--- _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 license: https://creativecommons.org/licenses/by/4.0/ 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' ...