a78e0589a932fe02 content_type: application/pdf creator: dernst date_created: 2019-11-18T16:16:18Z date_updated: 2020-07-14T12:47:37Z file_id: '7041' file_name: 2017_PlantPhysio_Synek.pdf file_size: 2176903 relation: main_file file_date_updated: 2020-07-14T12:47:37Z has_accepted_license: '1' intvolume: ' 174' issue: '1' language: - iso: eng month: '05' oa: 1 oa_version: Submitted Version page: 223 - 240 pmid: 1 publication: Plant Physiology publication_identifier: issn: - '00320889' publication_status: published publisher: American Society of Plant Biologists publist_id: '7058' quality_controlled: '1' scopus_import: 1 status: public title: EXO70C2 is a key regulatory factor for optimal tip growth of pollen type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 174 year: '2017' ... --- _id: '671' abstract: - lang: eng text: Humans routinely use conditionally cooperative strategies when interacting in repeated social dilemmas. They are more likely to cooperate if others cooperated before, and are ready to retaliate if others defected. To capture the emergence of reciprocity, most previous models consider subjects who can only choose from a restricted set of representative strategies, or who react to the outcome of the very last round only. As players memorize more rounds, the dimension of the strategy space increases exponentially. This increasing computational complexity renders simulations for individuals with higher cognitive abilities infeasible, especially if multiplayer interactions are taken into account. Here, we take an axiomatic approach instead. We propose several properties that a robust cooperative strategy for a repeated multiplayer dilemma should have. These properties naturally lead to a unique class of cooperative strategies, which contains the classical Win-Stay Lose-Shift rule as a special case. A comprehensive numerical analysis for the prisoner's dilemma and for the public goods game suggests that strategies of this class readily evolve across various memory-n spaces. Our results reveal that successful strategies depend not only on how cooperative others were in the past but also on the respective context of cooperation. article_processing_charge: Yes (in subscription journal) author: - first_name: Christian full_name: Hilbe, Christian id: 2FDF8F3C-F248-11E8-B48F-1D18A9856A87 last_name: Hilbe orcid: 0000-0001-5116-955X - first_name: Vaquero full_name: Martinez, Vaquero last_name: Martinez - first_name: Krishnendu full_name: Chatterjee, Krishnendu id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87 last_name: Chatterjee orcid: 0000-0002-4561-241X - first_name: Martin full_name: Nowak, Martin last_name: Nowak citation: ama: Hilbe C, Martinez V, Chatterjee K, Nowak M. Memory-n strategies of direct reciprocity. PNAS. 2017;114(18):4715-4720. doi:10.1073/pnas.1621239114 apa: Hilbe, C., Martinez, V., Chatterjee, K., & Nowak, M. (2017). Memory-n strategies of direct reciprocity. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1621239114 chicago: Hilbe, Christian, Vaquero Martinez, Krishnendu Chatterjee, and Martin Nowak. “Memory-n Strategies of Direct Reciprocity.” PNAS. National Academy of Sciences, 2017. https://doi.org/10.1073/pnas.1621239114. ieee: C. Hilbe, V. Martinez, K. Chatterjee, and M. Nowak, “Memory-n strategies of direct reciprocity,” PNAS, vol. 114, no. 18. National Academy of Sciences, pp. 4715–4720, 2017. ista: Hilbe C, Martinez V, Chatterjee K, Nowak M. 2017. Memory-n strategies of direct reciprocity. PNAS. 114(18), 4715–4720. mla: Hilbe, Christian, et al. “Memory-n Strategies of Direct Reciprocity.” PNAS, vol. 114, no. 18, National Academy of Sciences, 2017, pp. 4715–20, doi:10.1073/pnas.1621239114. short: C. Hilbe, V. Martinez, K. Chatterjee, M. Nowak, PNAS 114 (2017) 4715–4720. date_created: 2018-12-11T11:47:50Z date_published: 2017-05-02T00:00:00Z date_updated: 2021-01-12T08:08:37Z day: '02' department: - _id: KrCh doi: 10.1073/pnas.1621239114 ec_funded: 1 external_id: pmid: - '28420786' intvolume: ' 114' issue: '18' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5422766/ month: '05' oa: 1 oa_version: Published Version page: 4715 - 4720 pmid: 1 project: - _id: 2581B60A-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '279307' name: 'Quantitative Graph Games: Theory and Applications' - _id: 2584A770-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P 23499-N23 name: Modern Graph Algorithmic Techniques in Formal Verification - _id: 25863FF4-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S11407 name: Game Theory publication: PNAS publication_identifier: issn: - '00278424' publication_status: published publisher: National Academy of Sciences publist_id: '7053' quality_controlled: '1' scopus_import: 1 status: public title: Memory-n strategies of direct reciprocity type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 114 year: '2017' ... --- _id: '670' abstract: - lang: eng text: We propose an efficient method to model paper tearing in the context of interactive modeling. The method uses geometrical information to automatically detect potential starting points of tears. We further introduce a new hybrid geometrical and physical-based method to compute the trajectory of tears while procedurally synthesizing high resolution details of the tearing path using a texture based approach. The results obtained are compared with real paper and with previous studies on the expected geometric paths of paper that tears. article_processing_charge: No article_type: original author: - first_name: Camille full_name: Schreck, Camille id: 2B14B676-F248-11E8-B48F-1D18A9856A87 last_name: Schreck - first_name: Damien full_name: Rohmer, Damien last_name: Rohmer - first_name: Stefanie full_name: Hahmann, Stefanie last_name: Hahmann citation: ama: Schreck C, Rohmer D, Hahmann S. Interactive paper tearing. Computer Graphics Forum. 2017;36(2):95-106. doi:10.1111/cgf.13110 apa: Schreck, C., Rohmer, D., & Hahmann, S. (2017). Interactive paper tearing. Computer Graphics Forum. Wiley. https://doi.org/10.1111/cgf.13110 chicago: Schreck, Camille, Damien Rohmer, and Stefanie Hahmann. “Interactive Paper Tearing.” Computer Graphics Forum. Wiley, 2017. https://doi.org/10.1111/cgf.13110. ieee: C. Schreck, D. Rohmer, and S. Hahmann, “Interactive paper tearing,” Computer Graphics Forum, vol. 36, no. 2. Wiley, pp. 95–106, 2017. ista: Schreck C, Rohmer D, Hahmann S. 2017. Interactive paper tearing. Computer Graphics Forum. 36(2), 95–106. mla: Schreck, Camille, et al. “Interactive Paper Tearing.” Computer Graphics Forum, vol. 36, no. 2, Wiley, 2017, pp. 95–106, doi:10.1111/cgf.13110. short: C. Schreck, D. Rohmer, S. Hahmann, Computer Graphics Forum 36 (2017) 95–106. date_created: 2018-12-11T11:47:49Z date_published: 2017-05-01T00:00:00Z date_updated: 2021-01-12T08:08:37Z day: '01' ddc: - '000' department: - _id: ChWo doi: 10.1111/cgf.13110 intvolume: ' 36' issue: '2' language: - iso: eng main_file_link: - open_access: '1' url: https://hal.inria.fr/hal-01647113/file/eg_2017_schreck_paper_tearing.pdf month: '05' oa: 1 oa_version: Published Version page: 95 - 106 project: - _id: 25357BD2-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P 24352-N23 name: 'Deep Pictures: Creating Visual and Haptic Vector Images' publication: Computer Graphics Forum publication_identifier: issn: - '01677055' publication_status: published publisher: Wiley publist_id: '7056' quality_controlled: '1' scopus_import: 1 status: public title: Interactive paper tearing type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 36 year: '2017' ... --- _id: '672' abstract: - lang: eng text: Trafficking cells frequently transmigrate through epithelial and endothelial monolayers. How monolayers cooperate with the penetrating cells to support their transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic capillaries as a model system for transendothelial migration. We find that the chemokine CCL21, which is the decisive guidance cue for intravasation, mainly localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes extracellularly enriched at the sites of endothelial cell-cell junctions. When we reconstitute the transmigration process in vitro, we find that secretion of CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and selective calcium chelation in lymphatic endothelium attenuates transmigration. Altogether, our data demonstrate a chemokine-mediated feedback between DCs and lymphatic endothelium, which facilitates transendothelial migration. article_processing_charge: Yes author: - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner - first_name: Matthias full_name: Mehling, Matthias id: 3C23B994-F248-11E8-B48F-1D18A9856A87 last_name: Mehling orcid: 0000-0001-8599-1226 - first_name: Walter full_name: Kaufmann, Walter id: 3F99E422-F248-11E8-B48F-1D18A9856A87 last_name: Kaufmann orcid: 0000-0001-9735-5315 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027 apa: Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling, M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027 chicago: Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027. ieee: K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports, vol. 19, no. 5. Cell Press, pp. 902–909, 2017. ista: Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909. mla: Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports, vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027. short: K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling, W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909. date_created: 2018-12-11T11:47:50Z date_published: 2017-05-02T00:00:00Z date_updated: 2023-02-23T12:50:09Z day: '02' ddc: - '570' department: - _id: MiSi - _id: Bio - _id: EM-Fac doi: 10.1016/j.celrep.2017.04.027 ec_funded: 1 file: - access_level: open_access checksum: 8fdddaab1f1d76a6ec9ca94dcb6b07a2 content_type: application/pdf creator: system date_created: 2018-12-12T10:14:54Z date_updated: 2020-07-14T12:47:38Z file_id: '5109' file_name: IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf file_size: 2248814 relation: main_file file_date_updated: 2020-07-14T12:47:38Z has_accepted_license: '1' intvolume: ' 19' issue: '5' language: - iso: eng month: '05' oa: 1 oa_version: Published Version page: 902 - 909 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Cell Reports publication_identifier: issn: - '22111247' publication_status: published publisher: Cell Press publist_id: '7052' pubrep_id: '900' quality_controlled: '1' scopus_import: 1 status: public title: Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 19 year: '2017' ... --- _id: '674' abstract: - lang: eng text: Navigation of cells along gradients of guidance cues is a determining step in many developmental and immunological processes. Gradients can either be soluble or immobilized to tissues as demonstrated for the haptotactic migration of dendritic cells (DCs) toward higher concentrations of immobilized chemokine CCL21. To elucidate how gradient characteristics govern cellular response patterns, we here introduce an in vitro system allowing to track migratory responses of DCs to precisely controlled immobilized gradients of CCL21. We find that haptotactic sensing depends on the absolute CCL21 concentration and local steepness of the gradient, consistent with a scenario where DC directionality is governed by the signal-to-noise ratio of CCL21 binding to the receptor CCR7. We find that the conditions for optimal DC guidance are perfectly provided by the CCL21 gradients we measure in vivo. Furthermore, we find that CCR7 signal termination by the G-protein-coupled receptor kinase 6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient sensing in vitro and confirm those observations in vivo. These findings suggest that stable, tissue-bound CCL21 gradients as sustainable “roads” ensure optimal guidance in vivo. author: - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Veronika full_name: Bierbaum, Veronika id: 3FD04378-F248-11E8-B48F-1D18A9856A87 last_name: Bierbaum - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Teresa full_name: Tarrant, Teresa last_name: Tarrant - first_name: Tobias full_name: Bollenbach, Tobias id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87 last_name: Bollenbach orcid: 0000-0003-4398-476X - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 2017;27(9):1314-1325. doi:10.1016/j.cub.2017.04.004 apa: Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries, I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.04.004 chicago: Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.04.004. ieee: J. Schwarz et al., “Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6,” Current Biology, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017. ista: Schwarz J, Bierbaum V, Vaahtomeri K, Hauschild R, Brown M, de Vries I, Leithner AF, Reversat A, Merrin J, Tarrant T, Bollenbach MT, Sixt MK. 2017. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 27(9), 1314–1325. mla: Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:10.1016/j.cub.2017.04.004. short: J. Schwarz, V. Bierbaum, K. Vaahtomeri, R. Hauschild, M. Brown, I. de Vries, A.F. Leithner, A. Reversat, J. Merrin, T. Tarrant, M.T. Bollenbach, M.K. Sixt, Current Biology 27 (2017) 1314–1325. date_created: 2018-12-11T11:47:51Z date_published: 2017-05-09T00:00:00Z date_updated: 2023-02-23T12:50:44Z day: '09' department: - _id: MiSi - _id: Bio - _id: NanoFab doi: 10.1016/j.cub.2017.04.004 ec_funded: 1 intvolume: ' 27' issue: '9' language: - iso: eng month: '05' oa_version: None page: 1314 - 1325 project: - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Current Biology publication_identifier: issn: - '09609822' publication_status: published publisher: Cell Press publist_id: '7050' quality_controlled: '1' scopus_import: 1 status: public title: Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6 type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 27 year: '2017' ... --- _id: '677' abstract: - lang: eng text: The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler that acts in transcription, replication, and genome stability. It is required for resistance against genotoxic agents and is involved in the repair of DNA double-strand breaks (DSBs) by homologous recombination (HR). However, the causes of the HR defect in INO80-C mutant cells are controversial. Here, we unite previous findings using a system to study HR with high spatial resolution in budding yeast. We find that INO80-C has at least two distinct functions during HR—DNA end resection and presynaptic filament formation. Importantly, the second function is linked to the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic filament formation is the crucial INO80-C function during HR. author: - first_name: Claudio full_name: Lademann, Claudio last_name: Lademann - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Boris full_name: Pfander, Boris last_name: Pfander - first_name: Stefan full_name: Jentsch, Stefan last_name: Jentsch citation: ama: Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 2017;19(7):1294-1303. doi:10.1016/j.celrep.2017.04.051 apa: Lademann, C., Renkawitz, J., Pfander, B., & Jentsch, S. (2017). The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.051 chicago: Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.051. ieee: C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination,” Cell Reports, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017. ista: Lademann C, Renkawitz J, Pfander B, Jentsch S. 2017. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 19(7), 1294–1303. mla: Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” Cell Reports, vol. 19, no. 7, Cell Press, 2017, pp. 1294–303, doi:10.1016/j.celrep.2017.04.051. short: C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017) 1294–1303. date_created: 2018-12-11T11:47:52Z date_published: 2017-05-16T00:00:00Z date_updated: 2021-01-12T08:08:57Z day: '16' ddc: - '570' department: - _id: MiSi doi: 10.1016/j.celrep.2017.04.051 file: - access_level: open_access checksum: efc7287d9c6354983cb151880e9ad72a content_type: application/pdf creator: system date_created: 2018-12-12T10:15:48Z date_updated: 2020-07-14T12:47:40Z file_id: '5171' file_name: IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf file_size: 3005610 relation: main_file file_date_updated: 2020-07-14T12:47:40Z has_accepted_license: '1' intvolume: ' 19' issue: '7' language: - iso: eng month: '05' oa: 1 oa_version: Published Version page: 1294 - 1303 publication: Cell Reports publication_identifier: issn: - '22111247' publication_status: published publisher: Cell Press publist_id: '7046' pubrep_id: '899' quality_controlled: '1' scopus_import: 1 status: public title: The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 19 year: '2017' ...