---
_id: '657'
abstract:
- lang: eng
  text: Plant organs are typically organized into three main tissue layers. The middle
    ground tissue layer comprises the majority of the plant body and serves a wide
    range of functions, including photosynthesis, selective nutrient uptake and storage,
    and gravity sensing. Ground tissue patterning and maintenance in Arabidopsis are
    controlled by a well-established gene network revolving around the key regulator
    SHORT-ROOT (SHR). In contrast, it is completely unknown how ground tissue identity
    is first specified from totipotent precursor cells in the embryo. The plant signaling
    molecule auxin, acting through AUXIN RESPONSE FACTOR (ARF) transcription factors,
    is critical for embryo patterning. The auxin effector ARF5/MONOPTEROS (MP) acts
    both cell-autonomously and noncell-autonomously to control embryonic vascular
    tissue formation and root initiation, respectively. Here we show that auxin response
    and ARF activity cell-autonomously control the asymmetric division of the first
    ground tissue cells. By identifying embryonic target genes, we show that MP transcriptionally
    initiates the ground tissue lineage and acts upstream of the regulatory network
    that controls ground tissue patterning and maintenance. Strikingly, whereas the
    SHR network depends on MP, this MP function is, at least in part, SHR independent.
    Our study therefore identifies auxin response as a regulator of ground tissue
    specification in the embryonic root, and reveals that ground tissue initiation
    and maintenance use different regulators and mechanisms. Moreover, our data provide
    a framework for the simultaneous formation of multiple cell types by the same
    transcriptional regulator.
author:
- first_name: Barbara
  full_name: Möller, Barbara
  last_name: Möller
- first_name: Colette
  full_name: Ten Hove, Colette
  last_name: Ten Hove
- first_name: Daoquan
  full_name: Xiang, Daoquan
  last_name: Xiang
- first_name: Nerys
  full_name: Williams, Nerys
  last_name: Williams
- first_name: Lorena
  full_name: López, Lorena
  last_name: López
- first_name: Saiko
  full_name: Yoshida, Saiko
  id: 2E46069C-F248-11E8-B48F-1D18A9856A87
  last_name: Yoshida
- first_name: Margot
  full_name: Smit, Margot
  last_name: Smit
- first_name: Raju
  full_name: Datla, Raju
  last_name: Datla
- first_name: Dolf
  full_name: Weijers, Dolf
  last_name: Weijers
citation:
  ama: Möller B, Ten Hove C, Xiang D, et al. Auxin response cell autonomously controls
    ground tissue initiation in the early arabidopsis embryo. <i>PNAS</i>. 2017;114(12):E2533-E2539.
    doi:<a href="https://doi.org/10.1073/pnas.1616493114">10.1073/pnas.1616493114</a>
  apa: Möller, B., Ten Hove, C., Xiang, D., Williams, N., López, L., Yoshida, S.,
    … Weijers, D. (2017). Auxin response cell autonomously controls ground tissue
    initiation in the early arabidopsis embryo. <i>PNAS</i>. National Academy of Sciences.
    <a href="https://doi.org/10.1073/pnas.1616493114">https://doi.org/10.1073/pnas.1616493114</a>
  chicago: Möller, Barbara, Colette Ten Hove, Daoquan Xiang, Nerys Williams, Lorena
    López, Saiko Yoshida, Margot Smit, Raju Datla, and Dolf Weijers. “Auxin Response
    Cell Autonomously Controls Ground Tissue Initiation in the Early Arabidopsis Embryo.”
    <i>PNAS</i>. National Academy of Sciences, 2017. <a href="https://doi.org/10.1073/pnas.1616493114">https://doi.org/10.1073/pnas.1616493114</a>.
  ieee: B. Möller <i>et al.</i>, “Auxin response cell autonomously controls ground
    tissue initiation in the early arabidopsis embryo,” <i>PNAS</i>, vol. 114, no.
    12. National Academy of Sciences, pp. E2533–E2539, 2017.
  ista: Möller B, Ten Hove C, Xiang D, Williams N, López L, Yoshida S, Smit M, Datla
    R, Weijers D. 2017. Auxin response cell autonomously controls ground tissue initiation
    in the early arabidopsis embryo. PNAS. 114(12), E2533–E2539.
  mla: Möller, Barbara, et al. “Auxin Response Cell Autonomously Controls Ground Tissue
    Initiation in the Early Arabidopsis Embryo.” <i>PNAS</i>, vol. 114, no. 12, National
    Academy of Sciences, 2017, pp. E2533–39, doi:<a href="https://doi.org/10.1073/pnas.1616493114">10.1073/pnas.1616493114</a>.
  short: B. Möller, C. Ten Hove, D. Xiang, N. Williams, L. López, S. Yoshida, M. Smit,
    R. Datla, D. Weijers, PNAS 114 (2017) E2533–E2539.
date_created: 2018-12-11T11:47:45Z
date_published: 2017-03-21T00:00:00Z
date_updated: 2021-01-12T08:08:02Z
day: '21'
department:
- _id: JiFr
doi: 10.1073/pnas.1616493114
external_id:
  pmid:
  - '28265057'
intvolume: '       114'
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5373392/
month: '03'
oa: 1
oa_version: Submitted Version
page: E2533 - E2539
pmid: 1
publication: PNAS
publication_identifier:
  issn:
  - '00278424'
publication_status: published
publisher: National Academy of Sciences
publist_id: '7076'
quality_controlled: '1'
scopus_import: 1
status: public
title: Auxin response cell autonomously controls ground tissue initiation in the early
  arabidopsis embryo
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 114
year: '2017'
...
---
_id: '658'
abstract:
- lang: eng
  text: 'With the accelerated development of robot technologies, control becomes one
    of the central themes of research. In traditional approaches, the controller,
    by its internal functionality, finds appropriate actions on the basis of specific
    objectives for the task at hand. While very successful in many applications, self-organized
    control schemes seem to be favored in large complex systems with unknown dynamics
    or which are difficult to model. Reasons are the expected scalability, robustness,
    and resilience of self-organizing systems. The paper presents a self-learning
    neurocontroller based on extrinsic differential plasticity introduced recently,
    applying it to an anthropomorphic musculoskeletal robot arm with attached objects
    of unknown physical dynamics. The central finding of the paper is the following
    effect: by the mere feedback through the internal dynamics of the object, the
    robot is learning to relate each of the objects with a very specific sensorimotor
    pattern. Specifically, an attached pendulum pilots the arm into a circular motion,
    a half-filled bottle produces axis oriented shaking behavior, a wheel is getting
    rotated, and wiping patterns emerge automatically in a table-plus-brush setting.
    By these object-specific dynamical patterns, the robot may be said to recognize
    the object''s identity, or in other words, it discovers dynamical affordances
    of objects. Furthermore, when including hand coordinates obtained from a camera,
    a dedicated hand-eye coordination self-organizes spontaneously. These phenomena
    are discussed from a specific dynamical system perspective. Central is the dedicated
    working regime at the border to instability with its potentially infinite reservoir
    of (limit cycle) attractors &quot;waiting&quot; to be excited. Besides converging
    toward one of these attractors, variate behavior is also arising from a self-induced
    attractor morphing driven by the learning rule. We claim that experimental investigations
    with this anthropomorphic, self-learning robot not only generate interesting and
    potentially useful behaviors, but may also help to better understand what subjective
    human muscle feelings are, how they can be rooted in sensorimotor patterns, and
    how these concepts may feed back on robotics.'
article_number: '00008'
article_processing_charge: Yes
author:
- first_name: Ralf
  full_name: Der, Ralf
  last_name: Der
- first_name: Georg S
  full_name: Martius, Georg S
  id: 3A276B68-F248-11E8-B48F-1D18A9856A87
  last_name: Martius
citation:
  ama: Der R, Martius GS. Self organized behavior generation for musculoskeletal robots.
    <i>Frontiers in Neurorobotics</i>. 2017;11(MAR). doi:<a href="https://doi.org/10.3389/fnbot.2017.00008">10.3389/fnbot.2017.00008</a>
  apa: Der, R., &#38; Martius, G. S. (2017). Self organized behavior generation for
    musculoskeletal robots. <i>Frontiers in Neurorobotics</i>. Frontiers Research
    Foundation. <a href="https://doi.org/10.3389/fnbot.2017.00008">https://doi.org/10.3389/fnbot.2017.00008</a>
  chicago: Der, Ralf, and Georg S Martius. “Self Organized Behavior Generation for
    Musculoskeletal Robots.” <i>Frontiers in Neurorobotics</i>. Frontiers Research
    Foundation, 2017. <a href="https://doi.org/10.3389/fnbot.2017.00008">https://doi.org/10.3389/fnbot.2017.00008</a>.
  ieee: R. Der and G. S. Martius, “Self organized behavior generation for musculoskeletal
    robots,” <i>Frontiers in Neurorobotics</i>, vol. 11, no. MAR. Frontiers Research
    Foundation, 2017.
  ista: Der R, Martius GS. 2017. Self organized behavior generation for musculoskeletal
    robots. Frontiers in Neurorobotics. 11(MAR), 00008.
  mla: Der, Ralf, and Georg S. Martius. “Self Organized Behavior Generation for Musculoskeletal
    Robots.” <i>Frontiers in Neurorobotics</i>, vol. 11, no. MAR, 00008, Frontiers
    Research Foundation, 2017, doi:<a href="https://doi.org/10.3389/fnbot.2017.00008">10.3389/fnbot.2017.00008</a>.
  short: R. Der, G.S. Martius, Frontiers in Neurorobotics 11 (2017).
date_created: 2018-12-11T11:47:45Z
date_published: 2017-03-16T00:00:00Z
date_updated: 2021-01-12T08:08:04Z
day: '16'
ddc:
- '006'
department:
- _id: ChLa
- _id: GaTk
doi: 10.3389/fnbot.2017.00008
ec_funded: 1
file:
- access_level: open_access
  checksum: b1bc43f96d1df3313c03032c2a46388d
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:18:49Z
  date_updated: 2020-07-14T12:47:33Z
  file_id: '5371'
  file_name: IST-2017-903-v1+1_fnbot-11-00008.pdf
  file_size: 8439566
  relation: main_file
file_date_updated: 2020-07-14T12:47:33Z
has_accepted_license: '1'
intvolume: '        11'
issue: MAR
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
publication: Frontiers in Neurorobotics
publication_identifier:
  issn:
  - '16625218'
publication_status: published
publisher: Frontiers Research Foundation
publist_id: '7078'
pubrep_id: '903'
quality_controlled: '1'
scopus_import: 1
status: public
title: Self organized behavior generation for musculoskeletal robots
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2EBD1598-F248-11E8-B48F-1D18A9856A87
volume: 11
year: '2017'
...
---
_id: '659'
abstract:
- lang: eng
  text: Migration frequently involves Rac-mediated protrusion of lamellipodia, formed
    by Arp2/3 complex-dependent branching thought to be crucial for force generation
    and stability of these networks. The formins FMNL2 and FMNL3 are Cdc42 effectors
    targeting to the lamellipodium tip and shown here to nucleate and elongate actin
    filaments with complementary activities in vitro. In migrating B16-F1 melanoma
    cells, both formins contribute to the velocity of lamellipodium protrusion. Loss
    of FMNL2/3 function in melanoma cells and fibroblasts reduces lamellipodial width,
    actin filament density and -bundling, without changing patterns of Arp2/3 complex
    incorporation. Strikingly, in melanoma cells, FMNL2/3 gene inactivation almost
    completely abolishes protrusion forces exerted by lamellipodia and modifies their
    ultrastructural organization. Consistently, CRISPR/Cas-mediated depletion of FMNL2/3
    in fibroblasts reduces both migration and capability of cells to move against
    viscous media. Together, we conclude that force generation in lamellipodia strongly
    depends on FMNL formin activity, operating in addition to Arp2/3 complex-dependent
    filament branching.
article_number: '14832'
article_processing_charge: No
author:
- first_name: Frieda
  full_name: Kage, Frieda
  last_name: Kage
- first_name: Moritz
  full_name: Winterhoff, Moritz
  last_name: Winterhoff
- first_name: Vanessa
  full_name: Dimchev, Vanessa
  last_name: Dimchev
- first_name: Jan
  full_name: Müller, Jan
  id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
  last_name: Müller
- first_name: Tobias
  full_name: Thalheim, Tobias
  last_name: Thalheim
- first_name: Anika
  full_name: Freise, Anika
  last_name: Freise
- first_name: Stefan
  full_name: Brühmann, Stefan
  last_name: Brühmann
- first_name: Jana
  full_name: Kollasser, Jana
  last_name: Kollasser
- first_name: Jennifer
  full_name: Block, Jennifer
  last_name: Block
- first_name: Georgi A
  full_name: Dimchev, Georgi A
  last_name: Dimchev
- first_name: Matthias
  full_name: Geyer, Matthias
  last_name: Geyer
- first_name: Hams
  full_name: Schnittler, Hams
  last_name: Schnittler
- first_name: Cord
  full_name: Brakebusch, Cord
  last_name: Brakebusch
- first_name: Theresia
  full_name: Stradal, Theresia
  last_name: Stradal
- first_name: Marie
  full_name: Carlier, Marie
  last_name: Carlier
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
- first_name: Josef
  full_name: Käs, Josef
  last_name: Käs
- first_name: Jan
  full_name: Faix, Jan
  last_name: Faix
- first_name: Klemens
  full_name: Rottner, Klemens
  last_name: Rottner
citation:
  ama: Kage F, Winterhoff M, Dimchev V, et al. FMNL formins boost lamellipodial force
    generation. <i>Nature Communications</i>. 2017;8. doi:<a href="https://doi.org/10.1038/ncomms14832">10.1038/ncomms14832</a>
  apa: Kage, F., Winterhoff, M., Dimchev, V., Müller, J., Thalheim, T., Freise, A.,
    … Rottner, K. (2017). FMNL formins boost lamellipodial force generation. <i>Nature
    Communications</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/ncomms14832">https://doi.org/10.1038/ncomms14832</a>
  chicago: Kage, Frieda, Moritz Winterhoff, Vanessa Dimchev, Jan Müller, Tobias Thalheim,
    Anika Freise, Stefan Brühmann, et al. “FMNL Formins Boost Lamellipodial Force
    Generation.” <i>Nature Communications</i>. Nature Publishing Group, 2017. <a href="https://doi.org/10.1038/ncomms14832">https://doi.org/10.1038/ncomms14832</a>.
  ieee: F. Kage <i>et al.</i>, “FMNL formins boost lamellipodial force generation,”
    <i>Nature Communications</i>, vol. 8. Nature Publishing Group, 2017.
  ista: Kage F, Winterhoff M, Dimchev V, Müller J, Thalheim T, Freise A, Brühmann
    S, Kollasser J, Block J, Dimchev GA, Geyer M, Schnittler H, Brakebusch C, Stradal
    T, Carlier M, Sixt MK, Käs J, Faix J, Rottner K. 2017. FMNL formins boost lamellipodial
    force generation. Nature Communications. 8, 14832.
  mla: Kage, Frieda, et al. “FMNL Formins Boost Lamellipodial Force Generation.” <i>Nature
    Communications</i>, vol. 8, 14832, Nature Publishing Group, 2017, doi:<a href="https://doi.org/10.1038/ncomms14832">10.1038/ncomms14832</a>.
  short: F. Kage, M. Winterhoff, V. Dimchev, J. Müller, T. Thalheim, A. Freise, S.
    Brühmann, J. Kollasser, J. Block, G.A. Dimchev, M. Geyer, H. Schnittler, C. Brakebusch,
    T. Stradal, M. Carlier, M.K. Sixt, J. Käs, J. Faix, K. Rottner, Nature Communications
    8 (2017).
date_created: 2018-12-11T11:47:46Z
date_published: 2017-03-22T00:00:00Z
date_updated: 2021-01-12T08:08:06Z
day: '22'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1038/ncomms14832
file:
- access_level: open_access
  checksum: dae30190291c3630e8102d8714a8d23e
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:14:21Z
  date_updated: 2020-07-14T12:47:34Z
  file_id: '5072'
  file_name: IST-2017-902-v1+1_Kage_et_al-2017-Nature_Communications.pdf
  file_size: 9523746
  relation: main_file
file_date_updated: 2020-07-14T12:47:34Z
has_accepted_license: '1'
intvolume: '         8'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
  issn:
  - '20411723'
publication_status: published
publisher: Nature Publishing Group
publist_id: '7075'
pubrep_id: '902'
quality_controlled: '1'
scopus_import: 1
status: public
title: FMNL formins boost lamellipodial force generation
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2017'
...
---
_id: '660'
abstract:
- lang: eng
  text: Growing microtubules are protected from depolymerization by the presence of
    a GTP or GDP/Pi cap. End-binding proteins of the EB1 family bind to the stabilizing
    cap, allowing monitoring of its size in real time. The cap size has been shown
    to correlate with instantaneous microtubule stability. Here we have quantitatively
    characterized the properties of cap size fluctuations during steadystate growth
    and have developed a theory predicting their timescale and amplitude from the
    kinetics of microtubule growth and cap maturation. In contrast to growth speed
    fluctuations, cap size fluctuations show a characteristic timescale, which is
    defined by the lifetime of the cap sites. Growth fluctuations affect the amplitude
    of cap size fluctuations; however, cap size does not affect growth speed, indicating
    that microtubules are far from instability during most of their time of growth.
    Our theory provides the basis for a quantitative understanding of microtubule
    stability fluctuations during steady-state growth.
acknowledgement: We thank Philippe Cluzel for helpful discussions and Gunnar Pruessner
  for data analysis advice. This work was supported by the Francis Crick Institute,
  which receives its core funding from Cancer Research UK Grant FC001163, Medical
  Research Council Grant FC001163, and Wellcome Trust Grant FC001163. This work was
  also supported by European Research Council Advanced Grant Project 323042 (to C.D.
  and T.S.).
author:
- first_name: Jamie
  full_name: Rickman, Jamie
  last_name: Rickman
- first_name: Christian F
  full_name: Düllberg, Christian F
  id: 459064DC-F248-11E8-B48F-1D18A9856A87
  last_name: Düllberg
  orcid: 0000-0001-6335-9748
- first_name: Nicholas
  full_name: Cade, Nicholas
  last_name: Cade
- first_name: Lewis
  full_name: Griffin, Lewis
  last_name: Griffin
- first_name: Thomas
  full_name: Surrey, Thomas
  last_name: Surrey
citation:
  ama: Rickman J, Düllberg CF, Cade N, Griffin L, Surrey T. Steady state EB cap size
    fluctuations are determined by stochastic microtubule growth and maturation. <i>PNAS</i>.
    2017;114(13):3427-3432. doi:<a href="https://doi.org/10.1073/pnas.1620274114">10.1073/pnas.1620274114</a>
  apa: Rickman, J., Düllberg, C. F., Cade, N., Griffin, L., &#38; Surrey, T. (2017).
    Steady state EB cap size fluctuations are determined by stochastic microtubule
    growth and maturation. <i>PNAS</i>. National Academy of Sciences. <a href="https://doi.org/10.1073/pnas.1620274114">https://doi.org/10.1073/pnas.1620274114</a>
  chicago: Rickman, Jamie, Christian F Düllberg, Nicholas Cade, Lewis Griffin, and
    Thomas Surrey. “Steady State EB Cap Size Fluctuations Are Determined by Stochastic
    Microtubule Growth and Maturation.” <i>PNAS</i>. National Academy of Sciences,
    2017. <a href="https://doi.org/10.1073/pnas.1620274114">https://doi.org/10.1073/pnas.1620274114</a>.
  ieee: J. Rickman, C. F. Düllberg, N. Cade, L. Griffin, and T. Surrey, “Steady state
    EB cap size fluctuations are determined by stochastic microtubule growth and maturation,”
    <i>PNAS</i>, vol. 114, no. 13. National Academy of Sciences, pp. 3427–3432, 2017.
  ista: Rickman J, Düllberg CF, Cade N, Griffin L, Surrey T. 2017. Steady state EB
    cap size fluctuations are determined by stochastic microtubule growth and maturation.
    PNAS. 114(13), 3427–3432.
  mla: Rickman, Jamie, et al. “Steady State EB Cap Size Fluctuations Are Determined
    by Stochastic Microtubule Growth and Maturation.” <i>PNAS</i>, vol. 114, no. 13,
    National Academy of Sciences, 2017, pp. 3427–32, doi:<a href="https://doi.org/10.1073/pnas.1620274114">10.1073/pnas.1620274114</a>.
  short: J. Rickman, C.F. Düllberg, N. Cade, L. Griffin, T. Surrey, PNAS 114 (2017)
    3427–3432.
date_created: 2018-12-11T11:47:46Z
date_published: 2017-03-28T00:00:00Z
date_updated: 2021-01-12T08:08:09Z
day: '28'
department:
- _id: MaLo
doi: 10.1073/pnas.1620274114
external_id:
  pmid:
  - '28280102'
intvolume: '       114'
issue: '13'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380103/
month: '03'
oa: 1
oa_version: Submitted Version
page: 3427 - 3432
pmid: 1
publication: PNAS
publication_identifier:
  issn:
  - '00278424'
publication_status: published
publisher: National Academy of Sciences
publist_id: '7073'
quality_controlled: '1'
scopus_import: 1
status: public
title: Steady state EB cap size fluctuations are determined by stochastic microtubule
  growth and maturation
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 114
year: '2017'
...
---
_id: '661'
abstract:
- lang: eng
  text: During embryonic development, mechanical forces are essential for cellular
    rearrangements driving tissue morphogenesis. Here, we show that in the early zebrafish
    embryo, friction forces are generated at the interface between anterior axial
    mesoderm (prechordal plate, ppl) progenitors migrating towards the animal pole
    and neurectoderm progenitors moving in the opposite direction towards the vegetal
    pole of the embryo. These friction forces lead to global rearrangement of cells
    within the neurectoderm and determine the position of the neural anlage. Using
    a combination of experiments and simulations, we show that this process depends
    on hydrodynamic coupling between neurectoderm and ppl as a result of E-cadherin-mediated
    adhesion between those tissues. Our data thus establish the emergence of friction
    forces at the interface between moving tissues as a critical force-generating
    process shaping the embryo.
acknowledged_ssus:
- _id: SSU
author:
- first_name: Michael
  full_name: Smutny, Michael
  id: 3FE6E4E8-F248-11E8-B48F-1D18A9856A87
  last_name: Smutny
  orcid: 0000-0002-5920-9090
- first_name: Zsuzsa
  full_name: Ákos, Zsuzsa
  last_name: Ákos
- first_name: Silvia
  full_name: Grigolon, Silvia
  last_name: Grigolon
- first_name: Shayan
  full_name: Shamipour, Shayan
  id: 40B34FE2-F248-11E8-B48F-1D18A9856A87
  last_name: Shamipour
- first_name: Verena
  full_name: Ruprecht, Verena
  last_name: Ruprecht
- first_name: Daniel
  full_name: Capek, Daniel
  id: 31C42484-F248-11E8-B48F-1D18A9856A87
  last_name: Capek
  orcid: 0000-0001-5199-9940
- first_name: Martin
  full_name: Behrndt, Martin
  id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87
  last_name: Behrndt
- first_name: Ekaterina
  full_name: Papusheva, Ekaterina
  id: 41DB591E-F248-11E8-B48F-1D18A9856A87
  last_name: Papusheva
- first_name: Masazumi
  full_name: Tada, Masazumi
  last_name: Tada
- first_name: Björn
  full_name: Hof, Björn
  id: 3A374330-F248-11E8-B48F-1D18A9856A87
  last_name: Hof
  orcid: 0000-0003-2057-2754
- first_name: Tamás
  full_name: Vicsek, Tamás
  last_name: Vicsek
- first_name: Guillaume
  full_name: Salbreux, Guillaume
  last_name: Salbreux
- 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: Smutny M, Ákos Z, Grigolon S, et al. Friction forces position the neural anlage.
    <i>Nature Cell Biology</i>. 2017;19:306-317. doi:<a href="https://doi.org/10.1038/ncb3492">10.1038/ncb3492</a>
  apa: Smutny, M., Ákos, Z., Grigolon, S., Shamipour, S., Ruprecht, V., Capek, D.,
    … Heisenberg, C.-P. J. (2017). Friction forces position the neural anlage. <i>Nature
    Cell Biology</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/ncb3492">https://doi.org/10.1038/ncb3492</a>
  chicago: Smutny, Michael, Zsuzsa Ákos, Silvia Grigolon, Shayan Shamipour, Verena
    Ruprecht, Daniel Capek, Martin Behrndt, et al. “Friction Forces Position the Neural
    Anlage.” <i>Nature Cell Biology</i>. Nature Publishing Group, 2017. <a href="https://doi.org/10.1038/ncb3492">https://doi.org/10.1038/ncb3492</a>.
  ieee: M. Smutny <i>et al.</i>, “Friction forces position the neural anlage,” <i>Nature
    Cell Biology</i>, vol. 19. Nature Publishing Group, pp. 306–317, 2017.
  ista: Smutny M, Ákos Z, Grigolon S, Shamipour S, Ruprecht V, Capek D, Behrndt M,
    Papusheva E, Tada M, Hof B, Vicsek T, Salbreux G, Heisenberg C-PJ. 2017. Friction
    forces position the neural anlage. Nature Cell Biology. 19, 306–317.
  mla: Smutny, Michael, et al. “Friction Forces Position the Neural Anlage.” <i>Nature
    Cell Biology</i>, vol. 19, Nature Publishing Group, 2017, pp. 306–17, doi:<a href="https://doi.org/10.1038/ncb3492">10.1038/ncb3492</a>.
  short: M. Smutny, Z. Ákos, S. Grigolon, S. Shamipour, V. Ruprecht, D. Capek, M.
    Behrndt, E. Papusheva, M. Tada, B. Hof, T. Vicsek, G. Salbreux, C.-P.J. Heisenberg,
    Nature Cell Biology 19 (2017) 306–317.
date_created: 2018-12-11T11:47:46Z
date_published: 2017-03-27T00:00:00Z
date_updated: 2024-03-25T23:30:21Z
day: '27'
department:
- _id: CaHe
- _id: BjHo
- _id: Bio
doi: 10.1038/ncb3492
ec_funded: 1
external_id:
  pmid:
  - '28346437'
intvolume: '        19'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://europepmc.org/articles/pmc5635970
month: '03'
oa: 1
oa_version: Submitted Version
page: 306 - 317
pmid: 1
project:
- _id: 25152F3A-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '306589'
  name: Decoding the complexity of turbulence at its origin
- _id: 252ABD0A-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: I 930-B20
  name: Control of Epithelial Cell Layer Spreading in Zebrafish
publication: Nature Cell Biology
publication_identifier:
  issn:
  - '14657392'
publication_status: published
publisher: Nature Publishing Group
publist_id: '7074'
quality_controlled: '1'
related_material:
  record:
  - id: '50'
    relation: dissertation_contains
    status: public
  - id: '8350'
    relation: dissertation_contains
    status: public
scopus_import: 1
status: public
title: Friction forces position the neural anlage
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2017'
...
---
_id: '662'
abstract:
- lang: eng
  text: 'We report a direct-numerical-simulation study of the Taylor-Couette flow
    in the quasi-Keplerian regime at shear Reynolds numbers up to (105). Quasi-Keplerian
    rotating flow has been investigated for decades as a simplified model system to
    study the origin of turbulence in accretion disks that is not fully understood.
    The flow in this study is axially periodic and thus the experimental end-wall
    effects on the stability of the flow are avoided. Using optimal linear perturbations
    as initial conditions, our simulations find no sustained turbulence: the strong
    initial perturbations distort the velocity profile and trigger turbulence that
    eventually decays.'
article_number: '044107'
author:
- first_name: Liang
  full_name: Shi, Liang
  last_name: Shi
- first_name: Björn
  full_name: Hof, Björn
  id: 3A374330-F248-11E8-B48F-1D18A9856A87
  last_name: Hof
  orcid: 0000-0003-2057-2754
- first_name: Markus
  full_name: Rampp, Markus
  last_name: Rampp
- first_name: Marc
  full_name: Avila, Marc
  last_name: Avila
citation:
  ama: Shi L, Hof B, Rampp M, Avila M. Hydrodynamic turbulence in quasi Keplerian
    rotating flows. <i>Physics of Fluids</i>. 2017;29(4). doi:<a href="https://doi.org/10.1063/1.4981525">10.1063/1.4981525</a>
  apa: Shi, L., Hof, B., Rampp, M., &#38; Avila, M. (2017). Hydrodynamic turbulence
    in quasi Keplerian rotating flows. <i>Physics of Fluids</i>. American Institute
    of Physics. <a href="https://doi.org/10.1063/1.4981525">https://doi.org/10.1063/1.4981525</a>
  chicago: Shi, Liang, Björn Hof, Markus Rampp, and Marc Avila. “Hydrodynamic Turbulence
    in Quasi Keplerian Rotating Flows.” <i>Physics of Fluids</i>. American Institute
    of Physics, 2017. <a href="https://doi.org/10.1063/1.4981525">https://doi.org/10.1063/1.4981525</a>.
  ieee: L. Shi, B. Hof, M. Rampp, and M. Avila, “Hydrodynamic turbulence in quasi
    Keplerian rotating flows,” <i>Physics of Fluids</i>, vol. 29, no. 4. American
    Institute of Physics, 2017.
  ista: Shi L, Hof B, Rampp M, Avila M. 2017. Hydrodynamic turbulence in quasi Keplerian
    rotating flows. Physics of Fluids. 29(4), 044107.
  mla: Shi, Liang, et al. “Hydrodynamic Turbulence in Quasi Keplerian Rotating Flows.”
    <i>Physics of Fluids</i>, vol. 29, no. 4, 044107, American Institute of Physics,
    2017, doi:<a href="https://doi.org/10.1063/1.4981525">10.1063/1.4981525</a>.
  short: L. Shi, B. Hof, M. Rampp, M. Avila, Physics of Fluids 29 (2017).
date_created: 2018-12-11T11:47:47Z
date_published: 2017-04-01T00:00:00Z
date_updated: 2021-01-12T08:08:15Z
day: '01'
department:
- _id: BjHo
doi: 10.1063/1.4981525
intvolume: '        29'
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1703.01714
month: '04'
oa: 1
oa_version: Submitted Version
project:
- _id: 2511D90C-B435-11E9-9278-68D0E5697425
  grant_number: SFB 963  TP A8
  name: Astrophysical instability of currents and turbulences
publication: Physics of Fluids
publication_identifier:
  issn:
  - '10706631'
publication_status: published
publisher: American Institute of Physics
publist_id: '7072'
quality_controlled: '1'
scopus_import: 1
status: public
title: Hydrodynamic turbulence in quasi Keplerian rotating flows
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 29
year: '2017'
...
---
_id: '663'
abstract:
- lang: eng
  text: 'In this paper, we propose an approach to automatically compute invariant
    clusters for nonlinear semialgebraic hybrid systems. An invariant cluster for
    an ordinary differential equation (ODE) is a multivariate polynomial invariant
    g(u→, x→) = 0, parametric in u→, which can yield an infinite number of concrete
    invariants by assigning different values to u→ so that every trajectory of the
    system can be overapproximated precisely by the intersection of a group of concrete
    invariants. For semialgebraic systems, which involve ODEs with multivariate polynomial
    right-hand sides, given a template multivariate polynomial g(u→, x→), an invariant
    cluster can be obtained by first computing the remainder of the Lie derivative
    of g(u→, x→) divided by g(u→, x→) and then solving the system of polynomial equations
    obtained from the coefficients of the remainder. Based on invariant clusters and
    sum-of-squares (SOS) programming, we present a new method for the safety verification
    of hybrid systems. Experiments on nonlinear benchmark systems from biology and
    control theory show that our approach is efficient. '
author:
- first_name: Hui
  full_name: Kong, Hui
  id: 3BDE25AA-F248-11E8-B48F-1D18A9856A87
  last_name: Kong
  orcid: 0000-0002-3066-6941
- first_name: Sergiy
  full_name: Bogomolov, Sergiy
  last_name: Bogomolov
  orcid: 0000-0002-0686-0365
- first_name: Christian
  full_name: Schilling, Christian
  last_name: Schilling
- first_name: Yu
  full_name: Jiang, Yu
  last_name: Jiang
- first_name: Thomas A
  full_name: Henzinger, Thomas A
  id: 40876CD8-F248-11E8-B48F-1D18A9856A87
  last_name: Henzinger
  orcid: 0000−0002−2985−7724
citation:
  ama: 'Kong H, Bogomolov S, Schilling C, Jiang Y, Henzinger TA. Safety verification
    of nonlinear hybrid systems based on invariant clusters. In: <i>Proceedings of
    the 20th International Conference on Hybrid Systems</i>. ACM; 2017:163-172. doi:<a
    href="https://doi.org/10.1145/3049797.3049814">10.1145/3049797.3049814</a>'
  apa: 'Kong, H., Bogomolov, S., Schilling, C., Jiang, Y., &#38; Henzinger, T. A.
    (2017). Safety verification of nonlinear hybrid systems based on invariant clusters.
    In <i>Proceedings of the 20th International Conference on Hybrid Systems</i> (pp.
    163–172). Pittsburgh, PA, United States: ACM. <a href="https://doi.org/10.1145/3049797.3049814">https://doi.org/10.1145/3049797.3049814</a>'
  chicago: Kong, Hui, Sergiy Bogomolov, Christian Schilling, Yu Jiang, and Thomas
    A Henzinger. “Safety Verification of Nonlinear Hybrid Systems Based on Invariant
    Clusters.” In <i>Proceedings of the 20th International Conference on Hybrid Systems</i>,
    163–72. ACM, 2017. <a href="https://doi.org/10.1145/3049797.3049814">https://doi.org/10.1145/3049797.3049814</a>.
  ieee: H. Kong, S. Bogomolov, C. Schilling, Y. Jiang, and T. A. Henzinger, “Safety
    verification of nonlinear hybrid systems based on invariant clusters,” in <i>Proceedings
    of the 20th International Conference on Hybrid Systems</i>, Pittsburgh, PA, United
    States, 2017, pp. 163–172.
  ista: 'Kong H, Bogomolov S, Schilling C, Jiang Y, Henzinger TA. 2017. Safety verification
    of nonlinear hybrid systems based on invariant clusters. Proceedings of the 20th
    International Conference on Hybrid Systems. HSCC: Hybrid Systems Computation and
    Control , 163–172.'
  mla: Kong, Hui, et al. “Safety Verification of Nonlinear Hybrid Systems Based on
    Invariant Clusters.” <i>Proceedings of the 20th International Conference on Hybrid
    Systems</i>, ACM, 2017, pp. 163–72, doi:<a href="https://doi.org/10.1145/3049797.3049814">10.1145/3049797.3049814</a>.
  short: H. Kong, S. Bogomolov, C. Schilling, Y. Jiang, T.A. Henzinger, in:, Proceedings
    of the 20th International Conference on Hybrid Systems, ACM, 2017, pp. 163–172.
conference:
  end_date: 2017-04-20
  location: Pittsburgh, PA, United States
  name: 'HSCC: Hybrid Systems Computation and Control '
  start_date: 2017-04-18
date_created: 2018-12-11T11:47:47Z
date_published: 2017-04-01T00:00:00Z
date_updated: 2021-01-12T08:08:17Z
day: '01'
ddc:
- '000'
department:
- _id: ToHe
doi: 10.1145/3049797.3049814
file:
- access_level: open_access
  checksum: b7667434cbf5b5f0ade3bea1dbe5bf63
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:11:20Z
  date_updated: 2020-07-14T12:47:34Z
  file_id: '4873'
  file_name: IST-2017-817-v1+1_p163-kong.pdf
  file_size: 1650530
  relation: main_file
file_date_updated: 2020-07-14T12:47:34Z
has_accepted_license: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Submitted Version
page: 163 - 172
publication: Proceedings of the 20th International Conference on Hybrid Systems
publication_identifier:
  isbn:
  - 978-145034590-3
publication_status: published
publisher: ACM
publist_id: '7067'
pubrep_id: '817'
quality_controlled: '1'
scopus_import: 1
status: public
title: Safety verification of nonlinear hybrid systems based on invariant clusters
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2017'
...
---
_id: '664'
abstract:
- lang: eng
  text: Immune cells communicate using cytokine signals, but the quantitative rules
    of this communication aren't clear. In this issue of Immunity, Oyler-Yaniv et
    al. (2017) suggest that the distribution of a cytokine within a lymphatic organ
    is primarily governed by the local density of cells consuming it.
author:
- first_name: Frank P
  full_name: Assen, Frank P
  id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
  last_name: Assen
  orcid: 0000-0003-3470-6119
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
citation:
  ama: Assen FP, Sixt MK. The dynamic cytokine niche. <i>Immunity</i>. 2017;46(4):519-520.
    doi:<a href="https://doi.org/10.1016/j.immuni.2017.04.006">10.1016/j.immuni.2017.04.006</a>
  apa: Assen, F. P., &#38; Sixt, M. K. (2017). The dynamic cytokine niche. <i>Immunity</i>.
    Cell Press. <a href="https://doi.org/10.1016/j.immuni.2017.04.006">https://doi.org/10.1016/j.immuni.2017.04.006</a>
  chicago: Assen, Frank P, and Michael K Sixt. “The Dynamic Cytokine Niche.” <i>Immunity</i>.
    Cell Press, 2017. <a href="https://doi.org/10.1016/j.immuni.2017.04.006">https://doi.org/10.1016/j.immuni.2017.04.006</a>.
  ieee: F. P. Assen and M. K. Sixt, “The dynamic cytokine niche,” <i>Immunity</i>,
    vol. 46, no. 4. Cell Press, pp. 519–520, 2017.
  ista: Assen FP, Sixt MK. 2017. The dynamic cytokine niche. Immunity. 46(4), 519–520.
  mla: Assen, Frank P., and Michael K. Sixt. “The Dynamic Cytokine Niche.” <i>Immunity</i>,
    vol. 46, no. 4, Cell Press, 2017, pp. 519–20, doi:<a href="https://doi.org/10.1016/j.immuni.2017.04.006">10.1016/j.immuni.2017.04.006</a>.
  short: F.P. Assen, M.K. Sixt, Immunity 46 (2017) 519–520.
date_created: 2018-12-11T11:47:47Z
date_published: 2017-04-18T00:00:00Z
date_updated: 2024-03-25T23:30:05Z
day: '18'
department:
- _id: MiSi
doi: 10.1016/j.immuni.2017.04.006
intvolume: '        46'
issue: '4'
language:
- iso: eng
month: '04'
oa_version: None
page: 519 - 520
publication: Immunity
publication_identifier:
  issn:
  - '10747613'
publication_status: published
publisher: Cell Press
publist_id: '7065'
quality_controlled: '1'
related_material:
  record:
  - id: '6947'
    relation: dissertation_contains
    status: public
scopus_import: 1
status: public
title: The dynamic cytokine niche
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 46
year: '2017'
...
---
_id: '665'
abstract:
- lang: eng
  text: The molecular mechanisms underlying phenotypic variation in isogenic bacterial
    populations remain poorly understood.We report that AcrAB-TolC, the main multidrug
    efflux pump of Escherichia coli, exhibits a strong partitioning bias for old cell
    poles by a segregation mechanism that is mediated by ternary AcrAB-TolC complex
    formation. Mother cells inheriting old poles are phenotypically distinct and display
    increased drug efflux activity relative to daughters. Consequently, we find systematic
    and long-lived growth differences between mother and daughter cells in the presence
    of subinhibitory drug concentrations. A simple model for biased partitioning predicts
    a population structure of long-lived and highly heterogeneous phenotypes. This
    straightforward mechanism of generating sustained growth rate differences at subinhibitory
    antibiotic concentrations has implications for understanding the emergence of
    multidrug resistance in bacteria.
article_processing_charge: No
article_type: original
author:
- first_name: Tobias
  full_name: Bergmiller, Tobias
  id: 2C471CFA-F248-11E8-B48F-1D18A9856A87
  last_name: Bergmiller
  orcid: 0000-0001-5396-4346
- first_name: Anna M
  full_name: Andersson, Anna M
  id: 2B8A40DA-F248-11E8-B48F-1D18A9856A87
  last_name: Andersson
  orcid: 0000-0003-2912-6769
- first_name: Kathrin
  full_name: Tomasek, Kathrin
  id: 3AEC8556-F248-11E8-B48F-1D18A9856A87
  last_name: Tomasek
  orcid: 0000-0003-3768-877X
- first_name: Enrique
  full_name: Balleza, Enrique
  last_name: Balleza
- first_name: Daniel
  full_name: Kiviet, Daniel
  last_name: Kiviet
- first_name: Robert
  full_name: Hauschild, Robert
  id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
  last_name: Hauschild
  orcid: 0000-0001-9843-3522
- first_name: Gasper
  full_name: Tkacik, Gasper
  id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
  last_name: Tkacik
  orcid: 0000-0002-6699-1455
- first_name: Calin C
  full_name: Guet, Calin C
  id: 47F8433E-F248-11E8-B48F-1D18A9856A87
  last_name: Guet
  orcid: 0000-0001-6220-2052
citation:
  ama: Bergmiller T, Andersson AM, Tomasek K, et al. Biased partitioning of the multidrug
    efflux pump AcrAB TolC underlies long lived phenotypic heterogeneity. <i>Science</i>.
    2017;356(6335):311-315. doi:<a href="https://doi.org/10.1126/science.aaf4762">10.1126/science.aaf4762</a>
  apa: Bergmiller, T., Andersson, A. M., Tomasek, K., Balleza, E., Kiviet, D., Hauschild,
    R., … Guet, C. C. (2017). Biased partitioning of the multidrug efflux pump AcrAB
    TolC underlies long lived phenotypic heterogeneity. <i>Science</i>. American Association
    for the Advancement of Science. <a href="https://doi.org/10.1126/science.aaf4762">https://doi.org/10.1126/science.aaf4762</a>
  chicago: Bergmiller, Tobias, Anna M Andersson, Kathrin Tomasek, Enrique Balleza,
    Daniel Kiviet, Robert Hauschild, Gašper Tkačik, and Calin C Guet. “Biased Partitioning
    of the Multidrug Efflux Pump AcrAB TolC Underlies Long Lived Phenotypic Heterogeneity.”
    <i>Science</i>. American Association for the Advancement of Science, 2017. <a
    href="https://doi.org/10.1126/science.aaf4762">https://doi.org/10.1126/science.aaf4762</a>.
  ieee: T. Bergmiller <i>et al.</i>, “Biased partitioning of the multidrug efflux
    pump AcrAB TolC underlies long lived phenotypic heterogeneity,” <i>Science</i>,
    vol. 356, no. 6335. American Association for the Advancement of Science, pp. 311–315,
    2017.
  ista: Bergmiller T, Andersson AM, Tomasek K, Balleza E, Kiviet D, Hauschild R, Tkačik
    G, Guet CC. 2017. Biased partitioning of the multidrug efflux pump AcrAB TolC
    underlies long lived phenotypic heterogeneity. Science. 356(6335), 311–315.
  mla: Bergmiller, Tobias, et al. “Biased Partitioning of the Multidrug Efflux Pump
    AcrAB TolC Underlies Long Lived Phenotypic Heterogeneity.” <i>Science</i>, vol.
    356, no. 6335, American Association for the Advancement of Science, 2017, pp.
    311–15, doi:<a href="https://doi.org/10.1126/science.aaf4762">10.1126/science.aaf4762</a>.
  short: T. Bergmiller, A.M. Andersson, K. Tomasek, E. Balleza, D. Kiviet, R. Hauschild,
    G. Tkačik, C.C. Guet, Science 356 (2017) 311–315.
date_created: 2018-12-11T11:47:48Z
date_published: 2017-04-21T00:00:00Z
date_updated: 2024-02-21T13:49:00Z
day: '21'
department:
- _id: CaGu
- _id: GaTk
- _id: Bio
doi: 10.1126/science.aaf4762
intvolume: '       356'
issue: '6335'
language:
- iso: eng
month: '04'
oa_version: None
page: 311 - 315
project:
- _id: 254E9036-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P28844-B27
  name: Biophysics of information processing in gene regulation
publication: Science
publication_identifier:
  issn:
  - '00368075'
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7064'
quality_controlled: '1'
related_material:
  record:
  - id: '5560'
    relation: popular_science
    status: public
scopus_import: 1
status: public
title: Biased partitioning of the multidrug efflux pump AcrAB TolC underlies long
  lived phenotypic heterogeneity
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 356
year: '2017'
...
---
_id: '666'
abstract:
- lang: eng
  text: Antibiotics elicit drastic changes in microbial gene expression, including
    the induction of stress response genes. While certain stress responses are known
    to “cross-protect” bacteria from other stressors, it is unclear whether cellular
    responses to antibiotics have a similar protective role. By measuring the genome-wide
    transcriptional response dynamics of Escherichia coli to four antibiotics, we
    found that trimethoprim induces a rapid acid stress response that protects bacteria
    from subsequent exposure to acid. Combining microfluidics with time-lapse imaging
    to monitor survival and acid stress response in single cells revealed that the
    noisy expression of the acid resistance operon gadBC correlates with single-cell
    survival. Cells with higher gadBC expression following trimethoprim maintain higher
    intracellular pH and survive the acid stress longer. The seemingly random single-cell
    survival under acid stress can therefore be predicted from gadBC expression and
    rationalized in terms of GadB/C molecular function. Overall, we provide a roadmap
    for identifying the molecular mechanisms of single-cell cross-protection between
    antibiotics and other stressors.
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Karin
  full_name: Mitosch, Karin
  id: 39B66846-F248-11E8-B48F-1D18A9856A87
  last_name: Mitosch
- first_name: Georg
  full_name: Rieckh, Georg
  id: 34DA8BD6-F248-11E8-B48F-1D18A9856A87
  last_name: Rieckh
- first_name: Tobias
  full_name: Bollenbach, Tobias
  id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
  last_name: Bollenbach
  orcid: 0000-0003-4398-476X
citation:
  ama: Mitosch K, Rieckh G, Bollenbach MT. Noisy response to antibiotic stress predicts
    subsequent single cell survival in an acidic environment. <i>Cell Systems</i>.
    2017;4(4):393-403. doi:<a href="https://doi.org/10.1016/j.cels.2017.03.001">10.1016/j.cels.2017.03.001</a>
  apa: Mitosch, K., Rieckh, G., &#38; Bollenbach, M. T. (2017). Noisy response to
    antibiotic stress predicts subsequent single cell survival in an acidic environment.
    <i>Cell Systems</i>. Cell Press. <a href="https://doi.org/10.1016/j.cels.2017.03.001">https://doi.org/10.1016/j.cels.2017.03.001</a>
  chicago: Mitosch, Karin, Georg Rieckh, and Mark Tobias Bollenbach. “Noisy Response
    to Antibiotic Stress Predicts Subsequent Single Cell Survival in an Acidic Environment.”
    <i>Cell Systems</i>. Cell Press, 2017. <a href="https://doi.org/10.1016/j.cels.2017.03.001">https://doi.org/10.1016/j.cels.2017.03.001</a>.
  ieee: K. Mitosch, G. Rieckh, and M. T. Bollenbach, “Noisy response to antibiotic
    stress predicts subsequent single cell survival in an acidic environment,” <i>Cell
    Systems</i>, vol. 4, no. 4. Cell Press, pp. 393–403, 2017.
  ista: Mitosch K, Rieckh G, Bollenbach MT. 2017. Noisy response to antibiotic stress
    predicts subsequent single cell survival in an acidic environment. Cell Systems.
    4(4), 393–403.
  mla: Mitosch, Karin, et al. “Noisy Response to Antibiotic Stress Predicts Subsequent
    Single Cell Survival in an Acidic Environment.” <i>Cell Systems</i>, vol. 4, no.
    4, Cell Press, 2017, pp. 393–403, doi:<a href="https://doi.org/10.1016/j.cels.2017.03.001">10.1016/j.cels.2017.03.001</a>.
  short: K. Mitosch, G. Rieckh, M.T. Bollenbach, Cell Systems 4 (2017) 393–403.
date_created: 2018-12-11T11:47:48Z
date_published: 2017-04-26T00:00:00Z
date_updated: 2023-09-07T12:00:25Z
day: '26'
ddc:
- '576'
- '610'
department:
- _id: ToBo
- _id: GaTk
doi: 10.1016/j.cels.2017.03.001
ec_funded: 1
file:
- access_level: open_access
  checksum: 04ff20011c3d9a601c514aa999a5fe1a
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:13:54Z
  date_updated: 2020-07-14T12:47:35Z
  file_id: '5041'
  file_name: IST-2017-901-v1+1_1-s2.0-S2405471217300868-main.pdf
  file_size: 2438660
  relation: main_file
file_date_updated: 2020-07-14T12:47:35Z
has_accepted_license: '1'
intvolume: '         4'
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 393 - 403
project:
- _id: 25E83C2C-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '303507'
  name: Optimality principles in responses to antibiotics
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P27201-B22
  name: Revealing the mechanisms underlying drug interactions
- _id: 25EB3A80-B435-11E9-9278-68D0E5697425
  grant_number: RGP0042/2013
  name: Revealing the fundamental limits of cell growth
publication: Cell Systems
publication_identifier:
  issn:
  - '24054712'
publication_status: published
publisher: Cell Press
publist_id: '7061'
pubrep_id: '901'
quality_controlled: '1'
related_material:
  record:
  - id: '818'
    relation: dissertation_contains
    status: public
scopus_import: 1
status: public
title: Noisy response to antibiotic stress predicts subsequent single cell survival
  in an acidic environment
tmp:
  image: /images/cc_by_nc_nd.png
  legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
  name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
    (CC BY-NC-ND 4.0)
  short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 4
year: '2017'
...
---
_id: '667'
abstract:
- lang: eng
  text: Perinatal exposure to penicillin may result in longlasting gut and behavioral
    changes.
article_number: '2786'
author:
- first_name: Gaia
  full_name: Novarino, Gaia
  id: 3E57A680-F248-11E8-B48F-1D18A9856A87
  last_name: Novarino
  orcid: 0000-0002-7673-7178
citation:
  ama: Novarino G. The antisocial side of antibiotics. <i>Science Translational Medicine</i>.
    2017;9(387). doi:<a href="https://doi.org/10.1126/scitranslmed.aan2786">10.1126/scitranslmed.aan2786</a>
  apa: Novarino, G. (2017). The antisocial side of antibiotics. <i>Science Translational
    Medicine</i>. American Association for the Advancement of Science. <a href="https://doi.org/10.1126/scitranslmed.aan2786">https://doi.org/10.1126/scitranslmed.aan2786</a>
  chicago: Novarino, Gaia. “The Antisocial Side of Antibiotics.” <i>Science Translational
    Medicine</i>. American Association for the Advancement of Science, 2017. <a href="https://doi.org/10.1126/scitranslmed.aan2786">https://doi.org/10.1126/scitranslmed.aan2786</a>.
  ieee: G. Novarino, “The antisocial side of antibiotics,” <i>Science Translational
    Medicine</i>, vol. 9, no. 387. American Association for the Advancement of Science,
    2017.
  ista: Novarino G. 2017. The antisocial side of antibiotics. Science Translational
    Medicine. 9(387), 2786.
  mla: Novarino, Gaia. “The Antisocial Side of Antibiotics.” <i>Science Translational
    Medicine</i>, vol. 9, no. 387, 2786, American Association for the Advancement
    of Science, 2017, doi:<a href="https://doi.org/10.1126/scitranslmed.aan2786">10.1126/scitranslmed.aan2786</a>.
  short: G. Novarino, Science Translational Medicine 9 (2017).
date_created: 2018-12-11T11:47:48Z
date_published: 2017-04-26T00:00:00Z
date_updated: 2021-01-12T08:08:30Z
day: '26'
department:
- _id: GaNo
doi: 10.1126/scitranslmed.aan2786
intvolume: '         9'
issue: '387'
language:
- iso: eng
month: '04'
oa_version: None
publication: Science Translational Medicine
publication_identifier:
  issn:
  - '19466234'
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7060'
quality_controlled: '1'
scopus_import: 1
status: public
title: The antisocial side of antibiotics
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2017'
...
---
_id: '668'
abstract:
- lang: eng
  text: Macrophage filopodia, finger-like membrane protrusions, were first implicated
    in phagocytosis more than 100 years ago, but little is still known about the involvement
    of these actin-dependent structures in particle clearance. Using spinning disk
    confocal microscopy to image filopodial dynamics in mouse resident Lifeact-EGFP
    macrophages, we show that filopodia, or filopodia-like structures, support pathogen
    clearance by multiple means. Filopodia supported the phagocytic uptake of bacterial
    (Escherichia coli) particles by (i) capturing along the filopodial shaft and surfing
    toward the cell body, the most common mode of capture; (ii) capturing via the
    tip followed by retraction; (iii) combinations of surfing and retraction; or (iv)
    sweeping actions. In addition, filopodia supported the uptake of zymosan (Saccharomyces
    cerevisiae) particles by (i) providing fixation, (ii) capturing at the tip and
    filopodia-guided actin anterograde flow with phagocytic cup formation, and (iii)
    the rapid growth of new protrusions. To explore the role of filopodia-inducing
    Cdc42, we generated myeloid-restricted Cdc42 knock-out mice. Cdc42-deficient macrophages
    exhibited rapid phagocytic cup kinetics, but reduced particle clearance, which
    could be explained by the marked rounded-up morphology of these cells. Macrophages
    lacking Myo10, thought to act downstream of Cdc42, had normal morphology, motility,
    and phagocytic cup formation, but displayed markedly reduced filopodia formation.
    In conclusion, live-cell imaging revealed multiple mechanisms involving macrophage
    filopodia in particle capture and engulfment. Cdc42 is not critical for filopodia
    or phagocytic cup formation, but plays a key role in driving macrophage lamellipodial
    spreading.
article_type: original
author:
- first_name: Markus
  full_name: Horsthemke, Markus
  last_name: Horsthemke
- first_name: Anne
  full_name: Bachg, Anne
  last_name: Bachg
- first_name: Katharina
  full_name: Groll, Katharina
  last_name: Groll
- first_name: Sven
  full_name: Moyzio, Sven
  last_name: Moyzio
- first_name: Barbara
  full_name: Müther, Barbara
  last_name: Müther
- first_name: Sandra
  full_name: Hemkemeyer, Sandra
  last_name: Hemkemeyer
- first_name: Roland
  full_name: Wedlich Söldner, Roland
  last_name: Wedlich Söldner
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
- first_name: Sebastian
  full_name: Tacke, Sebastian
  last_name: Tacke
- first_name: Martin
  full_name: Bähler, Martin
  last_name: Bähler
- first_name: Peter
  full_name: Hanley, Peter
  last_name: Hanley
citation:
  ama: Horsthemke M, Bachg A, Groll K, et al. Multiple roles of filopodial dynamics
    in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion.
    <i>Journal of Biological Chemistry</i>. 2017;292(17):7258-7273. doi:<a href="https://doi.org/10.1074/jbc.M116.766923">10.1074/jbc.M116.766923</a>
  apa: Horsthemke, M., Bachg, A., Groll, K., Moyzio, S., Müther, B., Hemkemeyer, S.,
    … Hanley, P. (2017). Multiple roles of filopodial dynamics in particle capture
    and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. <i>Journal of Biological
    Chemistry</i>. American Society for Biochemistry and Molecular Biology. <a href="https://doi.org/10.1074/jbc.M116.766923">https://doi.org/10.1074/jbc.M116.766923</a>
  chicago: Horsthemke, Markus, Anne Bachg, Katharina Groll, Sven Moyzio, Barbara Müther,
    Sandra Hemkemeyer, Roland Wedlich Söldner, et al. “Multiple Roles of Filopodial
    Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10
    Deletion.” <i>Journal of Biological Chemistry</i>. American Society for Biochemistry
    and Molecular Biology, 2017. <a href="https://doi.org/10.1074/jbc.M116.766923">https://doi.org/10.1074/jbc.M116.766923</a>.
  ieee: M. Horsthemke <i>et al.</i>, “Multiple roles of filopodial dynamics in particle
    capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion,” <i>Journal
    of Biological Chemistry</i>, vol. 292, no. 17. American Society for Biochemistry
    and Molecular Biology, pp. 7258–7273, 2017.
  ista: Horsthemke M, Bachg A, Groll K, Moyzio S, Müther B, Hemkemeyer S, Wedlich
    Söldner R, Sixt MK, Tacke S, Bähler M, Hanley P. 2017. Multiple roles of filopodial
    dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10
    deletion. Journal of Biological Chemistry. 292(17), 7258–7273.
  mla: Horsthemke, Markus, et al. “Multiple Roles of Filopodial Dynamics in Particle
    Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” <i>Journal
    of Biological Chemistry</i>, vol. 292, no. 17, American Society for Biochemistry
    and Molecular Biology, 2017, pp. 7258–73, doi:<a href="https://doi.org/10.1074/jbc.M116.766923">10.1074/jbc.M116.766923</a>.
  short: M. Horsthemke, A. Bachg, K. Groll, S. Moyzio, B. Müther, S. Hemkemeyer, R.
    Wedlich Söldner, M.K. Sixt, S. Tacke, M. Bähler, P. Hanley, Journal of Biological
    Chemistry 292 (2017) 7258–7273.
date_created: 2018-12-11T11:47:49Z
date_published: 2017-04-28T00:00:00Z
date_updated: 2021-01-12T08:08:34Z
day: '28'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1074/jbc.M116.766923
file:
- access_level: open_access
  checksum: d488162874326a4bb056065fa549dc4a
  content_type: application/pdf
  creator: dernst
  date_created: 2019-10-24T15:25:42Z
  date_updated: 2020-07-14T12:47:37Z
  file_id: '6971'
  file_name: 2017_JBC_Horsthemke.pdf
  file_size: 5647880
  relation: main_file
file_date_updated: 2020-07-14T12:47:37Z
has_accepted_license: '1'
intvolume: '       292'
issue: '17'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 7258 - 7273
publication: Journal of Biological Chemistry
publication_identifier:
  issn:
  - '00219258'
publication_status: published
publisher: American Society for Biochemistry and Molecular Biology
publist_id: '7059'
quality_controlled: '1'
scopus_import: 1
status: public
title: Multiple roles of filopodial dynamics in particle capture and phagocytosis
  and phenotypes of Cdc42 and Myo10 deletion
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 292
year: '2017'
...
---
_id: '669'
abstract:
- lang: eng
  text: 'The exocyst, a eukaryotic tethering complex, coregulates targeted exocytosis
    as an effector of small GTPases in polarized cell growth. In land plants, several
    exocyst subunits are encoded by double or triple paralogs, culminating in tens
    of EXO70 paralogs. Out of 23 Arabidopsis thaliana EXO70 isoforms, we analyzed
    seven isoforms expressed in pollen. Genetic and microscopic analyses of single
    mutants in EXO70A2, EXO70C1, EXO70C2, EXO70F1, EXO70H3, EXO70H5, and EXO70H6 genes
    revealed that only a loss-of-function EXO70C2 allele resulted in a significant
    male-specific transmission defect (segregation 40%:51%:9%) due to aberrant pollen
    tube growth. Mutant pollen tubes grown in vitro exhibited an enhanced growth rate
    and a decreased thickness of the tip cell wall, causing tip bursts. However, exo70C2
    pollen tubes could frequently recover and restart their speedy elongation, resulting
    in a repetitive stop-and-go growth dynamics. A pollenspecific depletion of the
    closest paralog, EXO70C1, using artificial microRNA in the exo70C2 mutant background,
    resulted in a complete pollen-specific transmission defect, suggesting redundant
    functions of EXO70C1 and EXO70C2. Both EXO70C1 and EXO70C2, GFP tagged and expressed
    under the control of their native promoters, localized in the cytoplasm of pollen
    grains, pollen tubes, and also root trichoblast cells. The expression of EXO70C2-GFP
    complemented the aberrant growth of exo70C2 pollen tubes. The absent EXO70C2 interactions
    with core exocyst subunits in the yeast two-hybrid assay, cytoplasmic localization,
    and genetic effect suggest an unconventional EXO70 function possibly as a regulator
    of exocytosis outside the exocyst complex. In conclusion, EXO70C2 is a novel factor
    contributing to the regulation of optimal tip growth of Arabidopsis pollen tubes. '
article_processing_charge: No
article_type: original
author:
- first_name: Lukáš
  full_name: Synek, Lukáš
  last_name: Synek
- first_name: Nemanja
  full_name: Vukašinović, Nemanja
  last_name: Vukašinović
- first_name: Ivan
  full_name: Kulich, Ivan
  last_name: Kulich
- first_name: Michal
  full_name: Hála, Michal
  last_name: Hála
- first_name: Klára
  full_name: Aldorfová, Klára
  last_name: Aldorfová
- first_name: Matyas
  full_name: Fendrych, Matyas
  id: 43905548-F248-11E8-B48F-1D18A9856A87
  last_name: Fendrych
  orcid: 0000-0002-9767-8699
- first_name: Viktor
  full_name: Žárský, Viktor
  last_name: Žárský
citation:
  ama: Synek L, Vukašinović N, Kulich I, et al. EXO70C2 is a key regulatory factor
    for optimal tip growth of pollen. <i>Plant Physiology</i>. 2017;174(1):223-240.
    doi:<a href="https://doi.org/10.1104/pp.16.01282">10.1104/pp.16.01282</a>
  apa: Synek, L., Vukašinović, N., Kulich, I., Hála, M., Aldorfová, K., Fendrych,
    M., &#38; Žárský, V. (2017). EXO70C2 is a key regulatory factor for optimal tip
    growth of pollen. <i>Plant Physiology</i>. American Society of Plant Biologists.
    <a href="https://doi.org/10.1104/pp.16.01282">https://doi.org/10.1104/pp.16.01282</a>
  chicago: Synek, Lukáš, Nemanja Vukašinović, Ivan Kulich, Michal Hála, Klára Aldorfová,
    Matyas Fendrych, and Viktor Žárský. “EXO70C2 Is a Key Regulatory Factor for Optimal
    Tip Growth of Pollen.” <i>Plant Physiology</i>. American Society of Plant Biologists,
    2017. <a href="https://doi.org/10.1104/pp.16.01282">https://doi.org/10.1104/pp.16.01282</a>.
  ieee: L. Synek <i>et al.</i>, “EXO70C2 is a key regulatory factor for optimal tip
    growth of pollen,” <i>Plant Physiology</i>, vol. 174, no. 1. American Society
    of Plant Biologists, pp. 223–240, 2017.
  ista: Synek L, Vukašinović N, Kulich I, Hála M, Aldorfová K, Fendrych M, Žárský
    V. 2017. EXO70C2 is a key regulatory factor for optimal tip growth of pollen.
    Plant Physiology. 174(1), 223–240.
  mla: Synek, Lukáš, et al. “EXO70C2 Is a Key Regulatory Factor for Optimal Tip Growth
    of Pollen.” <i>Plant Physiology</i>, vol. 174, no. 1, American Society of Plant
    Biologists, 2017, pp. 223–40, doi:<a href="https://doi.org/10.1104/pp.16.01282">10.1104/pp.16.01282</a>.
  short: L. Synek, N. Vukašinović, I. Kulich, M. Hála, K. Aldorfová, M. Fendrych,
    V. Žárský, Plant Physiology 174 (2017) 223–240.
date_created: 2018-12-11T11:47:49Z
date_published: 2017-05-01T00:00:00Z
date_updated: 2021-01-12T08:08:35Z
day: '01'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.1104/pp.16.01282
external_id:
  pmid:
  - '28356503'
file:
- access_level: open_access
  checksum: 97155acc6aa5f0d0a78e0589a932fe02
  content_type: application/pdf
  creator: dernst
  date_created: 2019-11-18T16:16:18Z
  date_updated: 2020-07-14T12:47:37Z
  file_id: '7041'
  file_name: 2017_PlantPhysio_Synek.pdf
  file_size: 2176903
  relation: main_file
file_date_updated: 2020-07-14T12:47:37Z
has_accepted_license: '1'
intvolume: '       174'
issue: '1'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Submitted Version
page: 223 - 240
pmid: 1
publication: Plant Physiology
publication_identifier:
  issn:
  - '00320889'
publication_status: published
publisher: American Society of Plant Biologists
publist_id: '7058'
quality_controlled: '1'
scopus_import: 1
status: public
title: EXO70C2 is a key regulatory factor for optimal tip growth of pollen
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 174
year: '2017'
...
---
_id: '670'
abstract:
- lang: eng
  text: We propose an efficient method to model paper tearing in the context of interactive
    modeling. The method uses geometrical information to automatically detect potential
    starting points of tears. We further introduce a new hybrid geometrical and physical-based
    method to compute the trajectory of tears while procedurally synthesizing high
    resolution details of the tearing path using a texture based approach. The results
    obtained are compared with real paper and with previous studies on the expected
    geometric paths of paper that tears.
article_processing_charge: No
article_type: original
author:
- first_name: Camille
  full_name: Schreck, Camille
  id: 2B14B676-F248-11E8-B48F-1D18A9856A87
  last_name: Schreck
- first_name: Damien
  full_name: Rohmer, Damien
  last_name: Rohmer
- first_name: Stefanie
  full_name: Hahmann, Stefanie
  last_name: Hahmann
citation:
  ama: Schreck C, Rohmer D, Hahmann S. Interactive paper tearing. <i>Computer Graphics
    Forum</i>. 2017;36(2):95-106. doi:<a href="https://doi.org/10.1111/cgf.13110">10.1111/cgf.13110</a>
  apa: Schreck, C., Rohmer, D., &#38; Hahmann, S. (2017). Interactive paper tearing.
    <i>Computer Graphics Forum</i>. Wiley. <a href="https://doi.org/10.1111/cgf.13110">https://doi.org/10.1111/cgf.13110</a>
  chicago: Schreck, Camille, Damien Rohmer, and Stefanie Hahmann. “Interactive Paper
    Tearing.” <i>Computer Graphics Forum</i>. Wiley, 2017. <a href="https://doi.org/10.1111/cgf.13110">https://doi.org/10.1111/cgf.13110</a>.
  ieee: C. Schreck, D. Rohmer, and S. Hahmann, “Interactive paper tearing,” <i>Computer
    Graphics Forum</i>, vol. 36, no. 2. Wiley, pp. 95–106, 2017.
  ista: Schreck C, Rohmer D, Hahmann S. 2017. Interactive paper tearing. Computer
    Graphics Forum. 36(2), 95–106.
  mla: Schreck, Camille, et al. “Interactive Paper Tearing.” <i>Computer Graphics
    Forum</i>, vol. 36, no. 2, Wiley, 2017, pp. 95–106, doi:<a href="https://doi.org/10.1111/cgf.13110">10.1111/cgf.13110</a>.
  short: C. Schreck, D. Rohmer, S. Hahmann, Computer Graphics Forum 36 (2017) 95–106.
date_created: 2018-12-11T11:47:49Z
date_published: 2017-05-01T00:00:00Z
date_updated: 2021-01-12T08:08:37Z
day: '01'
ddc:
- '000'
department:
- _id: ChWo
doi: 10.1111/cgf.13110
intvolume: '        36'
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://hal.inria.fr/hal-01647113/file/eg_2017_schreck_paper_tearing.pdf
month: '05'
oa: 1
oa_version: Published Version
page: 95 - 106
project:
- _id: 25357BD2-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P 24352-N23
  name: 'Deep Pictures: Creating Visual and Haptic Vector Images'
publication: Computer Graphics Forum
publication_identifier:
  issn:
  - '01677055'
publication_status: published
publisher: Wiley
publist_id: '7056'
quality_controlled: '1'
scopus_import: 1
status: public
title: Interactive paper tearing
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 36
year: '2017'
...
---
_id: '671'
abstract:
- lang: eng
  text: Humans routinely use conditionally cooperative strategies when interacting
    in repeated social dilemmas. They are more likely to cooperate if others cooperated
    before, and are ready to retaliate if others defected. To capture the emergence
    of reciprocity, most previous models consider subjects who can only choose from
    a restricted set of representative strategies, or who react to the outcome of
    the very last round only. As players memorize more rounds, the dimension of the
    strategy space increases exponentially. This increasing computational complexity
    renders simulations for individuals with higher cognitive abilities infeasible,
    especially if multiplayer interactions are taken into account. Here, we take an
    axiomatic approach instead. We propose several properties that a robust cooperative
    strategy for a repeated multiplayer dilemma should have. These properties naturally
    lead to a unique class of cooperative strategies, which contains the classical
    Win-Stay Lose-Shift rule as a special case. A comprehensive numerical analysis
    for the prisoner's dilemma and for the public goods game suggests that strategies
    of this class readily evolve across various memory-n spaces. Our results reveal
    that successful strategies depend not only on how cooperative others were in the
    past but also on the respective context of cooperation.
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Christian
  full_name: Hilbe, Christian
  id: 2FDF8F3C-F248-11E8-B48F-1D18A9856A87
  last_name: Hilbe
  orcid: 0000-0001-5116-955X
- first_name: Vaquero
  full_name: Martinez, Vaquero
  last_name: Martinez
- first_name: Krishnendu
  full_name: Chatterjee, Krishnendu
  id: 2E5DCA20-F248-11E8-B48F-1D18A9856A87
  last_name: Chatterjee
  orcid: 0000-0002-4561-241X
- first_name: Martin
  full_name: Nowak, Martin
  last_name: Nowak
citation:
  ama: Hilbe C, Martinez V, Chatterjee K, Nowak M. Memory-n strategies of direct reciprocity.
    <i>PNAS</i>. 2017;114(18):4715-4720. doi:<a href="https://doi.org/10.1073/pnas.1621239114">10.1073/pnas.1621239114</a>
  apa: Hilbe, C., Martinez, V., Chatterjee, K., &#38; Nowak, M. (2017). Memory-n strategies
    of direct reciprocity. <i>PNAS</i>. National Academy of Sciences. <a href="https://doi.org/10.1073/pnas.1621239114">https://doi.org/10.1073/pnas.1621239114</a>
  chicago: Hilbe, Christian, Vaquero Martinez, Krishnendu Chatterjee, and Martin Nowak.
    “Memory-n Strategies of Direct Reciprocity.” <i>PNAS</i>. National Academy of
    Sciences, 2017. <a href="https://doi.org/10.1073/pnas.1621239114">https://doi.org/10.1073/pnas.1621239114</a>.
  ieee: C. Hilbe, V. Martinez, K. Chatterjee, and M. Nowak, “Memory-n strategies of
    direct reciprocity,” <i>PNAS</i>, vol. 114, no. 18. National Academy of Sciences,
    pp. 4715–4720, 2017.
  ista: Hilbe C, Martinez V, Chatterjee K, Nowak M. 2017. Memory-n strategies of direct
    reciprocity. PNAS. 114(18), 4715–4720.
  mla: Hilbe, Christian, et al. “Memory-n Strategies of Direct Reciprocity.” <i>PNAS</i>,
    vol. 114, no. 18, National Academy of Sciences, 2017, pp. 4715–20, doi:<a href="https://doi.org/10.1073/pnas.1621239114">10.1073/pnas.1621239114</a>.
  short: C. Hilbe, V. Martinez, K. Chatterjee, M. Nowak, PNAS 114 (2017) 4715–4720.
date_created: 2018-12-11T11:47:50Z
date_published: 2017-05-02T00:00:00Z
date_updated: 2021-01-12T08:08:37Z
day: '02'
department:
- _id: KrCh
doi: 10.1073/pnas.1621239114
ec_funded: 1
external_id:
  pmid:
  - '28420786'
intvolume: '       114'
issue: '18'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5422766/
month: '05'
oa: 1
oa_version: Published Version
page: 4715 - 4720
pmid: 1
project:
- _id: 2581B60A-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '279307'
  name: 'Quantitative Graph Games: Theory and Applications'
- _id: 2584A770-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P 23499-N23
  name: Modern Graph Algorithmic Techniques in Formal Verification
- _id: 25863FF4-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: S11407
  name: Game Theory
publication: PNAS
publication_identifier:
  issn:
  - '00278424'
publication_status: published
publisher: National Academy of Sciences
publist_id: '7053'
quality_controlled: '1'
scopus_import: 1
status: public
title: Memory-n strategies of direct reciprocity
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 114
year: '2017'
...
---
_id: '672'
abstract:
- lang: eng
  text: Trafficking cells frequently transmigrate through epithelial and endothelial
    monolayers. How monolayers cooperate with the penetrating cells to support their
    transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic
    capillaries as a model system for transendothelial migration. We find that the
    chemokine CCL21, which is the decisive guidance cue for intravasation, mainly
    localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial
    cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes
    extracellularly enriched at the sites of endothelial cell-cell junctions. When
    we reconstitute the transmigration process in vitro, we find that secretion of
    CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and
    selective calcium chelation in lymphatic endothelium attenuates transmigration.
    Altogether, our data demonstrate a chemokine-mediated feedback between DCs and
    lymphatic endothelium, which facilitates transendothelial migration.
article_processing_charge: Yes
author:
- first_name: Kari
  full_name: Vaahtomeri, Kari
  id: 368EE576-F248-11E8-B48F-1D18A9856A87
  last_name: Vaahtomeri
  orcid: 0000-0001-7829-3518
- first_name: Markus
  full_name: Brown, Markus
  id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
  last_name: Brown
- first_name: Robert
  full_name: Hauschild, Robert
  id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
  last_name: Hauschild
  orcid: 0000-0001-9843-3522
- first_name: Ingrid
  full_name: De Vries, Ingrid
  id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
  last_name: De Vries
- first_name: Alexander F
  full_name: Leithner, Alexander F
  id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
  last_name: Leithner
- first_name: Matthias
  full_name: Mehling, Matthias
  id: 3C23B994-F248-11E8-B48F-1D18A9856A87
  last_name: Mehling
  orcid: 0000-0001-8599-1226
- first_name: Walter
  full_name: Kaufmann, Walter
  id: 3F99E422-F248-11E8-B48F-1D18A9856A87
  last_name: Kaufmann
  orcid: 0000-0001-9735-5315
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
citation:
  ama: Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the
    chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia.
    <i>Cell Reports</i>. 2017;19(5):902-909. doi:<a href="https://doi.org/10.1016/j.celrep.2017.04.027">10.1016/j.celrep.2017.04.027</a>
  apa: Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling,
    M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes
    dendritic cell transmigration across lymphatic endothelia. <i>Cell Reports</i>.
    Cell Press. <a href="https://doi.org/10.1016/j.celrep.2017.04.027">https://doi.org/10.1016/j.celrep.2017.04.027</a>
  chicago: Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander
    F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered
    Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic
    Endothelia.” <i>Cell Reports</i>. Cell Press, 2017. <a href="https://doi.org/10.1016/j.celrep.2017.04.027">https://doi.org/10.1016/j.celrep.2017.04.027</a>.
  ieee: K. Vaahtomeri <i>et al.</i>, “Locally triggered release of the chemokine CCL21
    promotes dendritic cell transmigration across lymphatic endothelia,” <i>Cell Reports</i>,
    vol. 19, no. 5. Cell Press, pp. 902–909, 2017.
  ista: Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann
    W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic
    cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909.
  mla: Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21
    Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” <i>Cell Reports</i>,
    vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:<a href="https://doi.org/10.1016/j.celrep.2017.04.027">10.1016/j.celrep.2017.04.027</a>.
  short: K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling,
    W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.
date_created: 2018-12-11T11:47:50Z
date_published: 2017-05-02T00:00:00Z
date_updated: 2023-02-23T12:50:09Z
day: '02'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
- _id: EM-Fac
doi: 10.1016/j.celrep.2017.04.027
ec_funded: 1
file:
- access_level: open_access
  checksum: 8fdddaab1f1d76a6ec9ca94dcb6b07a2
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:14:54Z
  date_updated: 2020-07-14T12:47:38Z
  file_id: '5109'
  file_name: IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf
  file_size: 2248814
  relation: main_file
file_date_updated: 2020-07-14T12:47:38Z
has_accepted_license: '1'
intvolume: '        19'
issue: '5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 902 - 909
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '281556'
  name: Cytoskeletal force generation and force transduction of migrating leukocytes
    (EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: Y 564-B12
  name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Cell Reports
publication_identifier:
  issn:
  - '22111247'
publication_status: published
publisher: Cell Press
publist_id: '7052'
pubrep_id: '900'
quality_controlled: '1'
scopus_import: 1
status: public
title: Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration
  across lymphatic endothelia
tmp:
  image: /images/cc_by_nc_nd.png
  legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
  name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
    (CC BY-NC-ND 4.0)
  short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2017'
...
---
_id: '673'
abstract:
- lang: eng
  text: We present a numerical study of wavy supercritical cylindrical Couette flow
    between counter-rotating cylinders in which the wavy pattern propagates either
    prograde with the inner cylinder or retrograde opposite the rotation of the inner
    cylinder. The wave propagation reversals from prograde to retrograde and vice
    versa occur at distinct values of the inner cylinder Reynolds number when the
    associated frequency of the wavy instability vanishes. The reversal occurs for
    both twofold and threefold symmetric wavy vortices. Moreover, the wave propagation
    reversal only occurs for sufficiently strong counter-rotation. The flow pattern
    reversal appears to be intrinsic in the system as either periodic boundary conditions
    or fixed end wall boundary conditions for different system sizes always result
    in the wave propagation reversal. We present a detailed bifurcation sequence and
    parameter space diagram with respect to retrograde behavior of wavy flows. The
    retrograde propagation of the instability occurs when the inner Reynolds number
    is about two times the outer Reynolds number. The mechanism for the retrograde
    propagation is associated with the inviscidly unstable region near the inner cylinder
    and the direction of the global average azimuthal velocity. Flow dynamics, spatio-temporal
    behavior, global mean angular velocity, and torque of the flow with the wavy pattern
    are explored.
article_number: '053103'
article_processing_charge: No
author:
- first_name: Sebastian
  full_name: Altmeyer, Sebastian
  id: 2EE67FDC-F248-11E8-B48F-1D18A9856A87
  last_name: Altmeyer
  orcid: 0000-0001-5964-0203
- first_name: Richard
  full_name: Lueptow, Richard
  last_name: Lueptow
citation:
  ama: Altmeyer S, Lueptow R. Wave propagation reversal for wavy vortices in wide
    gap counter rotating cylindrical Couette flow. <i>Physical Review E</i>. 2017;95(5).
    doi:<a href="https://doi.org/10.1103/PhysRevE.95.053103">10.1103/PhysRevE.95.053103</a>
  apa: Altmeyer, S., &#38; Lueptow, R. (2017). Wave propagation reversal for wavy
    vortices in wide gap counter rotating cylindrical Couette flow. <i>Physical Review
    E</i>. American Physical Society. <a href="https://doi.org/10.1103/PhysRevE.95.053103">https://doi.org/10.1103/PhysRevE.95.053103</a>
  chicago: Altmeyer, Sebastian, and Richard Lueptow. “Wave Propagation Reversal for
    Wavy Vortices in Wide Gap Counter Rotating Cylindrical Couette Flow.” <i>Physical
    Review E</i>. American Physical Society, 2017. <a href="https://doi.org/10.1103/PhysRevE.95.053103">https://doi.org/10.1103/PhysRevE.95.053103</a>.
  ieee: S. Altmeyer and R. Lueptow, “Wave propagation reversal for wavy vortices in
    wide gap counter rotating cylindrical Couette flow,” <i>Physical Review E</i>,
    vol. 95, no. 5. American Physical Society, 2017.
  ista: Altmeyer S, Lueptow R. 2017. Wave propagation reversal for wavy vortices in
    wide gap counter rotating cylindrical Couette flow. Physical Review E. 95(5),
    053103.
  mla: Altmeyer, Sebastian, and Richard Lueptow. “Wave Propagation Reversal for Wavy
    Vortices in Wide Gap Counter Rotating Cylindrical Couette Flow.” <i>Physical Review
    E</i>, vol. 95, no. 5, 053103, American Physical Society, 2017, doi:<a href="https://doi.org/10.1103/PhysRevE.95.053103">10.1103/PhysRevE.95.053103</a>.
  short: S. Altmeyer, R. Lueptow, Physical Review E 95 (2017).
date_created: 2018-12-11T11:47:50Z
date_published: 2017-05-10T00:00:00Z
date_updated: 2023-10-10T13:30:03Z
day: '10'
department:
- _id: BjHo
doi: 10.1103/PhysRevE.95.053103
intvolume: '        95'
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/pdf/physics/0505164.pdf
month: '05'
oa: 1
oa_version: Submitted Version
publication: Physical Review E
publication_identifier:
  issn:
  - 2470-0045
publication_status: published
publisher: American Physical Society
publist_id: '7049'
scopus_import: '1'
status: public
title: Wave propagation reversal for wavy vortices in wide gap counter rotating cylindrical
  Couette flow
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 95
year: '2017'
...
---
_id: '674'
abstract:
- lang: eng
  text: Navigation of cells along gradients of guidance cues is a determining step
    in many developmental and immunological processes. Gradients can either be soluble
    or immobilized to tissues as demonstrated for the haptotactic migration of dendritic
    cells (DCs) toward higher concentrations of immobilized chemokine CCL21. To elucidate
    how gradient characteristics govern cellular response patterns, we here introduce
    an in vitro system allowing to track migratory responses of DCs to precisely controlled
    immobilized gradients of CCL21. We find that haptotactic sensing depends on the
    absolute CCL21 concentration and local steepness of the gradient, consistent with
    a scenario where DC directionality is governed by the signal-to-noise ratio of
    CCL21 binding to the receptor CCR7. We find that the conditions for optimal DC
    guidance are perfectly provided by the CCL21 gradients we measure in vivo. Furthermore,
    we find that CCR7 signal termination by the G-protein-coupled receptor kinase
    6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient
    sensing in vitro and confirm those observations in vivo. These findings suggest
    that stable, tissue-bound CCL21 gradients as sustainable “roads” ensure optimal
    guidance in vivo.
author:
- first_name: Jan
  full_name: Schwarz, Jan
  id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
  last_name: Schwarz
- first_name: Veronika
  full_name: Bierbaum, Veronika
  id: 3FD04378-F248-11E8-B48F-1D18A9856A87
  last_name: Bierbaum
- first_name: Kari
  full_name: Vaahtomeri, Kari
  id: 368EE576-F248-11E8-B48F-1D18A9856A87
  last_name: Vaahtomeri
  orcid: 0000-0001-7829-3518
- first_name: Robert
  full_name: Hauschild, Robert
  id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
  last_name: Hauschild
  orcid: 0000-0001-9843-3522
- first_name: Markus
  full_name: Brown, Markus
  id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
  last_name: Brown
- first_name: Ingrid
  full_name: De Vries, Ingrid
  id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
  last_name: De Vries
- first_name: Alexander F
  full_name: Leithner, Alexander F
  id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
  last_name: Leithner
- first_name: Anne
  full_name: Reversat, Anne
  id: 35B76592-F248-11E8-B48F-1D18A9856A87
  last_name: Reversat
  orcid: 0000-0003-0666-8928
- first_name: Jack
  full_name: Merrin, Jack
  id: 4515C308-F248-11E8-B48F-1D18A9856A87
  last_name: Merrin
  orcid: 0000-0001-5145-4609
- first_name: Teresa
  full_name: Tarrant, Teresa
  last_name: Tarrant
- first_name: Tobias
  full_name: Bollenbach, Tobias
  id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
  last_name: Bollenbach
  orcid: 0000-0003-4398-476X
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
citation:
  ama: Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic
    chemokine gradients in a manner governed by signal to noise ratio and dependent
    on GRK6. <i>Current Biology</i>. 2017;27(9):1314-1325. doi:<a href="https://doi.org/10.1016/j.cub.2017.04.004">10.1016/j.cub.2017.04.004</a>
  apa: Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries,
    I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients
    in a manner governed by signal to noise ratio and dependent on GRK6. <i>Current
    Biology</i>. Cell Press. <a href="https://doi.org/10.1016/j.cub.2017.04.004">https://doi.org/10.1016/j.cub.2017.04.004</a>
  chicago: Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus
    Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret
    Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio
    and Dependent on GRK6.” <i>Current Biology</i>. Cell Press, 2017. <a href="https://doi.org/10.1016/j.cub.2017.04.004">https://doi.org/10.1016/j.cub.2017.04.004</a>.
  ieee: J. Schwarz <i>et al.</i>, “Dendritic cells interpret haptotactic chemokine
    gradients in a manner governed by signal to noise ratio and dependent on GRK6,”
    <i>Current Biology</i>, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017.
  ista: Schwarz J, Bierbaum V, Vaahtomeri K, Hauschild R, Brown M, de Vries I, Leithner
    AF, Reversat A, Merrin J, Tarrant T, Bollenbach MT, Sixt MK. 2017. Dendritic cells
    interpret haptotactic chemokine gradients in a manner governed by signal to noise
    ratio and dependent on GRK6. Current Biology. 27(9), 1314–1325.
  mla: Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients
    in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” <i>Current
    Biology</i>, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:<a href="https://doi.org/10.1016/j.cub.2017.04.004">10.1016/j.cub.2017.04.004</a>.
  short: J. Schwarz, V. Bierbaum, K. Vaahtomeri, R. Hauschild, M. Brown, I. de Vries,
    A.F. Leithner, A. Reversat, J. Merrin, T. Tarrant, M.T. Bollenbach, M.K. Sixt,
    Current Biology 27 (2017) 1314–1325.
date_created: 2018-12-11T11:47:51Z
date_published: 2017-05-09T00:00:00Z
date_updated: 2023-02-23T12:50:44Z
day: '09'
department:
- _id: MiSi
- _id: Bio
- _id: NanoFab
doi: 10.1016/j.cub.2017.04.004
ec_funded: 1
intvolume: '        27'
issue: '9'
language:
- iso: eng
month: '05'
oa_version: None
page: 1314 - 1325
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: Y 564-B12
  name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Current Biology
publication_identifier:
  issn:
  - '09609822'
publication_status: published
publisher: Cell Press
publist_id: '7050'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dendritic cells interpret haptotactic chemokine gradients in a manner governed
  by signal to noise ratio and dependent on GRK6
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 27
year: '2017'
...
---
_id: '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:
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month: '05'
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oa_version: Published Version
page: 1798 - 1806
pmid: 1
publication: Development
publication_identifier:
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  - '09501991'
publication_status: published
publisher: Company of Biologists
publist_id: '7047'
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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:
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  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'
...
