---
_id: '676'
abstract:
- lang: eng
  text: The segregation of different cell types into distinct tissues is a fundamental
    process in metazoan development. Differences in cell adhesion and cortex tension
    are commonly thought to drive cell sorting by regulating tissue surface tension
    (TST). However, the role that differential TST plays in cell segregation within
    the developing embryo is as yet unclear. Here, we have analyzed the role of differential
    TST for germ layer progenitor cell segregation during zebrafish gastrulation.
    Contrary to previous observations that differential TST drives germ layer progenitor
    cell segregation in vitro, we show that germ layers display indistinguishable
    TST within the gastrulating embryo, arguing against differential TST driving germ
    layer progenitor cell segregation in vivo. We further show that the osmolarity
    of the interstitial fluid (IF) is an important factor that influences germ layer
    TST in vivo, and that lower osmolarity of the IF compared with standard cell culture
    medium can explain why germ layers display differential TST in culture but not
    in vivo. Finally, we show that directed migration of mesendoderm progenitors is
    required for germ layer progenitor cell segregation and germ layer formation.
article_processing_charge: No
article_type: original
author:
- first_name: Gabriel
  full_name: Krens, Gabriel
  id: 2B819732-F248-11E8-B48F-1D18A9856A87
  last_name: Krens
  orcid: 0000-0003-4761-5996
- first_name: Jim
  full_name: Veldhuis, Jim
  last_name: Veldhuis
- first_name: Vanessa
  full_name: Barone, Vanessa
  id: 419EECCC-F248-11E8-B48F-1D18A9856A87
  last_name: Barone
  orcid: 0000-0003-2676-3367
- first_name: Daniel
  full_name: Capek, Daniel
  id: 31C42484-F248-11E8-B48F-1D18A9856A87
  last_name: Capek
  orcid: 0000-0001-5199-9940
- first_name: Jean-Léon
  full_name: Maître, Jean-Léon
  id: 48F1E0D8-F248-11E8-B48F-1D18A9856A87
  last_name: Maître
  orcid: 0000-0002-3688-1474
- first_name: Wayne
  full_name: Brodland, Wayne
  last_name: Brodland
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Krens G, Veldhuis J, Barone V, et al. Interstitial fluid osmolarity modulates
    the action of differential tissue surface tension in progenitor cell segregation
    during gastrulation. <i>Development</i>. 2017;144(10):1798-1806. doi:<a href="https://doi.org/10.1242/dev.144964">10.1242/dev.144964</a>
  apa: Krens, G., Veldhuis, J., Barone, V., Capek, D., Maître, J.-L., Brodland, W.,
    &#38; Heisenberg, C.-P. J. (2017). Interstitial fluid osmolarity modulates the
    action of differential tissue surface tension in progenitor cell segregation during
    gastrulation. <i>Development</i>. Company of Biologists. <a href="https://doi.org/10.1242/dev.144964">https://doi.org/10.1242/dev.144964</a>
  chicago: Krens, Gabriel, Jim Veldhuis, Vanessa Barone, Daniel Capek, Jean-Léon Maître,
    Wayne Brodland, and Carl-Philipp J Heisenberg. “Interstitial Fluid Osmolarity
    Modulates the Action of Differential Tissue Surface Tension in Progenitor Cell
    Segregation during Gastrulation.” <i>Development</i>. Company of Biologists, 2017.
    <a href="https://doi.org/10.1242/dev.144964">https://doi.org/10.1242/dev.144964</a>.
  ieee: G. Krens <i>et al.</i>, “Interstitial fluid osmolarity modulates the action
    of differential tissue surface tension in progenitor cell segregation during gastrulation,”
    <i>Development</i>, vol. 144, no. 10. Company of Biologists, pp. 1798–1806, 2017.
  ista: Krens G, Veldhuis J, Barone V, Capek D, Maître J-L, Brodland W, Heisenberg
    C-PJ. 2017. Interstitial fluid osmolarity modulates the action of differential
    tissue surface tension in progenitor cell segregation during gastrulation. Development.
    144(10), 1798–1806.
  mla: Krens, Gabriel, et al. “Interstitial Fluid Osmolarity Modulates the Action
    of Differential Tissue Surface Tension in Progenitor Cell Segregation during Gastrulation.”
    <i>Development</i>, vol. 144, no. 10, Company of Biologists, 2017, pp. 1798–806,
    doi:<a href="https://doi.org/10.1242/dev.144964">10.1242/dev.144964</a>.
  short: G. Krens, J. Veldhuis, V. Barone, D. Capek, J.-L. Maître, W. Brodland, C.-P.J.
    Heisenberg, Development 144 (2017) 1798–1806.
date_created: 2018-12-11T11:47:52Z
date_published: 2017-05-15T00:00:00Z
date_updated: 2024-03-25T23:30:13Z
day: '15'
ddc:
- '570'
department:
- _id: Bio
- _id: CaHe
doi: 10.1242/dev.144964
external_id:
  pmid:
  - '28512197'
file:
- access_level: open_access
  checksum: bc25125fb664706cdf180e061429f91d
  content_type: application/pdf
  creator: dernst
  date_created: 2019-09-24T06:56:22Z
  date_updated: 2020-07-14T12:47:39Z
  file_id: '6905'
  file_name: 2017_Development_Krens.pdf
  file_size: 8194516
  relation: main_file
file_date_updated: 2020-07-14T12:47:39Z
has_accepted_license: '1'
intvolume: '       144'
issue: '10'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 1798 - 1806
pmid: 1
publication: Development
publication_identifier:
  issn:
  - '09501991'
publication_status: published
publisher: Company of Biologists
publist_id: '7047'
quality_controlled: '1'
related_material:
  record:
  - id: '961'
    relation: dissertation_contains
    status: public
  - id: '50'
    relation: dissertation_contains
    status: public
scopus_import: 1
status: public
title: Interstitial fluid osmolarity modulates the action of differential tissue surface
  tension in progenitor cell segregation during gastrulation
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: 144
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. <i>Cell
    Reports</i>. 2017;19(7):1294-1303. doi:<a href="https://doi.org/10.1016/j.celrep.2017.04.051">10.1016/j.celrep.2017.04.051</a>
  apa: Lademann, C., Renkawitz, J., Pfander, B., &#38; Jentsch, S. (2017). The INO80
    complex removes H2A.Z to promote presynaptic filament formation during homologous
    recombination. <i>Cell Reports</i>. Cell Press. <a href="https://doi.org/10.1016/j.celrep.2017.04.051">https://doi.org/10.1016/j.celrep.2017.04.051</a>
  chicago: Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The
    INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous
    Recombination.” <i>Cell Reports</i>. Cell Press, 2017. <a href="https://doi.org/10.1016/j.celrep.2017.04.051">https://doi.org/10.1016/j.celrep.2017.04.051</a>.
  ieee: C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex
    removes H2A.Z to promote presynaptic filament formation during homologous recombination,”
    <i>Cell Reports</i>, 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.” <i>Cell Reports</i>, vol.
    19, no. 7, Cell Press, 2017, pp. 1294–303, doi:<a href="https://doi.org/10.1016/j.celrep.2017.04.051">10.1016/j.celrep.2017.04.051</a>.
  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'
...
---
_id: '678'
abstract:
- lang: eng
  text: The seminal observation that mechanical signals can elicit changes in biochemical
    signalling within cells, a process commonly termed mechanosensation and mechanotransduction,
    has revolutionized our understanding of the role of cell mechanics in various
    fundamental biological processes, such as cell motility, adhesion, proliferation
    and differentiation. In this Review, we will discuss how the interplay and feedback
    between mechanical and biochemical signals control tissue morphogenesis and cell
    fate specification in embryonic development.
author:
- first_name: Nicoletta
  full_name: Petridou, Nicoletta
  id: 2A003F6C-F248-11E8-B48F-1D18A9856A87
  last_name: Petridou
  orcid: 0000-0002-8451-1195
- first_name: Zoltan P
  full_name: Spiro, Zoltan P
  id: 426AD026-F248-11E8-B48F-1D18A9856A87
  last_name: Spiro
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Petridou N, Spiro ZP, Heisenberg C-PJ. Multiscale force sensing in development.
    <i>Nature Cell Biology</i>. 2017;19(6):581-588. doi:<a href="https://doi.org/10.1038/ncb3524">10.1038/ncb3524</a>
  apa: Petridou, N., Spiro, Z. P., &#38; Heisenberg, C.-P. J. (2017). Multiscale force
    sensing in development. <i>Nature Cell Biology</i>. Nature Publishing Group. <a
    href="https://doi.org/10.1038/ncb3524">https://doi.org/10.1038/ncb3524</a>
  chicago: Petridou, Nicoletta, Zoltan P Spiro, and Carl-Philipp J Heisenberg. “Multiscale
    Force Sensing in Development.” <i>Nature Cell Biology</i>. Nature Publishing Group,
    2017. <a href="https://doi.org/10.1038/ncb3524">https://doi.org/10.1038/ncb3524</a>.
  ieee: N. Petridou, Z. P. Spiro, and C.-P. J. Heisenberg, “Multiscale force sensing
    in development,” <i>Nature Cell Biology</i>, vol. 19, no. 6. Nature Publishing
    Group, pp. 581–588, 2017.
  ista: Petridou N, Spiro ZP, Heisenberg C-PJ. 2017. Multiscale force sensing in development.
    Nature Cell Biology. 19(6), 581–588.
  mla: Petridou, Nicoletta, et al. “Multiscale Force Sensing in Development.” <i>Nature
    Cell Biology</i>, vol. 19, no. 6, Nature Publishing Group, 2017, pp. 581–88, doi:<a
    href="https://doi.org/10.1038/ncb3524">10.1038/ncb3524</a>.
  short: N. Petridou, Z.P. Spiro, C.-P.J. Heisenberg, Nature Cell Biology 19 (2017)
    581–588.
date_created: 2018-12-11T11:47:53Z
date_published: 2017-05-31T00:00:00Z
date_updated: 2021-01-12T08:08:59Z
day: '31'
department:
- _id: CaHe
doi: 10.1038/ncb3524
intvolume: '        19'
issue: '6'
language:
- iso: eng
month: '05'
oa_version: None
page: 581 - 588
project:
- _id: 25236028-B435-11E9-9278-68D0E5697425
  grant_number: ALTF534-2016
  name: The generation and function of anisotropic tissue tension in zebrafish epiboly
    (EMBO Fellowship)
publication: Nature Cell Biology
publication_identifier:
  issn:
  - '14657392'
publication_status: published
publisher: Nature Publishing Group
publist_id: '7040'
quality_controlled: '1'
scopus_import: 1
status: public
title: Multiscale force sensing in development
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2017'
...
---
_id: '679'
abstract:
- lang: eng
  text: Protective responses against pathogens require a rapid mobilization of resting
    neutrophils and the timely removal of activated ones. Neutrophils are exceptionally
    short-lived leukocytes, yet it remains unclear whether the lifespan of pathogen-engaged
    neutrophils is regulated differently from that in the circulating steady-state
    pool. Here, we have found that under homeostatic conditions, the mRNA-destabilizing
    protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated
    infiltrating murine neutrophils but not neutrophil cellularity. Activated TTP-deficient
    neutrophils exhibited decreased apoptosis and enhanced accumulation at the infection
    site. In the context of myeloid-specific deletion of Ttp, the potentiation of
    neutrophil deployment protected mice against lethal soft tissue infection with
    Streptococcus pyogenes and prevented bacterial dissemination. Neutrophil transcriptome
    analysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically
    associated with elevated expression of myeloid cell leukemia 1 (Mcl1) but not
    other antiapoptotic B cell leukemia/ lymphoma 2 (Bcl2) family members. Higher
    Mcl1 expression resulted from stabilization of Mcl1 mRNA in the absence of TTP.
    The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable
    to that of transgenic Mcl1-overexpressing neutrophils. Our study demonstrates
    that posttranscriptional gene regulation by TTP schedules the termination of the
    antimicrobial engagement of neutrophils. The balancing role of TTP comes at the
    cost of an increased risk of bacterial infections.
acknowledgement: This work was supported by grants from the Austrian Science Fund
  (FWF) (P27538-B21, I1621-B22, and SFB 43, to PK); by funding from the European Union
  Seventh Framework Programme Marie Curie Initial Training Networks (FP7-PEOPLE-2012-ITN)
  for the project INBIONET (INfection BIOlogy Training NETwork under grant agreement
  PITN-GA-2012-316682; and by a joint research cluster initiative of the University
  of Vienna and the Medical University of Vienna.
author:
- first_name: Florian
  full_name: Ebner, Florian
  last_name: Ebner
- first_name: Vitaly
  full_name: Sedlyarov, Vitaly
  last_name: Sedlyarov
- first_name: Saren
  full_name: Tasciyan, Saren
  id: 4323B49C-F248-11E8-B48F-1D18A9856A87
  last_name: Tasciyan
  orcid: 0000-0003-1671-393X
- first_name: Masa
  full_name: Ivin, Masa
  last_name: Ivin
- first_name: Franz
  full_name: Kratochvill, Franz
  last_name: Kratochvill
- first_name: Nina
  full_name: Gratz, Nina
  last_name: Gratz
- first_name: Lukas
  full_name: Kenner, Lukas
  last_name: Kenner
- first_name: Andreas
  full_name: Villunger, Andreas
  last_name: Villunger
- 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: Pavel
  full_name: Kovarik, Pavel
  last_name: Kovarik
citation:
  ama: Ebner F, Sedlyarov V, Tasciyan S, et al. The RNA-binding protein tristetraprolin
    schedules apoptosis of pathogen-engaged neutrophils during bacterial infection.
    <i>The Journal of Clinical Investigation</i>. 2017;127(6):2051-2065. doi:<a href="https://doi.org/10.1172/JCI80631">10.1172/JCI80631</a>
  apa: Ebner, F., Sedlyarov, V., Tasciyan, S., Ivin, M., Kratochvill, F., Gratz, N.,
    … Kovarik, P. (2017). The RNA-binding protein tristetraprolin schedules apoptosis
    of pathogen-engaged neutrophils during bacterial infection. <i>The Journal of
    Clinical Investigation</i>. American Society for Clinical Investigation. <a href="https://doi.org/10.1172/JCI80631">https://doi.org/10.1172/JCI80631</a>
  chicago: Ebner, Florian, Vitaly Sedlyarov, Saren Tasciyan, Masa Ivin, Franz Kratochvill,
    Nina Gratz, Lukas Kenner, Andreas Villunger, Michael K Sixt, and Pavel Kovarik.
    “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged
    Neutrophils during Bacterial Infection.” <i>The Journal of Clinical Investigation</i>.
    American Society for Clinical Investigation, 2017. <a href="https://doi.org/10.1172/JCI80631">https://doi.org/10.1172/JCI80631</a>.
  ieee: F. Ebner <i>et al.</i>, “The RNA-binding protein tristetraprolin schedules
    apoptosis of pathogen-engaged neutrophils during bacterial infection,” <i>The
    Journal of Clinical Investigation</i>, vol. 127, no. 6. American Society for Clinical
    Investigation, pp. 2051–2065, 2017.
  ista: Ebner F, Sedlyarov V, Tasciyan S, Ivin M, Kratochvill F, Gratz N, Kenner L,
    Villunger A, Sixt MK, Kovarik P. 2017. The RNA-binding protein tristetraprolin
    schedules apoptosis of pathogen-engaged neutrophils during bacterial infection.
    The Journal of Clinical Investigation. 127(6), 2051–2065.
  mla: Ebner, Florian, et al. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis
    of Pathogen-Engaged Neutrophils during Bacterial Infection.” <i>The Journal of
    Clinical Investigation</i>, vol. 127, no. 6, American Society for Clinical Investigation,
    2017, pp. 2051–65, doi:<a href="https://doi.org/10.1172/JCI80631">10.1172/JCI80631</a>.
  short: F. Ebner, V. Sedlyarov, S. Tasciyan, M. Ivin, F. Kratochvill, N. Gratz, L.
    Kenner, A. Villunger, M.K. Sixt, P. Kovarik, The Journal of Clinical Investigation
    127 (2017) 2051–2065.
date_created: 2018-12-11T11:47:53Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2024-03-25T23:30:12Z
day: '01'
department:
- _id: MiSi
doi: 10.1172/JCI80631
external_id:
  pmid:
  - '28504646'
intvolume: '       127'
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451238/
month: '06'
oa: 1
oa_version: Submitted Version
page: 2051 - 2065
pmid: 1
project:
- _id: 25985A36-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: T00817-B21
  name: The biochemical basis of PAR polarization
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P27201-B22
  name: Revealing the mechanisms underlying drug interactions
publication: The Journal of Clinical Investigation
publication_identifier:
  issn:
  - '00219738'
publication_status: published
publisher: American Society for Clinical Investigation
publist_id: '7038'
quality_controlled: '1'
related_material:
  record:
  - id: '12401'
    relation: dissertation_contains
    status: public
scopus_import: 1
status: public
title: The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged
  neutrophils during bacterial infection
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 127
year: '2017'
...
---
_id: '680'
abstract:
- lang: eng
  text: In order to respond reliably to specific features of their environment, sensory
    neurons need to integrate multiple incoming noisy signals. Crucially, they also
    need to compete for the interpretation of those signals with other neurons representing
    similar features. The form that this competition should take depends critically
    on the noise corrupting these signals. In this study we show that for the type
    of noise commonly observed in sensory systems, whose variance scales with the
    mean signal, sensory neurons should selectively divide their input signals by
    their predictions, suppressing ambiguous cues while amplifying others. Any change
    in the stimulus context alters which inputs are suppressed, leading to a deep
    dynamic reshaping of neural receptive fields going far beyond simple surround
    suppression. Paradoxically, these highly variable receptive fields go alongside
    and are in fact required for an invariant representation of external sensory features.
    In addition to offering a normative account of context-dependent changes in sensory
    responses, perceptual inference in the presence of signal-dependent noise accounts
    for ubiquitous features of sensory neurons such as divisive normalization, gain
    control and contrast dependent temporal dynamics.
article_number: e1005582
author:
- first_name: Matthew J
  full_name: Chalk, Matthew J
  id: 2BAAC544-F248-11E8-B48F-1D18A9856A87
  last_name: Chalk
  orcid: 0000-0001-7782-4436
- first_name: Paul
  full_name: Masset, Paul
  last_name: Masset
- first_name: Boris
  full_name: Gutkin, Boris
  last_name: Gutkin
- first_name: Sophie
  full_name: Denève, Sophie
  last_name: Denève
citation:
  ama: Chalk MJ, Masset P, Gutkin B, Denève S. Sensory noise predicts divisive reshaping
    of receptive fields. <i>PLoS Computational Biology</i>. 2017;13(6). doi:<a href="https://doi.org/10.1371/journal.pcbi.1005582">10.1371/journal.pcbi.1005582</a>
  apa: Chalk, M. J., Masset, P., Gutkin, B., &#38; Denève, S. (2017). Sensory noise
    predicts divisive reshaping of receptive fields. <i>PLoS Computational Biology</i>.
    Public Library of Science. <a href="https://doi.org/10.1371/journal.pcbi.1005582">https://doi.org/10.1371/journal.pcbi.1005582</a>
  chicago: Chalk, Matthew J, Paul Masset, Boris Gutkin, and Sophie Denève. “Sensory
    Noise Predicts Divisive Reshaping of Receptive Fields.” <i>PLoS Computational
    Biology</i>. Public Library of Science, 2017. <a href="https://doi.org/10.1371/journal.pcbi.1005582">https://doi.org/10.1371/journal.pcbi.1005582</a>.
  ieee: M. J. Chalk, P. Masset, B. Gutkin, and S. Denève, “Sensory noise predicts
    divisive reshaping of receptive fields,” <i>PLoS Computational Biology</i>, vol.
    13, no. 6. Public Library of Science, 2017.
  ista: Chalk MJ, Masset P, Gutkin B, Denève S. 2017. Sensory noise predicts divisive
    reshaping of receptive fields. PLoS Computational Biology. 13(6), e1005582.
  mla: Chalk, Matthew J., et al. “Sensory Noise Predicts Divisive Reshaping of Receptive
    Fields.” <i>PLoS Computational Biology</i>, vol. 13, no. 6, e1005582, Public Library
    of Science, 2017, doi:<a href="https://doi.org/10.1371/journal.pcbi.1005582">10.1371/journal.pcbi.1005582</a>.
  short: M.J. Chalk, P. Masset, B. Gutkin, S. Denève, PLoS Computational Biology 13
    (2017).
date_created: 2018-12-11T11:47:53Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2023-02-23T14:10:54Z
day: '01'
ddc:
- '571'
department:
- _id: GaTk
doi: 10.1371/journal.pcbi.1005582
file:
- access_level: open_access
  checksum: 796a1026076af6f4405a47d985bc7b68
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:07:47Z
  date_updated: 2020-07-14T12:47:40Z
  file_id: '4645'
  file_name: IST-2017-898-v1+1_journal.pcbi.1005582.pdf
  file_size: 14555676
  relation: main_file
file_date_updated: 2020-07-14T12:47:40Z
has_accepted_license: '1'
intvolume: '        13'
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: PLoS Computational Biology
publication_identifier:
  issn:
  - 1553734X
publication_status: published
publisher: Public Library of Science
publist_id: '7035'
pubrep_id: '898'
quality_controlled: '1'
related_material:
  record:
  - id: '9855'
    relation: research_data
    status: public
scopus_import: 1
status: public
title: Sensory noise predicts divisive reshaping of receptive fields
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: 13
year: '2017'
...
---
_id: '681'
abstract:
- lang: eng
  text: Two-player games on graphs provide the theoretical framework for many important
    problems such as reactive synthesis. While the traditional study of two-player
    zero-sum games has been extended to multi-player games with several notions of
    equilibria, they are decidable only for perfect-information games, whereas several
    applications require imperfect-information. In this paper we propose a new notion
    of equilibria, called doomsday equilibria, which is a strategy profile where all
    players satisfy their own objective, and if any coalition of players deviates
    and violates even one of the players' objective, then the objective of every player
    is violated. We present algorithms and complexity results for deciding the existence
    of doomsday equilibria for various classes of ω-regular objectives, both for imperfect-information
    games, and for perfect-information games. We provide optimal complexity bounds
    for imperfect-information games, and in most cases for perfect-information games.
article_processing_charge: No
article_type: original
arxiv: 1
author:
- first_name: Krishnendu
  full_name: Chatterjee, Krishnendu
  id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87
  last_name: Chatterjee
  orcid: 0000-0002-4561-241X
- first_name: Laurent
  full_name: Doyen, Laurent
  last_name: Doyen
- first_name: Emmanuel
  full_name: Filiot, Emmanuel
  last_name: Filiot
- first_name: Jean
  full_name: Raskin, Jean
  last_name: Raskin
citation:
  ama: Chatterjee K, Doyen L, Filiot E, Raskin J. Doomsday equilibria for omega-regular
    games. <i>Information and Computation</i>. 2017;254:296-315. doi:<a href="https://doi.org/10.1016/j.ic.2016.10.012">10.1016/j.ic.2016.10.012</a>
  apa: Chatterjee, K., Doyen, L., Filiot, E., &#38; Raskin, J. (2017). Doomsday equilibria
    for omega-regular games. <i>Information and Computation</i>. Elsevier. <a href="https://doi.org/10.1016/j.ic.2016.10.012">https://doi.org/10.1016/j.ic.2016.10.012</a>
  chicago: Chatterjee, Krishnendu, Laurent Doyen, Emmanuel Filiot, and Jean Raskin.
    “Doomsday Equilibria for Omega-Regular Games.” <i>Information and Computation</i>.
    Elsevier, 2017. <a href="https://doi.org/10.1016/j.ic.2016.10.012">https://doi.org/10.1016/j.ic.2016.10.012</a>.
  ieee: K. Chatterjee, L. Doyen, E. Filiot, and J. Raskin, “Doomsday equilibria for
    omega-regular games,” <i>Information and Computation</i>, vol. 254. Elsevier,
    pp. 296–315, 2017.
  ista: Chatterjee K, Doyen L, Filiot E, Raskin J. 2017. Doomsday equilibria for omega-regular
    games. Information and Computation. 254, 296–315.
  mla: Chatterjee, Krishnendu, et al. “Doomsday Equilibria for Omega-Regular Games.”
    <i>Information and Computation</i>, vol. 254, Elsevier, 2017, pp. 296–315, doi:<a
    href="https://doi.org/10.1016/j.ic.2016.10.012">10.1016/j.ic.2016.10.012</a>.
  short: K. Chatterjee, L. Doyen, E. Filiot, J. Raskin, Information and Computation
    254 (2017) 296–315.
date_created: 2018-12-11T11:47:53Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2023-02-21T16:06:02Z
day: '01'
department:
- _id: KrCh
doi: 10.1016/j.ic.2016.10.012
ec_funded: 1
external_id:
  arxiv:
  - '1311.3238'
intvolume: '       254'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1311.3238
month: '06'
oa: 1
oa_version: Submitted Version
page: 296 - 315
project:
- _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
- _id: 2581B60A-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '279307'
  name: 'Quantitative Graph Games: Theory and Applications'
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
publication: Information and Computation
publication_identifier:
  issn:
  - '08905401'
publication_status: published
publisher: Elsevier
publist_id: '7036'
quality_controlled: '1'
related_material:
  record:
  - id: '10885'
    relation: earlier_version
    status: public
scopus_import: '1'
status: public
title: Doomsday equilibria for omega-regular games
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 254
year: '2017'
...
---
_id: '682'
abstract:
- lang: eng
  text: Left-right asymmetry is a fundamental feature of higher-order brain structure;
    however, the molecular basis of brain asymmetry remains unclear. We recently identified
    structural and functional asymmetries in mouse hippocampal circuitry that result
    from the asymmetrical distribution of two distinct populations of pyramidal cell
    synapses that differ in the density of the NMDA receptor subunit GluRε2 (also
    known as NR2B, GRIN2B or GluN2B). By examining the synaptic distribution of ε2
    subunits, we previously found that β2-microglobulin-deficient mice, which lack
    cell surface expression of the vast majority of major histocompatibility complex
    class I (MHCI) proteins, do not exhibit circuit asymmetry. In the present study,
    we conducted electrophysiological and anatomical analyses on the hippocampal circuitry
    of mice with a knockout of the paired immunoglobulin-like receptor B (PirB), an
    MHCI receptor. As in β2-microglobulin-deficient mice, the PirB-deficient hippocampus
    lacked circuit asymmetries. This finding that MHCI loss-of-function mice and PirB
    knockout mice have identical phenotypes suggests that MHCI signals that produce
    hippocampal asymmetries are transduced through PirB. Our results provide evidence
    for a critical role of the MHCI/PirB signaling system in the generation of asymmetries
    in hippocampal circuitry.
article_number: e0179377
article_type: original
author:
- first_name: Hikari
  full_name: Ukai, Hikari
  last_name: Ukai
- first_name: Aiko
  full_name: Kawahara, Aiko
  last_name: Kawahara
- first_name: Keiko
  full_name: Hirayama, Keiko
  last_name: Hirayama
- first_name: Matthew J
  full_name: Case, Matthew J
  id: 44B7CA5A-F248-11E8-B48F-1D18A9856A87
  last_name: Case
- first_name: Shotaro
  full_name: Aino, Shotaro
  last_name: Aino
- first_name: Masahiro
  full_name: Miyabe, Masahiro
  last_name: Miyabe
- first_name: Ken
  full_name: Wakita, Ken
  last_name: Wakita
- first_name: Ryohei
  full_name: Oogi, Ryohei
  last_name: Oogi
- first_name: Michiyo
  full_name: Kasayuki, Michiyo
  last_name: Kasayuki
- first_name: Shihomi
  full_name: Kawashima, Shihomi
  last_name: Kawashima
- first_name: Shunichi
  full_name: Sugimoto, Shunichi
  last_name: Sugimoto
- first_name: Kanako
  full_name: Chikamatsu, Kanako
  last_name: Chikamatsu
- first_name: Noritaka
  full_name: Nitta, Noritaka
  last_name: Nitta
- first_name: Tsuneyuki
  full_name: Koga, Tsuneyuki
  last_name: Koga
- first_name: Ryuichi
  full_name: Shigemoto, Ryuichi
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Toshiyuki
  full_name: Takai, Toshiyuki
  last_name: Takai
- first_name: Isao
  full_name: Ito, Isao
  last_name: Ito
citation:
  ama: Ukai H, Kawahara A, Hirayama K, et al. PirB regulates asymmetries in hippocampal
    circuitry. <i>PLoS One</i>. 2017;12(6). doi:<a href="https://doi.org/10.1371/journal.pone.0179377">10.1371/journal.pone.0179377</a>
  apa: Ukai, H., Kawahara, A., Hirayama, K., Case, M. J., Aino, S., Miyabe, M., …
    Ito, I. (2017). PirB regulates asymmetries in hippocampal circuitry. <i>PLoS One</i>.
    Public Library of Science. <a href="https://doi.org/10.1371/journal.pone.0179377">https://doi.org/10.1371/journal.pone.0179377</a>
  chicago: Ukai, Hikari, Aiko Kawahara, Keiko Hirayama, Matthew J Case, Shotaro Aino,
    Masahiro Miyabe, Ken Wakita, et al. “PirB Regulates Asymmetries in Hippocampal
    Circuitry.” <i>PLoS One</i>. Public Library of Science, 2017. <a href="https://doi.org/10.1371/journal.pone.0179377">https://doi.org/10.1371/journal.pone.0179377</a>.
  ieee: H. Ukai <i>et al.</i>, “PirB regulates asymmetries in hippocampal circuitry,”
    <i>PLoS One</i>, vol. 12, no. 6. Public Library of Science, 2017.
  ista: Ukai H, Kawahara A, Hirayama K, Case MJ, Aino S, Miyabe M, Wakita K, Oogi
    R, Kasayuki M, Kawashima S, Sugimoto S, Chikamatsu K, Nitta N, Koga T, Shigemoto
    R, Takai T, Ito I. 2017. PirB regulates asymmetries in hippocampal circuitry.
    PLoS One. 12(6), e0179377.
  mla: Ukai, Hikari, et al. “PirB Regulates Asymmetries in Hippocampal Circuitry.”
    <i>PLoS One</i>, vol. 12, no. 6, e0179377, Public Library of Science, 2017, doi:<a
    href="https://doi.org/10.1371/journal.pone.0179377">10.1371/journal.pone.0179377</a>.
  short: H. Ukai, A. Kawahara, K. Hirayama, M.J. Case, S. Aino, M. Miyabe, K. Wakita,
    R. Oogi, M. Kasayuki, S. Kawashima, S. Sugimoto, K. Chikamatsu, N. Nitta, T. Koga,
    R. Shigemoto, T. Takai, I. Ito, PLoS One 12 (2017).
date_created: 2018-12-11T11:47:54Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2024-03-25T23:30:07Z
day: '01'
ddc:
- '571'
department:
- _id: RySh
doi: 10.1371/journal.pone.0179377
file:
- access_level: open_access
  checksum: 24dd19c46fb1c761b0bcbbcd1025a3a8
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:12:16Z
  date_updated: 2020-07-14T12:47:40Z
  file_id: '4934'
  file_name: IST-2017-897-v1+1_journal.pone.0179377.pdf
  file_size: 5798454
  relation: main_file
file_date_updated: 2020-07-14T12:47:40Z
has_accepted_license: '1'
intvolume: '        12'
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_identifier:
  issn:
  - '19326203'
publication_status: published
publisher: Public Library of Science
publist_id: '7034'
pubrep_id: '897'
quality_controlled: '1'
related_material:
  record:
  - id: '51'
    relation: dissertation_contains
    status: public
scopus_import: 1
status: public
title: PirB regulates asymmetries in hippocampal circuitry
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: 12
year: '2017'
...
---
_id: '683'
abstract:
- lang: eng
  text: 'Given a triangulation of a point set in the plane, a flip deletes an edge
    e whose removal leaves a convex quadrilateral, and replaces e by the opposite
    diagonal of the quadrilateral. It is well known that any triangulation of a point
    set can be reconfigured to any other triangulation by some sequence of flips.
    We explore this question in the setting where each edge of a triangulation has
    a label, and a flip transfers the label of the removed edge to the new edge. It
    is not true that every labelled triangulation of a point set can be reconfigured
    to every other labelled triangulation via a sequence of flips, but we characterize
    when this is possible. There is an obvious necessary condition: for each label
    l, if edge e has label l in the first triangulation and edge f has label l in
    the second triangulation, then there must be some sequence of flips that moves
    label l from e to f, ignoring all other labels. Bose, Lubiw, Pathak and Verdonschot
    formulated the Orbit Conjecture, which states that this necessary condition is
    also sufficient, i.e. that all labels can be simultaneously mapped to their destination
    if and only if each label individually can be mapped to its destination. We prove
    this conjecture. Furthermore, we give a polynomial-time algorithm to find a sequence
    of flips to reconfigure one labelled triangulation to another, if such a sequence
    exists, and we prove an upper bound of O(n7) on the length of the flip sequence.
    Our proof uses the topological result that the sets of pairwise non-crossing edges
    on a planar point set form a simplicial complex that is homeomorphic to a high-dimensional
    ball (this follows from a result of Orden and Santos; we give a different proof
    based on a shelling argument). The dual cell complex of this simplicial ball,
    called the flip complex, has the usual flip graph as its 1-skeleton. We use properties
    of the 2-skeleton of the flip complex to prove the Orbit Conjecture.'
alternative_title:
- LIPIcs
article_number: '49'
author:
- first_name: Anna
  full_name: Lubiw, Anna
  last_name: Lubiw
- first_name: Zuzana
  full_name: Masárová, Zuzana
  id: 45CFE238-F248-11E8-B48F-1D18A9856A87
  last_name: Masárová
  orcid: 0000-0002-6660-1322
- first_name: Uli
  full_name: Wagner, Uli
  id: 36690CA2-F248-11E8-B48F-1D18A9856A87
  last_name: Wagner
  orcid: 0000-0002-1494-0568
citation:
  ama: 'Lubiw A, Masárová Z, Wagner U. A proof of the orbit conjecture for flipping
    edge labelled triangulations. In: Vol 77. Schloss Dagstuhl - Leibniz-Zentrum für
    Informatik; 2017. doi:<a href="https://doi.org/10.4230/LIPIcs.SoCG.2017.49">10.4230/LIPIcs.SoCG.2017.49</a>'
  apa: 'Lubiw, A., Masárová, Z., &#38; Wagner, U. (2017). A proof of the orbit conjecture
    for flipping edge labelled triangulations (Vol. 77). Presented at the SoCG: Symposium
    on Computational Geometry, Brisbane, Australia: Schloss Dagstuhl - Leibniz-Zentrum
    für Informatik. <a href="https://doi.org/10.4230/LIPIcs.SoCG.2017.49">https://doi.org/10.4230/LIPIcs.SoCG.2017.49</a>'
  chicago: Lubiw, Anna, Zuzana Masárová, and Uli Wagner. “A Proof of the Orbit Conjecture
    for Flipping Edge Labelled Triangulations,” Vol. 77. Schloss Dagstuhl - Leibniz-Zentrum
    für Informatik, 2017. <a href="https://doi.org/10.4230/LIPIcs.SoCG.2017.49">https://doi.org/10.4230/LIPIcs.SoCG.2017.49</a>.
  ieee: 'A. Lubiw, Z. Masárová, and U. Wagner, “A proof of the orbit conjecture for
    flipping edge labelled triangulations,” presented at the SoCG: Symposium on Computational
    Geometry, Brisbane, Australia, 2017, vol. 77.'
  ista: 'Lubiw A, Masárová Z, Wagner U. 2017. A proof of the orbit conjecture for
    flipping edge labelled triangulations. SoCG: Symposium on Computational Geometry,
    LIPIcs, vol. 77, 49.'
  mla: Lubiw, Anna, et al. <i>A Proof of the Orbit Conjecture for Flipping Edge Labelled
    Triangulations</i>. Vol. 77, 49, Schloss Dagstuhl - Leibniz-Zentrum für Informatik,
    2017, doi:<a href="https://doi.org/10.4230/LIPIcs.SoCG.2017.49">10.4230/LIPIcs.SoCG.2017.49</a>.
  short: A. Lubiw, Z. Masárová, U. Wagner, in:, Schloss Dagstuhl - Leibniz-Zentrum
    für Informatik, 2017.
conference:
  end_date: 2017-07-07
  location: Brisbane, Australia
  name: 'SoCG: Symposium on Computational Geometry'
  start_date: 2017-07-04
date_created: 2018-12-11T11:47:54Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2023-09-05T15:01:43Z
day: '01'
ddc:
- '514'
- '516'
department:
- _id: UlWa
doi: 10.4230/LIPIcs.SoCG.2017.49
file:
- access_level: open_access
  checksum: 24fdde981cc513352a78dcf9b0660ae9
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:17:12Z
  date_updated: 2020-07-14T12:47:41Z
  file_id: '5265'
  file_name: IST-2017-896-v1+1_LIPIcs-SoCG-2017-49.pdf
  file_size: 710007
  relation: main_file
file_date_updated: 2020-07-14T12:47:41Z
has_accepted_license: '1'
intvolume: '        77'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication_status: published
publisher: Schloss Dagstuhl - Leibniz-Zentrum für Informatik
publist_id: '7033'
pubrep_id: '896'
quality_controlled: '1'
related_material:
  record:
  - id: '5986'
    relation: later_version
    status: public
scopus_import: 1
status: public
title: A proof of the orbit conjecture for flipping edge labelled triangulations
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: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 77
year: '2017'
...
---
_id: '684'
abstract:
- lang: eng
  text: We generalize winning conditions in two-player games by adding a structural
    acceptance condition called obligations. Obligations are orthogonal to the linear
    winning conditions that define whether a play is winning. Obligations are a declaration
    that player 0 can achieve a certain value from a configuration. If the obligation
    is met, the value of that configuration for player 0 is 1. We define the value
    in such games and show that obligation games are determined. For Markov chains
    with Borel objectives and obligations, and finite turn-based stochastic parity
    games with obligations we give an alternative and simpler characterization of
    the value function. Based on this simpler definition we show that the decision
    problem of winning finite turn-based stochastic parity games with obligations
    is in NP∩co-NP. We also show that obligation games provide a game framework for
    reasoning about p-automata. © 2017 The Association for Symbolic Logic.
article_processing_charge: No
author:
- first_name: Krishnendu
  full_name: Chatterjee, Krishnendu
  id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87
  last_name: Chatterjee
  orcid: 0000-0002-4561-241X
- first_name: Nir
  full_name: Piterman, Nir
  last_name: Piterman
citation:
  ama: Chatterjee K, Piterman N. Obligation blackwell games and p-automata. <i>Journal
    of Symbolic Logic</i>. 2017;82(2):420-452. doi:<a href="https://doi.org/10.1017/jsl.2016.71">10.1017/jsl.2016.71</a>
  apa: Chatterjee, K., &#38; Piterman, N. (2017). Obligation blackwell games and p-automata.
    <i>Journal of Symbolic Logic</i>. Cambridge University Press. <a href="https://doi.org/10.1017/jsl.2016.71">https://doi.org/10.1017/jsl.2016.71</a>
  chicago: Chatterjee, Krishnendu, and Nir Piterman. “Obligation Blackwell Games and
    P-Automata.” <i>Journal of Symbolic Logic</i>. Cambridge University Press, 2017.
    <a href="https://doi.org/10.1017/jsl.2016.71">https://doi.org/10.1017/jsl.2016.71</a>.
  ieee: K. Chatterjee and N. Piterman, “Obligation blackwell games and p-automata,”
    <i>Journal of Symbolic Logic</i>, vol. 82, no. 2. Cambridge University Press,
    pp. 420–452, 2017.
  ista: Chatterjee K, Piterman N. 2017. Obligation blackwell games and p-automata.
    Journal of Symbolic Logic. 82(2), 420–452.
  mla: Chatterjee, Krishnendu, and Nir Piterman. “Obligation Blackwell Games and P-Automata.”
    <i>Journal of Symbolic Logic</i>, vol. 82, no. 2, Cambridge University Press,
    2017, pp. 420–52, doi:<a href="https://doi.org/10.1017/jsl.2016.71">10.1017/jsl.2016.71</a>.
  short: K. Chatterjee, N. Piterman, Journal of Symbolic Logic 82 (2017) 420–452.
date_created: 2018-12-11T11:47:54Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2021-04-16T12:10:53Z
day: '01'
department:
- _id: KrCh
doi: 10.1017/jsl.2016.71
intvolume: '        82'
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1206.5174
month: '06'
oa: 1
oa_version: Submitted Version
page: 420 - 452
publication: Journal of Symbolic Logic
publication_identifier:
  eissn:
  - 1943-5886
  issn:
  - 0022-4812
publication_status: published
publisher: Cambridge University Press
publist_id: '7026'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Obligation blackwell games and p-automata
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 82
year: '2017'
...
---
_id: '6841'
abstract:
- lang: eng
  text: In classical machine learning, regression is treated as a black box process
    of identifying a suitable function from a hypothesis set without attempting to
    gain insight into the mechanism connecting inputs and outputs. In the natural
    sciences, however, finding an interpretable function for a phenomenon is the prime
    goal as it allows to understand and generalize results. This paper proposes a
    novel type of function learning network, called equation learner (EQL), that can
    learn analytical expressions and is able to extrapolate to unseen domains. It
    is implemented as an end-to-end differentiable feed-forward network and allows
    for efficient gradient based training. Due to sparsity regularization concise
    interpretable expressions can be obtained. Often the true underlying source expression
    is identified.
arxiv: 1
author:
- first_name: Georg S
  full_name: Martius, Georg S
  id: 3A276B68-F248-11E8-B48F-1D18A9856A87
  last_name: Martius
- first_name: Christoph
  full_name: Lampert, Christoph
  id: 40C20FD2-F248-11E8-B48F-1D18A9856A87
  last_name: Lampert
  orcid: 0000-0001-8622-7887
citation:
  ama: 'Martius GS, Lampert C. Extrapolation and learning equations. In: <i>5th International
    Conference on Learning Representations, ICLR 2017 - Workshop Track Proceedings</i>.
    International Conference on Learning Representations; 2017.'
  apa: 'Martius, G. S., &#38; Lampert, C. (2017). Extrapolation and learning equations.
    In <i>5th International Conference on Learning Representations, ICLR 2017 - Workshop
    Track Proceedings</i>. Toulon, France: International Conference on Learning Representations.'
  chicago: Martius, Georg S, and Christoph Lampert. “Extrapolation and Learning Equations.”
    In <i>5th International Conference on Learning Representations, ICLR 2017 - Workshop
    Track Proceedings</i>. International Conference on Learning Representations, 2017.
  ieee: G. S. Martius and C. Lampert, “Extrapolation and learning equations,” in <i>5th
    International Conference on Learning Representations, ICLR 2017 - Workshop Track
    Proceedings</i>, Toulon, France, 2017.
  ista: 'Martius GS, Lampert C. 2017. Extrapolation and learning equations. 5th International
    Conference on Learning Representations, ICLR 2017 - Workshop Track Proceedings.
    ICLR: International Conference on Learning Representations.'
  mla: Martius, Georg S., and Christoph Lampert. “Extrapolation and Learning Equations.”
    <i>5th International Conference on Learning Representations, ICLR 2017 - Workshop
    Track Proceedings</i>, International Conference on Learning Representations, 2017.
  short: G.S. Martius, C. Lampert, in:, 5th International Conference on Learning Representations,
    ICLR 2017 - Workshop Track Proceedings, International Conference on Learning Representations,
    2017.
conference:
  end_date: 2017-04-26
  location: Toulon, France
  name: 'ICLR: International Conference on Learning Representations'
  start_date: 2017-04-24
date_created: 2019-09-01T22:01:00Z
date_published: 2017-02-21T00:00:00Z
date_updated: 2021-01-12T08:09:17Z
day: '21'
department:
- _id: ChLa
ec_funded: 1
external_id:
  arxiv:
  - '1610.02995'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1610.02995
month: '02'
oa: 1
oa_version: Preprint
project:
- _id: 2532554C-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '308036'
  name: Lifelong Learning of Visual Scene Understanding
publication: 5th International Conference on Learning Representations, ICLR 2017 -
  Workshop Track Proceedings
publication_status: published
publisher: International Conference on Learning Representations
quality_controlled: '1'
scopus_import: 1
status: public
title: Extrapolation and learning equations
type: conference
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
year: '2017'
...
---
_id: '685'
abstract:
- lang: eng
  text: By applying methods and principles from the physical sciences to biological
    problems, D'Arcy Thompson's On Growth and Form demonstrated how mathematical reasoning
    reveals elegant, simple explanations for seemingly complex processes. This has
    had a profound influence on subsequent generations of developmental biologists.
    We discuss how this influence can be traced through twentieth century morphologists,
    embryologists and theoreticians to current research that explores the molecular
    and cellular mechanisms of tissue growth and patterning, including our own studies
    of the vertebrate neural tube.
author:
- first_name: James
  full_name: Briscoe, James
  last_name: Briscoe
- first_name: Anna
  full_name: Kicheva, Anna
  id: 3959A2A0-F248-11E8-B48F-1D18A9856A87
  last_name: Kicheva
  orcid: 0000-0003-4509-4998
citation:
  ama: Briscoe J, Kicheva A. The physics of development 100 years after D’Arcy Thompson’s
    “on growth and form.” <i>Mechanisms of Development</i>. 2017;145:26-31. doi:<a
    href="https://doi.org/10.1016/j.mod.2017.03.005">10.1016/j.mod.2017.03.005</a>
  apa: Briscoe, J., &#38; Kicheva, A. (2017). The physics of development 100 years
    after D’Arcy Thompson’s “on growth and form.” <i>Mechanisms of Development</i>.
    Elsevier. <a href="https://doi.org/10.1016/j.mod.2017.03.005">https://doi.org/10.1016/j.mod.2017.03.005</a>
  chicago: Briscoe, James, and Anna Kicheva. “The Physics of Development 100 Years
    after D’Arcy Thompson’s ‘on Growth and Form.’” <i>Mechanisms of Development</i>.
    Elsevier, 2017. <a href="https://doi.org/10.1016/j.mod.2017.03.005">https://doi.org/10.1016/j.mod.2017.03.005</a>.
  ieee: J. Briscoe and A. Kicheva, “The physics of development 100 years after D’Arcy
    Thompson’s ‘on growth and form,’” <i>Mechanisms of Development</i>, vol. 145.
    Elsevier, pp. 26–31, 2017.
  ista: Briscoe J, Kicheva A. 2017. The physics of development 100 years after D’Arcy
    Thompson’s “on growth and form”. Mechanisms of Development. 145, 26–31.
  mla: Briscoe, James, and Anna Kicheva. “The Physics of Development 100 Years after
    D’Arcy Thompson’s ‘on Growth and Form.’” <i>Mechanisms of Development</i>, vol.
    145, Elsevier, 2017, pp. 26–31, doi:<a href="https://doi.org/10.1016/j.mod.2017.03.005">10.1016/j.mod.2017.03.005</a>.
  short: J. Briscoe, A. Kicheva, Mechanisms of Development 145 (2017) 26–31.
date_created: 2018-12-11T11:47:55Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2021-01-12T08:09:20Z
day: '01'
ddc:
- '571'
department:
- _id: AnKi
doi: 10.1016/j.mod.2017.03.005
ec_funded: 1
external_id:
  pmid:
  - '28366718'
file:
- access_level: open_access
  checksum: 727043d2e4199fbef6b3704e6d1ac105
  content_type: application/pdf
  creator: dernst
  date_created: 2019-04-17T07:58:48Z
  date_updated: 2020-07-14T12:47:42Z
  file_id: '6335'
  file_name: 2017_Briscoe_Kicheva_and_DArcy_accepted_version.pdf
  file_size: 652313
  relation: main_file
file_date_updated: 2020-07-14T12:47:42Z
has_accepted_license: '1'
intvolume: '       145'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Submitted Version
page: 26 - 31
pmid: 1
project:
- _id: B6FC0238-B512-11E9-945C-1524E6697425
  call_identifier: H2020
  grant_number: '680037'
  name: Coordination of Patterning And Growth In the Spinal Cord
publication: Mechanisms of Development
publication_identifier:
  issn:
  - '09254773'
publication_status: published
publisher: Elsevier
publist_id: '7025'
pubrep_id: '985'
quality_controlled: '1'
scopus_import: 1
status: public
title: The physics of development 100 years after D'Arcy Thompson's “on growth and
  form”
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 145
year: '2017'
...
---
_id: '686'
abstract:
- lang: eng
  text: Tissues are thought to behave like fluids with a given surface tension. Differences
    in tissue surface tension (TST) have been proposed to trigger cell sorting and
    tissue envelopment. D'Arcy Thompson in his seminal book ‘On Growth and Form’ has
    introduced this concept of differential TST as a key physical mechanism dictating
    tissue formation and organization within the developing organism. Over the past
    century, many studies have picked up the concept of differential TST and analyzed
    the role and cell biological basis of TST in development, underlining the importance
    and influence of this concept in developmental biology.
author:
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: 'Heisenberg C-PJ. D’Arcy Thompson’s ‘on growth and form’: From soap bubbles
    to tissue self organization. <i>Mechanisms of Development</i>. 2017;145:32-37.
    doi:<a href="https://doi.org/10.1016/j.mod.2017.03.006">10.1016/j.mod.2017.03.006</a>'
  apa: 'Heisenberg, C.-P. J. (2017). D’Arcy Thompson’s ‘on growth and form’: From
    soap bubbles to tissue self organization. <i>Mechanisms of Development</i>. Elsevier.
    <a href="https://doi.org/10.1016/j.mod.2017.03.006">https://doi.org/10.1016/j.mod.2017.03.006</a>'
  chicago: 'Heisenberg, Carl-Philipp J. “D’Arcy Thompson’s ‘on Growth and Form’: From
    Soap Bubbles to Tissue Self Organization.” <i>Mechanisms of Development</i>. Elsevier,
    2017. <a href="https://doi.org/10.1016/j.mod.2017.03.006">https://doi.org/10.1016/j.mod.2017.03.006</a>.'
  ieee: 'C.-P. J. Heisenberg, “D’Arcy Thompson’s ‘on growth and form’: From soap bubbles
    to tissue self organization,” <i>Mechanisms of Development</i>, vol. 145. Elsevier,
    pp. 32–37, 2017.'
  ista: 'Heisenberg C-PJ. 2017. D’Arcy Thompson’s ‘on growth and form’: From soap
    bubbles to tissue self organization. Mechanisms of Development. 145, 32–37.'
  mla: 'Heisenberg, Carl-Philipp J. “D’Arcy Thompson’s ‘on Growth and Form’: From
    Soap Bubbles to Tissue Self Organization.” <i>Mechanisms of Development</i>, vol.
    145, Elsevier, 2017, pp. 32–37, doi:<a href="https://doi.org/10.1016/j.mod.2017.03.006">10.1016/j.mod.2017.03.006</a>.'
  short: C.-P.J. Heisenberg, Mechanisms of Development 145 (2017) 32–37.
date_created: 2018-12-11T11:47:55Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2021-01-12T08:09:23Z
day: '01'
department:
- _id: CaHe
doi: 10.1016/j.mod.2017.03.006
intvolume: '       145'
language:
- iso: eng
month: '06'
oa_version: None
page: 32 - 37
publication: Mechanisms of Development
publication_identifier:
  issn:
  - '09254773'
publication_status: published
publisher: Elsevier
publist_id: '7024'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'D''Arcy Thompson''s ‘on growth and form’: From soap bubbles to tissue self
  organization'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 145
year: '2017'
...
---
_id: '687'
abstract:
- lang: eng
  text: Pursuing the similarity between the Kontsevich-Soibelman construction of the
    cohomological Hall algebra (CoHA) of BPS states and Lusztig's construction of
    canonical bases for quantum enveloping algebras, and the similarity between the
    integrality conjecture for motivic Donaldson-Thomas invariants and the PBW theorem
    for quantum enveloping algebras, we build a coproduct on the CoHA associated to
    a quiver with potential. We also prove a cohomological dimensional reduction theorem,
    further linking a special class of CoHAs with Yangians, and explaining how to
    connect the study of character varieties with the study of CoHAs.
author:
- first_name: Ben
  full_name: Davison, Ben
  id: 4634AB1E-F248-11E8-B48F-1D18A9856A87
  last_name: Davison
  orcid: 0000-0002-8944-4390
citation:
  ama: Davison B. The critical CoHA of a quiver with potential. <i>Quarterly Journal
    of Mathematics</i>. 2017;68(2):635-703. doi:<a href="https://doi.org/10.1093/qmath/haw053">10.1093/qmath/haw053</a>
  apa: Davison, B. (2017). The critical CoHA of a quiver with potential. <i>Quarterly
    Journal of Mathematics</i>. Oxford University Press. <a href="https://doi.org/10.1093/qmath/haw053">https://doi.org/10.1093/qmath/haw053</a>
  chicago: Davison, Ben. “The Critical CoHA of a Quiver with Potential.” <i>Quarterly
    Journal of Mathematics</i>. Oxford University Press, 2017. <a href="https://doi.org/10.1093/qmath/haw053">https://doi.org/10.1093/qmath/haw053</a>.
  ieee: B. Davison, “The critical CoHA of a quiver with potential,” <i>Quarterly Journal
    of Mathematics</i>, vol. 68, no. 2. Oxford University Press, pp. 635–703, 2017.
  ista: Davison B. 2017. The critical CoHA of a quiver with potential. Quarterly Journal
    of Mathematics. 68(2), 635–703.
  mla: Davison, Ben. “The Critical CoHA of a Quiver with Potential.” <i>Quarterly
    Journal of Mathematics</i>, vol. 68, no. 2, Oxford University Press, 2017, pp.
    635–703, doi:<a href="https://doi.org/10.1093/qmath/haw053">10.1093/qmath/haw053</a>.
  short: B. Davison, Quarterly Journal of Mathematics 68 (2017) 635–703.
date_created: 2018-12-11T11:47:55Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2021-01-12T08:09:24Z
day: '01'
department:
- _id: TaHa
doi: 10.1093/qmath/haw053
ec_funded: 1
intvolume: '        68'
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1311.7172
month: '06'
oa: 1
oa_version: Submitted Version
page: 635 - 703
project:
- _id: 25E549F4-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '320593'
  name: Arithmetic and physics of Higgs moduli spaces
publication: Quarterly Journal of Mathematics
publication_identifier:
  issn:
  - '00335606'
publication_status: published
publisher: Oxford University Press
publist_id: '7022'
quality_controlled: '1'
scopus_import: 1
status: public
title: The critical CoHA of a quiver with potential
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 68
year: '2017'
...
---
_id: '688'
abstract:
- lang: eng
  text: 'We show that the framework of topological data analysis can be extended from
    metrics to general Bregman divergences, widening the scope of possible applications.
    Examples are the Kullback - Leibler divergence, which is commonly used for comparing
    text and images, and the Itakura - Saito divergence, popular for speech and sound.
    In particular, we prove that appropriately generalized čech and Delaunay (alpha)
    complexes capture the correct homotopy type, namely that of the corresponding
    union of Bregman balls. Consequently, their filtrations give the correct persistence
    diagram, namely the one generated by the uniformly growing Bregman balls. Moreover,
    we show that unlike the metric setting, the filtration of Vietoris-Rips complexes
    may fail to approximate the persistence diagram. We propose algorithms to compute
    the thus generalized čech, Vietoris-Rips and Delaunay complexes and experimentally
    test their efficiency. Lastly, we explain their surprisingly good performance
    by making a connection with discrete Morse theory. '
alternative_title:
- LIPIcs
author:
- first_name: Herbert
  full_name: Edelsbrunner, Herbert
  id: 3FB178DA-F248-11E8-B48F-1D18A9856A87
  last_name: Edelsbrunner
  orcid: 0000-0002-9823-6833
- first_name: Hubert
  full_name: Wagner, Hubert
  id: 379CA8B8-F248-11E8-B48F-1D18A9856A87
  last_name: Wagner
citation:
  ama: 'Edelsbrunner H, Wagner H. Topological data analysis with Bregman divergences.
    In: Vol 77. Schloss Dagstuhl - Leibniz-Zentrum für Informatik; 2017:391-3916.
    doi:<a href="https://doi.org/10.4230/LIPIcs.SoCG.2017.39">10.4230/LIPIcs.SoCG.2017.39</a>'
  apa: 'Edelsbrunner, H., &#38; Wagner, H. (2017). Topological data analysis with
    Bregman divergences (Vol. 77, pp. 391–3916). Presented at the Symposium on Computational
    Geometry, SoCG, Brisbane, Australia: Schloss Dagstuhl - Leibniz-Zentrum für Informatik.
    <a href="https://doi.org/10.4230/LIPIcs.SoCG.2017.39">https://doi.org/10.4230/LIPIcs.SoCG.2017.39</a>'
  chicago: Edelsbrunner, Herbert, and Hubert Wagner. “Topological Data Analysis with
    Bregman Divergences,” 77:391–3916. Schloss Dagstuhl - Leibniz-Zentrum für Informatik,
    2017. <a href="https://doi.org/10.4230/LIPIcs.SoCG.2017.39">https://doi.org/10.4230/LIPIcs.SoCG.2017.39</a>.
  ieee: H. Edelsbrunner and H. Wagner, “Topological data analysis with Bregman divergences,”
    presented at the Symposium on Computational Geometry, SoCG, Brisbane, Australia,
    2017, vol. 77, pp. 391–3916.
  ista: Edelsbrunner H, Wagner H. 2017. Topological data analysis with Bregman divergences.
    Symposium on Computational Geometry, SoCG, LIPIcs, vol. 77, 391–3916.
  mla: Edelsbrunner, Herbert, and Hubert Wagner. <i>Topological Data Analysis with
    Bregman Divergences</i>. Vol. 77, Schloss Dagstuhl - Leibniz-Zentrum für Informatik,
    2017, pp. 391–3916, doi:<a href="https://doi.org/10.4230/LIPIcs.SoCG.2017.39">10.4230/LIPIcs.SoCG.2017.39</a>.
  short: H. Edelsbrunner, H. Wagner, in:, Schloss Dagstuhl - Leibniz-Zentrum für Informatik,
    2017, pp. 391–3916.
conference:
  end_date: 2017-07-07
  location: Brisbane, Australia
  name: Symposium on Computational Geometry, SoCG
  start_date: 2017-07-04
date_created: 2018-12-11T11:47:56Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2021-01-12T08:09:26Z
day: '01'
ddc:
- '514'
- '516'
department:
- _id: HeEd
- _id: UlWa
doi: 10.4230/LIPIcs.SoCG.2017.39
file:
- access_level: open_access
  checksum: 067ab0cb3f962bae6c3af6bf0094e0f3
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:11:03Z
  date_updated: 2020-07-14T12:47:42Z
  file_id: '4856'
  file_name: IST-2017-895-v1+1_LIPIcs-SoCG-2017-39.pdf
  file_size: 990546
  relation: main_file
file_date_updated: 2020-07-14T12:47:42Z
has_accepted_license: '1'
intvolume: '        77'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 391-3916
publication_identifier:
  issn:
  - '18688969'
publication_status: published
publisher: Schloss Dagstuhl - Leibniz-Zentrum für Informatik
publist_id: '7021'
pubrep_id: '895'
quality_controlled: '1'
scopus_import: 1
status: public
title: Topological data analysis with Bregman divergences
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: conference
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 77
year: '2017'
...
---
_id: '689'
abstract:
- lang: eng
  text: Rett syndrome modeling in monkey mirrors the human disorder.
article_number: eaan8196
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. Rett syndrome modeling goes simian. <i>Science Translational Medicine</i>.
    2017;9(393). doi:<a href="https://doi.org/10.1126/scitranslmed.aan8196">10.1126/scitranslmed.aan8196</a>
  apa: Novarino, G. (2017). Rett syndrome modeling goes simian. <i>Science Translational
    Medicine</i>. American Association for the Advancement of Science. <a href="https://doi.org/10.1126/scitranslmed.aan8196">https://doi.org/10.1126/scitranslmed.aan8196</a>
  chicago: Novarino, Gaia. “Rett Syndrome Modeling Goes Simian.” <i>Science Translational
    Medicine</i>. American Association for the Advancement of Science, 2017. <a href="https://doi.org/10.1126/scitranslmed.aan8196">https://doi.org/10.1126/scitranslmed.aan8196</a>.
  ieee: G. Novarino, “Rett syndrome modeling goes simian,” <i>Science Translational
    Medicine</i>, vol. 9, no. 393. American Association for the Advancement of Science,
    2017.
  ista: Novarino G. 2017. Rett syndrome modeling goes simian. Science Translational
    Medicine. 9(393), eaan8196.
  mla: Novarino, Gaia. “Rett Syndrome Modeling Goes Simian.” <i>Science Translational
    Medicine</i>, vol. 9, no. 393, eaan8196, American Association for the Advancement
    of Science, 2017, doi:<a href="https://doi.org/10.1126/scitranslmed.aan8196">10.1126/scitranslmed.aan8196</a>.
  short: G. Novarino, Science Translational Medicine 9 (2017).
date_created: 2018-12-11T11:47:56Z
date_published: 2017-06-07T00:00:00Z
date_updated: 2021-01-12T08:09:29Z
day: '07'
department:
- _id: GaNo
doi: 10.1126/scitranslmed.aan8196
intvolume: '         9'
issue: '393'
language:
- iso: eng
month: '06'
oa_version: None
publication: Science Translational Medicine
publication_identifier:
  issn:
  - '19466234'
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7019'
quality_controlled: '1'
scopus_import: 1
status: public
title: Rett syndrome modeling goes simian
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2017'
...
---
_id: '693'
abstract:
- lang: eng
  text: 'Many central synapses contain a single presynaptic active zone and a single
    postsynaptic density. Vesicular release statistics at such “simple synapses” indicate
    that they contain a small complement of docking sites where vesicles repetitively
    dock and fuse. In this work, we investigate functional and morphological aspects
    of docking sites at simple synapses made between cerebellar parallel fibers and
    molecular layer interneurons. Using immunogold labeling of SDS-treated freeze-fracture
    replicas, we find that Cav2.1 channels form several clusters per active zone with
    about nine channels per cluster. The mean value and range of intersynaptic variation
    are similar for Cav2.1 cluster numbers and for functional estimates of docking-site
    numbers obtained from the maximum numbers of released vesicles per action potential.
    Both numbers grow in relation with synaptic size and decrease by a similar extent
    with age between 2 wk and 4 wk postnatal. Thus, the mean docking-site numbers
    were 3.15 at 2 wk (range: 1–10) and 2.03 at 4 wk (range: 1–4), whereas the mean
    numbers of Cav2.1 clusters were 2.84 at 2 wk (range: 1–8) and 2.37 at 4 wk (range:
    1–5). These changes were accompanied by decreases of miniature current amplitude
    (from 93 pA to 56 pA), active-zone surface area (from 0.0427 μm2 to 0.0234 μm2),
    and initial success rate (from 0.609 to 0.353), indicating a tightening of synaptic
    transmission with development. Altogether, these results suggest a close correspondence
    between the number of functionally defined vesicular docking sites and that of
    clusters of voltage-gated calcium channels. '
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Takafumi
  full_name: Miki, Takafumi
  last_name: Miki
- first_name: Walter
  full_name: Kaufmann, Walter
  id: 3F99E422-F248-11E8-B48F-1D18A9856A87
  last_name: Kaufmann
  orcid: 0000-0001-9735-5315
- first_name: Gerardo
  full_name: Malagon, Gerardo
  last_name: Malagon
- first_name: Laura
  full_name: Gomez, Laura
  last_name: Gomez
- first_name: Katsuhiko
  full_name: Tabuchi, Katsuhiko
  last_name: Tabuchi
- first_name: Masahiko
  full_name: Watanabe, Masahiko
  last_name: Watanabe
- first_name: Ryuichi
  full_name: Shigemoto, Ryuichi
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Alain
  full_name: Marty, Alain
  last_name: Marty
citation:
  ama: Miki T, Kaufmann W, Malagon G, et al. Numbers of presynaptic Ca2+ channel clusters
    match those of functionally defined vesicular docking sites in single central
    synapses. <i>PNAS</i>. 2017;114(26):E5246-E5255. doi:<a href="https://doi.org/10.1073/pnas.1704470114">10.1073/pnas.1704470114</a>
  apa: Miki, T., Kaufmann, W., Malagon, G., Gomez, L., Tabuchi, K., Watanabe, M.,
    … Marty, A. (2017). Numbers of presynaptic Ca2+ channel clusters match those of
    functionally defined vesicular docking sites in single central synapses. <i>PNAS</i>.
    National Academy of Sciences. <a href="https://doi.org/10.1073/pnas.1704470114">https://doi.org/10.1073/pnas.1704470114</a>
  chicago: Miki, Takafumi, Walter Kaufmann, Gerardo Malagon, Laura Gomez, Katsuhiko
    Tabuchi, Masahiko Watanabe, Ryuichi Shigemoto, and Alain Marty. “Numbers of Presynaptic
    Ca2+ Channel Clusters Match Those of Functionally Defined Vesicular Docking Sites
    in Single Central Synapses.” <i>PNAS</i>. National Academy of Sciences, 2017.
    <a href="https://doi.org/10.1073/pnas.1704470114">https://doi.org/10.1073/pnas.1704470114</a>.
  ieee: T. Miki <i>et al.</i>, “Numbers of presynaptic Ca2+ channel clusters match
    those of functionally defined vesicular docking sites in single central synapses,”
    <i>PNAS</i>, vol. 114, no. 26. National Academy of Sciences, pp. E5246–E5255,
    2017.
  ista: Miki T, Kaufmann W, Malagon G, Gomez L, Tabuchi K, Watanabe M, Shigemoto R,
    Marty A. 2017. Numbers of presynaptic Ca2+ channel clusters match those of functionally
    defined vesicular docking sites in single central synapses. PNAS. 114(26), E5246–E5255.
  mla: Miki, Takafumi, et al. “Numbers of Presynaptic Ca2+ Channel Clusters Match
    Those of Functionally Defined Vesicular Docking Sites in Single Central Synapses.”
    <i>PNAS</i>, vol. 114, no. 26, National Academy of Sciences, 2017, pp. E5246–55,
    doi:<a href="https://doi.org/10.1073/pnas.1704470114">10.1073/pnas.1704470114</a>.
  short: T. Miki, W. Kaufmann, G. Malagon, L. Gomez, K. Tabuchi, M. Watanabe, R. Shigemoto,
    A. Marty, PNAS 114 (2017) E5246–E5255.
date_created: 2018-12-11T11:47:57Z
date_published: 2017-06-27T00:00:00Z
date_updated: 2023-02-23T12:54:57Z
day: '27'
ddc:
- '570'
department:
- _id: EM-Fac
- _id: RySh
doi: 10.1073/pnas.1704470114
external_id:
  pmid:
  - '28607047'
file:
- access_level: open_access
  checksum: 2ab75d554f3df4a34d20fa8040589b7e
  content_type: application/pdf
  creator: kschuh
  date_created: 2020-01-03T13:27:29Z
  date_updated: 2020-07-14T12:47:44Z
  file_id: '7223'
  file_name: 2017_PNAS_Miki.pdf
  file_size: 2721544
  relation: main_file
file_date_updated: 2020-07-14T12:47:44Z
has_accepted_license: '1'
intvolume: '       114'
issue: '26'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: E5246 - E5255
pmid: 1
publication: PNAS
publication_identifier:
  issn:
  - '00278424'
publication_status: published
publisher: National Academy of Sciences
publist_id: '7013'
quality_controlled: '1'
scopus_import: 1
status: public
title: Numbers of presynaptic Ca2+ channel clusters match those of functionally defined
  vesicular docking sites in single central synapses
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 114
year: '2017'
...
---
_id: '6932'
abstract:
- lang: eng
  text: "LCLs or locally checkable labelling problems (e.g. maximal independent set,
    maximal matching, and vertex colouring) in the LOCAL model of computation are
    very well-understood in cycles (toroidal 1-dimensional grids): every problem has
    a complexity of O(1), Θ(log* n), or Θ(n), and the design of optimal algorithms
    can be fully automated. This work develops the complexity theory of LCL problems
    for toroidal 2-dimensional grids. The complexity classes are the same as in the
    1-dimensional case: O(1), Θ(log* n), and Θ(n). However, given an LCL problem it
    is undecidable whether its complexity is Θ(log* n) or Θ(n) in 2-dimensional grids.\r\nNevertheless,
    if we correctly guess that the complexity of a problem is Θ(log* n), we can completely
    automate the design of optimal algorithms. For any problem we can find an algorithm
    that is of a normal form A' o Sk, where A' is a finite function, Sk is an algorithm
    for finding a maximal independent set in kth power of the grid, and k is a constant.\r\nFinally,
    partially with the help of automated design tools, we classify the complexity
    of several concrete LCL problems related to colourings and orientations."
article_processing_charge: No
author:
- first_name: Sebastian
  full_name: Brandt, Sebastian
  last_name: Brandt
- first_name: Juho
  full_name: Hirvonen, Juho
  last_name: Hirvonen
- first_name: Janne H.
  full_name: Korhonen, Janne H.
  last_name: Korhonen
- first_name: Tuomo
  full_name: Lempiäinen, Tuomo
  last_name: Lempiäinen
- first_name: Patric R.J.
  full_name: Östergård, Patric R.J.
  last_name: Östergård
- first_name: Christopher
  full_name: Purcell, Christopher
  last_name: Purcell
- first_name: Joel
  full_name: Rybicki, Joel
  id: 334EFD2E-F248-11E8-B48F-1D18A9856A87
  last_name: Rybicki
  orcid: 0000-0002-6432-6646
- first_name: Jukka
  full_name: Suomela, Jukka
  last_name: Suomela
- first_name: Przemysław
  full_name: Uznański, Przemysław
  last_name: Uznański
citation:
  ama: 'Brandt S, Hirvonen J, Korhonen JH, et al. LCL problems on grids. In: ACM Press;
    2017:101-110. doi:<a href="https://doi.org/10.1145/3087801.3087833">10.1145/3087801.3087833</a>'
  apa: 'Brandt, S., Hirvonen, J., Korhonen, J. H., Lempiäinen, T., Östergård, P. R.
    J., Purcell, C., … Uznański, P. (2017). LCL problems on grids (pp. 101–110). Presented
    at the PODC: Principles of Distributed Computing, Washington, DC, United States:
    ACM Press. <a href="https://doi.org/10.1145/3087801.3087833">https://doi.org/10.1145/3087801.3087833</a>'
  chicago: Brandt, Sebastian, Juho Hirvonen, Janne H. Korhonen, Tuomo Lempiäinen,
    Patric R.J. Östergård, Christopher Purcell, Joel Rybicki, Jukka Suomela, and Przemysław
    Uznański. “LCL Problems on Grids,” 101–10. ACM Press, 2017. <a href="https://doi.org/10.1145/3087801.3087833">https://doi.org/10.1145/3087801.3087833</a>.
  ieee: 'S. Brandt <i>et al.</i>, “LCL problems on grids,” presented at the PODC:
    Principles of Distributed Computing, Washington, DC, United States, 2017, pp.
    101–110.'
  ista: 'Brandt S, Hirvonen J, Korhonen JH, Lempiäinen T, Östergård PRJ, Purcell C,
    Rybicki J, Suomela J, Uznański P. 2017. LCL problems on grids. PODC: Principles
    of Distributed Computing, 101–110.'
  mla: Brandt, Sebastian, et al. <i>LCL Problems on Grids</i>. ACM Press, 2017, pp.
    101–10, doi:<a href="https://doi.org/10.1145/3087801.3087833">10.1145/3087801.3087833</a>.
  short: S. Brandt, J. Hirvonen, J.H. Korhonen, T. Lempiäinen, P.R.J. Östergård, C.
    Purcell, J. Rybicki, J. Suomela, P. Uznański, in:, ACM Press, 2017, pp. 101–110.
conference:
  end_date: 2017-07-27
  location: Washington, DC, United States
  name: 'PODC: Principles of Distributed Computing'
  start_date: 2017-07-25
date_created: 2019-10-08T12:47:46Z
date_published: 2017-07-01T00:00:00Z
date_updated: 2021-01-12T08:09:39Z
day: '01'
doi: 10.1145/3087801.3087833
extern: '1'
language:
- iso: eng
month: '07'
oa_version: None
page: 101-110
publication_identifier:
  isbn:
  - '9781450349925'
publication_status: published
publisher: ACM Press
quality_controlled: '1'
status: public
title: LCL problems on grids
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2017'
...
---
_id: '694'
abstract:
- lang: eng
  text: A change regarding the extent of adhesion - hereafter referred to as adhesion
    plasticity - between adhesive and less-adhesive states of mammalian cells is important
    for their behavior. To investigate adhesion plasticity, we have selected a stable
    isogenic subpopulation of human MDA-MB-468 breast carcinoma cells growing in suspension.
    These suspension cells are unable to re-adhere to various matrices or to contract
    three-dimensional collagen lattices. By using transcriptome analysis, we identified
    the focal adhesion protein tensin3 (Tns3) as a determinant of adhesion plasticity.
    Tns3 is strongly reduced at mRNA and protein levels in suspension cells. Furthermore,
    by transiently challenging breast cancer cells to grow under non-adherent conditions
    markedly reduces Tns3 protein expression, which is regained upon re-adhesion.
    Stable knockdown of Tns3 in parental MDA-MB-468 cells results in defective adhesion,
    spreading and migration. Tns3-knockdown cells display impaired structure and dynamics
    of focal adhesion complexes as determined by immunostaining. Restoration of Tns3
    protein expression in suspension cells partially rescues adhesion and focal contact
    composition. Our work identifies Tns3 as a crucial focal adhesion component regulated
    by, and functionally contributing to, the switch between adhesive and non-adhesive
    states in MDA-MB-468 cancer cells.
article_type: original
author:
- first_name: Astrid
  full_name: Veß, Astrid
  last_name: Veß
- first_name: Ulrich
  full_name: Blache, Ulrich
  last_name: Blache
- first_name: Laura
  full_name: Leitner, Laura
  last_name: Leitner
- first_name: Angela
  full_name: Kurz, Angela
  last_name: Kurz
- first_name: Anja
  full_name: Ehrenpfordt, Anja
  last_name: Ehrenpfordt
- 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: Guido
  full_name: Posern, Guido
  last_name: Posern
citation:
  ama: Veß A, Blache U, Leitner L, et al. A dual phenotype of MDA MB 468 cancer cells
    reveals mutual regulation of tensin3 and adhesion plasticity. <i>Journal of Cell
    Science</i>. 2017;130(13):2172-2184. doi:<a href="https://doi.org/10.1242/jcs.200899">10.1242/jcs.200899</a>
  apa: Veß, A., Blache, U., Leitner, L., Kurz, A., Ehrenpfordt, A., Sixt, M. K., &#38;
    Posern, G. (2017). A dual phenotype of MDA MB 468 cancer cells reveals mutual
    regulation of tensin3 and adhesion plasticity. <i>Journal of Cell Science</i>.
    Company of Biologists. <a href="https://doi.org/10.1242/jcs.200899">https://doi.org/10.1242/jcs.200899</a>
  chicago: Veß, Astrid, Ulrich Blache, Laura Leitner, Angela Kurz, Anja Ehrenpfordt,
    Michael K Sixt, and Guido Posern. “A Dual Phenotype of MDA MB 468 Cancer Cells
    Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” <i>Journal of Cell
    Science</i>. Company of Biologists, 2017. <a href="https://doi.org/10.1242/jcs.200899">https://doi.org/10.1242/jcs.200899</a>.
  ieee: A. Veß <i>et al.</i>, “A dual phenotype of MDA MB 468 cancer cells reveals
    mutual regulation of tensin3 and adhesion plasticity,” <i>Journal of Cell Science</i>,
    vol. 130, no. 13. Company of Biologists, pp. 2172–2184, 2017.
  ista: Veß A, Blache U, Leitner L, Kurz A, Ehrenpfordt A, Sixt MK, Posern G. 2017.
    A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3
    and adhesion plasticity. Journal of Cell Science. 130(13), 2172–2184.
  mla: Veß, Astrid, et al. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual
    Regulation of Tensin3 and Adhesion Plasticity.” <i>Journal of Cell Science</i>,
    vol. 130, no. 13, Company of Biologists, 2017, pp. 2172–84, doi:<a href="https://doi.org/10.1242/jcs.200899">10.1242/jcs.200899</a>.
  short: A. Veß, U. Blache, L. Leitner, A. Kurz, A. Ehrenpfordt, M.K. Sixt, G. Posern,
    Journal of Cell Science 130 (2017) 2172–2184.
date_created: 2018-12-11T11:47:58Z
date_published: 2017-07-01T00:00:00Z
date_updated: 2021-01-12T08:09:41Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1242/jcs.200899
external_id:
  pmid:
  - '28515231'
file:
- access_level: open_access
  checksum: 42c81a0a4fc3128883b391c3af3f74bc
  content_type: application/pdf
  creator: dernst
  date_created: 2019-10-24T09:43:56Z
  date_updated: 2020-07-14T12:47:45Z
  file_id: '6966'
  file_name: 2017_CellScience_Vess.pdf
  file_size: 10847596
  relation: main_file
file_date_updated: 2020-07-14T12:47:45Z
has_accepted_license: '1'
intvolume: '       130'
issue: '13'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: 2172 - 2184
pmid: 1
publication: Journal of Cell Science
publication_identifier:
  issn:
  - '00219533'
publication_status: published
publisher: Company of Biologists
publist_id: '7008'
quality_controlled: '1'
scopus_import: 1
status: public
title: A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3
  and adhesion plasticity
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 130
year: '2017'
...
---
_id: '695'
abstract:
- lang: eng
  text: It has been known since Stefan Vogel's observations in 1969 that solitary
    female oil bees collect fatty floral oils from specialized oil-secreting plants
    with the aid of hairy patches on either their legs or abdomen, a reward used as
    food for their larvae and/or to line their brood cells. Similar adaptations are
    also known from male oil bees, although the purpose of their oil-collecting behavior
    has not yet been clarified. Here, we describe a novel pollination system involving
    male Paratetrapedia oil bees and the tropical herb Anthurium acutifolium. We present
    ultrastructural morphological details of bee and plant structures involved in
    this interaction and the composition of floral scents likely mediating pollinator
    attraction. Inflorescences of A. acutifolium were visited almost exclusively by
    male P. chocoensis oil bees. The bees mopped with a hairy patch of their abdominal
    sterna 3 across the inflorescence surface. During this activity on both staminate
    and pistillate stage inflorescences, bees’ abdomens and legs became loaded with
    pollen and contacted receptive stigmas. In contrast to what has been observed
    in other angiosperms visited for the collection of fatty floral oils, the inflorescences/flowers
    of A. acutifolium do not have structures specialized in oil secretion, i.e., elaiophores.
    These inflorescences, nonetheless, were strongly scented during the time interval
    they were visited by the bees. Gas chromatography/mass spectrometry (GC/MS) analyses
    of dynamic headspace floral samples revealed that inflorescences of both anthetic
    phases emitted scent bouquets consisting mainly of aliphatic esters, indole and
    uncommmon terpenoids (megastigmanes). Interestingly enough, our data suggest that
    the unusual floral scent of A. acutifolium is a perfume reward collected by male
    P. chocoensis oil bees. This pollination system thus bears a remarkable resemblence
    with the interactions between perfume-collecting male euglossine bees and their
    preferred flowers, discovered by Stefan Vogel half a century ago.
author:
- first_name: Florian
  full_name: Etl, Florian
  last_name: Etl
- first_name: Anna
  full_name: Franschitz, Anna
  id: 480826C8-F248-11E8-B48F-1D18A9856A87
  last_name: Franschitz
- first_name: Antonio
  full_name: Aguiar, Antonio
  last_name: Aguiar
- first_name: Jürg
  full_name: Schönenberger, Jürg
  last_name: Schönenberger
- first_name: Stefan
  full_name: Dötterl, Stefan
  last_name: Dötterl
citation:
  ama: 'Etl F, Franschitz A, Aguiar A, Schönenberger J, Dötterl S. A perfume collecting
    male oil bee? Evidences of a novel pollination system involving Anthurium acutifolium
    Araceae and Paratetrapedia chocoensis Apidae Tapinotaspidini. <i>Flora: Morphology,
    Distribution, Functional Ecology of Plants</i>. 2017;232:7-15. doi:<a href="https://doi.org/10.1016/j.flora.2017.02.020">10.1016/j.flora.2017.02.020</a>'
  apa: 'Etl, F., Franschitz, A., Aguiar, A., Schönenberger, J., &#38; Dötterl, S.
    (2017). A perfume collecting male oil bee? Evidences of a novel pollination system
    involving Anthurium acutifolium Araceae and Paratetrapedia chocoensis Apidae Tapinotaspidini.
    <i>Flora: Morphology, Distribution, Functional Ecology of Plants</i>. Elsevier.
    <a href="https://doi.org/10.1016/j.flora.2017.02.020">https://doi.org/10.1016/j.flora.2017.02.020</a>'
  chicago: 'Etl, Florian, Anna Franschitz, Antonio Aguiar, Jürg Schönenberger, and
    Stefan Dötterl. “A Perfume Collecting Male Oil Bee? Evidences of a Novel Pollination
    System Involving Anthurium Acutifolium Araceae and Paratetrapedia Chocoensis Apidae
    Tapinotaspidini.” <i>Flora: Morphology, Distribution, Functional Ecology of Plants</i>.
    Elsevier, 2017. <a href="https://doi.org/10.1016/j.flora.2017.02.020">https://doi.org/10.1016/j.flora.2017.02.020</a>.'
  ieee: 'F. Etl, A. Franschitz, A. Aguiar, J. Schönenberger, and S. Dötterl, “A perfume
    collecting male oil bee? Evidences of a novel pollination system involving Anthurium
    acutifolium Araceae and Paratetrapedia chocoensis Apidae Tapinotaspidini,” <i>Flora:
    Morphology, Distribution, Functional Ecology of Plants</i>, vol. 232. Elsevier,
    pp. 7–15, 2017.'
  ista: 'Etl F, Franschitz A, Aguiar A, Schönenberger J, Dötterl S. 2017. A perfume
    collecting male oil bee? Evidences of a novel pollination system involving Anthurium
    acutifolium Araceae and Paratetrapedia chocoensis Apidae Tapinotaspidini. Flora:
    Morphology, Distribution, Functional Ecology of Plants. 232, 7–15.'
  mla: 'Etl, Florian, et al. “A Perfume Collecting Male Oil Bee? Evidences of a Novel
    Pollination System Involving Anthurium Acutifolium Araceae and Paratetrapedia
    Chocoensis Apidae Tapinotaspidini.” <i>Flora: Morphology, Distribution, Functional
    Ecology of Plants</i>, vol. 232, Elsevier, 2017, pp. 7–15, doi:<a href="https://doi.org/10.1016/j.flora.2017.02.020">10.1016/j.flora.2017.02.020</a>.'
  short: 'F. Etl, A. Franschitz, A. Aguiar, J. Schönenberger, S. Dötterl, Flora: Morphology,
    Distribution, Functional Ecology of Plants 232 (2017) 7–15.'
date_created: 2018-12-11T11:47:58Z
date_published: 2017-07-01T00:00:00Z
date_updated: 2021-01-12T08:09:44Z
day: '01'
doi: 10.1016/j.flora.2017.02.020
extern: '1'
intvolume: '       232'
language:
- iso: eng
month: '07'
oa_version: None
page: 7 - 15
publication: 'Flora: Morphology, Distribution, Functional Ecology of Plants'
publication_identifier:
  issn:
  - '03672530'
publication_status: published
publisher: Elsevier
publist_id: '7007'
quality_controlled: '1'
status: public
title: A perfume collecting male oil bee? Evidences of a novel pollination system
  involving Anthurium acutifolium Araceae and Paratetrapedia chocoensis Apidae Tapinotaspidini
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 232
year: '2017'
...
---
_id: '696'
abstract:
- lang: eng
  text: Mutator strains are expected to evolve when the availability and effect of
    beneficial mutations are high enough to counteract the disadvantage from deleterious
    mutations that will inevitably accumulate. As the population becomes more adapted
    to its environment, both availability and effect of beneficial mutations necessarily
    decrease and mutation rates are predicted to decrease. It has been shown that
    certain molecular mechanisms can lead to increased mutation rates when the organism
    finds itself in a stressful environment. While this may be a correlated response
    to other functions, it could also be an adaptive mechanism, raising mutation rates
    only when it is most advantageous. Here, we use a mathematical model to investigate
    the plausibility of the adaptive hypothesis. We show that such a mechanism can
    be mantained if the population is subjected to diverse stresses. By simulating
    various antibiotic treatment schemes, we find that combination treatments can
    reduce the effectiveness of second-order selection on stress-induced mutagenesis.
    We discuss the implications of our results to strategies of antibiotic therapy.
article_number: e1005609
article_type: original
author:
- first_name: Marta
  full_name: Lukacisinova, Marta
  id: 4342E402-F248-11E8-B48F-1D18A9856A87
  last_name: Lukacisinova
  orcid: 0000-0002-2519-8004
- first_name: Sebastian
  full_name: Novak, Sebastian
  id: 461468AE-F248-11E8-B48F-1D18A9856A87
  last_name: Novak
  orcid: 0000-0002-2519-824X
- first_name: Tiago
  full_name: Paixao, Tiago
  id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
  last_name: Paixao
  orcid: 0000-0003-2361-3953
citation:
  ama: 'Lukacisinova M, Novak S, Paixao T. Stress induced mutagenesis: Stress diversity
    facilitates the persistence of mutator genes. <i>PLoS Computational Biology</i>.
    2017;13(7). doi:<a href="https://doi.org/10.1371/journal.pcbi.1005609">10.1371/journal.pcbi.1005609</a>'
  apa: 'Lukacisinova, M., Novak, S., &#38; Paixao, T. (2017). Stress induced mutagenesis:
    Stress diversity facilitates the persistence of mutator genes. <i>PLoS Computational
    Biology</i>. Public Library of Science. <a href="https://doi.org/10.1371/journal.pcbi.1005609">https://doi.org/10.1371/journal.pcbi.1005609</a>'
  chicago: 'Lukacisinova, Marta, Sebastian Novak, and Tiago Paixao. “Stress Induced
    Mutagenesis: Stress Diversity Facilitates the Persistence of Mutator Genes.” <i>PLoS
    Computational Biology</i>. Public Library of Science, 2017. <a href="https://doi.org/10.1371/journal.pcbi.1005609">https://doi.org/10.1371/journal.pcbi.1005609</a>.'
  ieee: 'M. Lukacisinova, S. Novak, and T. Paixao, “Stress induced mutagenesis: Stress
    diversity facilitates the persistence of mutator genes,” <i>PLoS Computational
    Biology</i>, vol. 13, no. 7. Public Library of Science, 2017.'
  ista: 'Lukacisinova M, Novak S, Paixao T. 2017. Stress induced mutagenesis: Stress
    diversity facilitates the persistence of mutator genes. PLoS Computational Biology.
    13(7), e1005609.'
  mla: 'Lukacisinova, Marta, et al. “Stress Induced Mutagenesis: Stress Diversity
    Facilitates the Persistence of Mutator Genes.” <i>PLoS Computational Biology</i>,
    vol. 13, no. 7, e1005609, Public Library of Science, 2017, doi:<a href="https://doi.org/10.1371/journal.pcbi.1005609">10.1371/journal.pcbi.1005609</a>.'
  short: M. Lukacisinova, S. Novak, T. Paixao, PLoS Computational Biology 13 (2017).
date_created: 2018-12-11T11:47:58Z
date_published: 2017-07-18T00:00:00Z
date_updated: 2024-03-25T23:30:14Z
day: '18'
ddc:
- '576'
department:
- _id: ToBo
- _id: NiBa
- _id: CaGu
doi: 10.1371/journal.pcbi.1005609
ec_funded: 1
file:
- access_level: open_access
  checksum: 9143c290fa6458ed2563bff4b295554a
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:15:01Z
  date_updated: 2020-07-14T12:47:46Z
  file_id: '5117'
  file_name: IST-2017-894-v1+1_journal.pcbi.1005609.pdf
  file_size: 3775716
  relation: main_file
file_date_updated: 2020-07-14T12:47:46Z
has_accepted_license: '1'
intvolume: '        13'
issue: '7'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
project:
- _id: 25B1EC9E-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '618091'
  name: Speed of Adaptation in Population Genetics and Evolutionary Computation
publication: PLoS Computational Biology
publication_identifier:
  issn:
  - 1553734X
publication_status: published
publisher: Public Library of Science
publist_id: '7004'
pubrep_id: '894'
quality_controlled: '1'
related_material:
  record:
  - id: '9849'
    relation: research_data
    status: public
  - id: '9850'
    relation: research_data
    status: public
  - id: '9851'
    relation: research_data
    status: public
  - id: '9852'
    relation: research_data
    status: public
  - id: '6263'
    relation: dissertation_contains
    status: public
scopus_import: 1
status: public
title: 'Stress induced mutagenesis: Stress diversity facilitates the persistence of
  mutator genes'
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: 13
year: '2017'
...
