---
_id: '544'
abstract:
- lang: eng
  text: Drosophila melanogaster plasmatocytes, the phagocytic cells among hemocytes,
    are essential for immune responses, but also play key roles from early development
    to death through their interactions with other cell types. They regulate homeostasis
    and signaling during development, stem cell proliferation, metabolism, cancer,
    wound responses and aging, displaying intriguing molecular and functional conservation
    with vertebrate macrophages. Given the relative ease of genetics in Drosophila
    compared to vertebrates, tools permitting visualization and genetic manipulation
    of plasmatocytes and surrounding tissues independently at all stages would greatly
    aid in fully understanding these processes, but are lacking. Here we describe
    a comprehensive set of transgenic lines that allow this. These include extremely
    brightly fluorescing mCherry-based lines that allow GAL4-independent visualization
    of plasmatocyte nuclei, cytoplasm or actin cytoskeleton from embryonic Stage 8
    through adulthood in both live and fixed samples even as heterozygotes, greatly
    facilitating screening. These lines allow live visualization and tracking of embryonic
    plasmatocytes, as well as larval plasmatocytes residing at the body wall or flowing
    with the surrounding hemolymph. With confocal imaging, interactions of plasmatocytes
    and inner tissues can be seen in live or fixed embryos, larvae and adults. They
    permit efficient GAL4-independent FACS analysis/sorting of plasmatocytes throughout
    life. To facilitate genetic analysis of reciprocal signaling, we have also made
    a plasmatocyte-expressing QF2 line that in combination with extant GAL4 drivers
    allows independent genetic manipulation of both plasmatocytes and surrounding
    tissues, and a GAL80 line that blocks GAL4 drivers from affecting plasmatocytes,
    both of which function from the early embryo to the adult.
acknowledged_ssus:
- _id: LifeSc
acknowledgement: ' A. Ratheesh also by Marie Curie IIF GA-2012-32950BB:DICJI, Marko
  Roblek by the provincial government of Lower Austria, K. Valoskova and S. Wachner
  by DOC Fellowships from the Austrian Academy of Sciences, '
article_processing_charge: No
author:
- first_name: Attila
  full_name: György, Attila
  id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
  last_name: György
  orcid: 0000-0002-1819-198X
- first_name: Marko
  full_name: Roblek, Marko
  id: 3047D808-F248-11E8-B48F-1D18A9856A87
  last_name: Roblek
  orcid: 0000-0001-9588-1389
- first_name: Aparna
  full_name: Ratheesh, Aparna
  id: 2F064CFE-F248-11E8-B48F-1D18A9856A87
  last_name: Ratheesh
  orcid: 0000-0001-7190-0776
- first_name: Katarina
  full_name: Valosková, Katarina
  id: 46F146FC-F248-11E8-B48F-1D18A9856A87
  last_name: Valosková
  orcid: 0000-0002-7926-0221
- first_name: Vera
  full_name: Belyaeva, Vera
  id: 47F080FE-F248-11E8-B48F-1D18A9856A87
  last_name: Belyaeva
- first_name: Stephanie
  full_name: Wachner, Stephanie
  id: 2A95E7B0-F248-11E8-B48F-1D18A9856A87
  last_name: Wachner
- first_name: Yutaka
  full_name: Matsubayashi, Yutaka
  last_name: Matsubayashi
- first_name: Besaiz
  full_name: Sanchez Sanchez, Besaiz
  last_name: Sanchez Sanchez
- first_name: Brian
  full_name: Stramer, Brian
  last_name: Stramer
- first_name: Daria E
  full_name: Siekhaus, Daria E
  id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
  last_name: Siekhaus
  orcid: 0000-0001-8323-8353
citation:
  ama: 'György A, Roblek M, Ratheesh A, et al. Tools allowing independent visualization
    and genetic manipulation of Drosophila melanogaster macrophages and surrounding
    tissues. <i>G3: Genes, Genomes, Genetics</i>. 2018;8(3):845-857. doi:<a href="https://doi.org/10.1534/g3.117.300452">10.1534/g3.117.300452</a>'
  apa: 'György, A., Roblek, M., Ratheesh, A., Valosková, K., Belyaeva, V., Wachner,
    S., … Siekhaus, D. E. (2018). Tools allowing independent visualization and genetic
    manipulation of Drosophila melanogaster macrophages and surrounding tissues. <i>G3:
    Genes, Genomes, Genetics</i>. Genetics Society of America. <a href="https://doi.org/10.1534/g3.117.300452">https://doi.org/10.1534/g3.117.300452</a>'
  chicago: 'György, Attila, Marko Roblek, Aparna Ratheesh, Katarina Valosková, Vera
    Belyaeva, Stephanie Wachner, Yutaka Matsubayashi, Besaiz Sanchez Sanchez, Brian
    Stramer, and Daria E Siekhaus. “Tools Allowing Independent Visualization and Genetic
    Manipulation of Drosophila Melanogaster Macrophages and Surrounding Tissues.”
    <i>G3: Genes, Genomes, Genetics</i>. Genetics Society of America, 2018. <a href="https://doi.org/10.1534/g3.117.300452">https://doi.org/10.1534/g3.117.300452</a>.'
  ieee: 'A. György <i>et al.</i>, “Tools allowing independent visualization and genetic
    manipulation of Drosophila melanogaster macrophages and surrounding tissues,”
    <i>G3: Genes, Genomes, Genetics</i>, vol. 8, no. 3. Genetics Society of America,
    pp. 845–857, 2018.'
  ista: 'György A, Roblek M, Ratheesh A, Valosková K, Belyaeva V, Wachner S, Matsubayashi
    Y, Sanchez Sanchez B, Stramer B, Siekhaus DE. 2018. Tools allowing independent
    visualization and genetic manipulation of Drosophila melanogaster macrophages
    and surrounding tissues. G3: Genes, Genomes, Genetics. 8(3), 845–857.'
  mla: 'György, Attila, et al. “Tools Allowing Independent Visualization and Genetic
    Manipulation of Drosophila Melanogaster Macrophages and Surrounding Tissues.”
    <i>G3: Genes, Genomes, Genetics</i>, vol. 8, no. 3, Genetics Society of America,
    2018, pp. 845–57, doi:<a href="https://doi.org/10.1534/g3.117.300452">10.1534/g3.117.300452</a>.'
  short: 'A. György, M. Roblek, A. Ratheesh, K. Valosková, V. Belyaeva, S. Wachner,
    Y. Matsubayashi, B. Sanchez Sanchez, B. Stramer, D.E. Siekhaus, G3: Genes, Genomes,
    Genetics 8 (2018) 845–857.'
corr_author: '1'
date_created: 2018-12-11T11:47:05Z
date_published: 2018-03-01T00:00:00Z
date_updated: 2026-08-10T22:30:25Z
day: '01'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.1534/g3.117.300452
ec_funded: 1
external_id:
  isi:
  - '000426693300011'
file:
- access_level: open_access
  checksum: 7d9d28b915159078a4ca7add568010e8
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:11:48Z
  date_updated: 2020-07-14T12:46:56Z
  file_id: '4905'
  file_name: IST-2018-990-v1+1_2018_Gyoergy_Tools_allowing.pdf
  file_size: 2251222
  relation: main_file
file_date_updated: 2020-07-14T12:46:56Z
has_accepted_license: '1'
intvolume: '         8'
isi: 1
issue: '3'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 845 - 857
project:
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P29638
  name: The role of Drosophila TNF alpha in immune cell invasion
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P29638
  name: The role of Drosophila TNF alpha in immune cell invasion
- _id: 2637E9C0-B435-11E9-9278-68D0E5697425
  grant_number: LSC16-021
  name: Investigating the role of the novel major superfamily facilitator transporter
    family member MFSD1 in metastasis
- _id: 2536F660-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '334077'
  name: Investigating the role of transporters in invasive migration through junctions
publication: 'G3: Genes, Genomes, Genetics'
publication_status: published
publisher: Genetics Society of America
publist_id: '7271'
pubrep_id: '990'
quality_controlled: '1'
related_material:
  record:
  - id: '6530'
    relation: research_paper
  - id: '6543'
    relation: research_paper
  - id: '11193'
    relation: dissertation_contains
    status: public
  - id: '6546'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Tools allowing independent visualization and genetic manipulation of Drosophila
  melanogaster macrophages and surrounding tissues
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 8
year: '2018'
...
---
_id: '15'
abstract:
- lang: eng
  text: Although much is known about the physiological framework of T cell motility,
    and numerous rate-limiting molecules have been identified through loss-of-function
    approaches, an integrated functional concept of T cell motility is lacking. Here,
    we used in vivo precision morphometry together with analysis of cytoskeletal dynamics
    in vitro to deconstruct the basic mechanisms of T cell migration within lymphatic
    organs. We show that the contributions of the integrin LFA-1 and the chemokine
    receptor CCR7 are complementary rather than positioned in a linear pathway, as
    they are during leukocyte extravasation from the blood vasculature. Our data demonstrate
    that CCR7 controls cortical actin flows, whereas integrins mediate substrate friction
    that is sufficient to drive locomotion in the absence of considerable surface
    adhesions and plasma membrane flux.
acknowledged_ssus:
- _id: SSU
acknowledgement: This work was funded by grants from the European Research Council
  (ERC StG 281556 and CoG 724373) and the Austrian Science Foundation (FWF) to M.S.
  and by Swiss National Foundation (SNF) project grants 31003A_135649, 31003A_153457
  and CR23I3_156234 to J.V.S. F.G. received funding from the European Union’s Horizon
  2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement
  no. 747687, and J.R. was funded by an EMBO long-term fellowship (ALTF 1396-2014).
article_processing_charge: No
author:
- first_name: Miroslav
  full_name: Hons, Miroslav
  id: 4167FE56-F248-11E8-B48F-1D18A9856A87
  last_name: Hons
  orcid: 0000-0002-6625-3348
- first_name: Aglaja
  full_name: Kopf, Aglaja
  id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
  last_name: Kopf
  orcid: 0000-0002-2187-6656
- first_name: Robert
  full_name: Hauschild, Robert
  id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
  last_name: Hauschild
  orcid: 0000-0001-9843-3522
- first_name: Alexander F
  full_name: Leithner, Alexander F
  id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
  last_name: Leithner
  orcid: 0000-0002-1073-744X
- first_name: Florian R
  full_name: Gärtner, Florian R
  id: 397A88EE-F248-11E8-B48F-1D18A9856A87
  last_name: Gärtner
  orcid: 0000-0001-6120-3723
- first_name: Jun
  full_name: Abe, Jun
  last_name: Abe
- first_name: Jörg
  full_name: Renkawitz, Jörg
  id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
  last_name: Renkawitz
  orcid: 0000-0003-2856-3369
- first_name: Jens
  full_name: Stein, Jens
  last_name: Stein
- 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: Hons M, Kopf A, Hauschild R, et al. Chemokines and integrins independently
    tune actin flow and substrate friction during intranodal migration of T cells.
    <i>Nature Immunology</i>. 2018;19(6):606-616. doi:<a href="https://doi.org/10.1038/s41590-018-0109-z">10.1038/s41590-018-0109-z</a>
  apa: Hons, M., Kopf, A., Hauschild, R., Leithner, A. F., Gärtner, F. R., Abe, J.,
    … Sixt, M. K. (2018). Chemokines and integrins independently tune actin flow and
    substrate friction during intranodal migration of T cells. <i>Nature Immunology</i>.
    Nature Publishing Group. <a href="https://doi.org/10.1038/s41590-018-0109-z">https://doi.org/10.1038/s41590-018-0109-z</a>
  chicago: Hons, Miroslav, Aglaja Kopf, Robert Hauschild, Alexander F Leithner, Florian
    R Gärtner, Jun Abe, Jörg Renkawitz, Jens Stein, and Michael K Sixt. “Chemokines
    and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal
    Migration of T Cells.” <i>Nature Immunology</i>. Nature Publishing Group, 2018.
    <a href="https://doi.org/10.1038/s41590-018-0109-z">https://doi.org/10.1038/s41590-018-0109-z</a>.
  ieee: M. Hons <i>et al.</i>, “Chemokines and integrins independently tune actin
    flow and substrate friction during intranodal migration of T cells,” <i>Nature
    Immunology</i>, vol. 19, no. 6. Nature Publishing Group, pp. 606–616, 2018.
  ista: Hons M, Kopf A, Hauschild R, Leithner AF, Gärtner FR, Abe J, Renkawitz J,
    Stein J, Sixt MK. 2018. Chemokines and integrins independently tune actin flow
    and substrate friction during intranodal migration of T cells. Nature Immunology.
    19(6), 606–616.
  mla: Hons, Miroslav, et al. “Chemokines and Integrins Independently Tune Actin Flow
    and Substrate Friction during Intranodal Migration of T Cells.” <i>Nature Immunology</i>,
    vol. 19, no. 6, Nature Publishing Group, 2018, pp. 606–16, doi:<a href="https://doi.org/10.1038/s41590-018-0109-z">10.1038/s41590-018-0109-z</a>.
  short: M. Hons, A. Kopf, R. Hauschild, A.F. Leithner, F.R. Gärtner, J. Abe, J. Renkawitz,
    J. Stein, M.K. Sixt, Nature Immunology 19 (2018) 606–616.
date_created: 2018-12-11T11:44:10Z
date_published: 2018-05-18T00:00:00Z
date_updated: 2026-08-10T22:30:24Z
day: '18'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
doi: 10.1038/s41590-018-0109-z
ec_funded: 1
external_id:
  isi:
  - '000433041500026'
  pmid:
  - '29777221'
intvolume: '        19'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pubmed/29777221
month: '05'
oa: 1
oa_version: Published Version
page: 606 - 616
pmid: 1
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '724373'
  name: Cellular Navigation Along Spatial Gradients
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '747687'
  name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
- _id: 25A48D24-B435-11E9-9278-68D0E5697425
  grant_number: ALTF 1396-2014
  name: Molecular and system level view of immune cell migration
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '281556'
  name: Cytoskeletal force generation and force transduction of migrating leukocytes
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '8040'
quality_controlled: '1'
related_material:
  record:
  - id: '6891'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Chemokines and integrins independently tune actin flow and substrate friction
  during intranodal migration of T cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2018'
...
---
_id: '422'
abstract:
- lang: eng
  text: We show that a rather simple, steady modification of the streamwise velocity
    profile in a pipe can lead to a complete collapse of turbulence and the flow fully
    relaminarizes. Two different devices, a stationary obstacle (inset) and a device
    which injects fluid through an annular gap close to the wall, are used to control
    the flow. Both devices modify the streamwise velocity profile such that the flow
    in the center of the pipe is decelerated and the flow in the near wall region
    is accelerated. We present measurements with stereoscopic particle image velocimetry
    to investigate and capture the development of the relaminarizing flow downstream
    these devices and the specific circumstances responsible for relaminarization.
    We find total relaminarization up to Reynolds numbers of 6000, where the skin
    friction in the far downstream distance is reduced by a factor of 3.4 due to relaminarization.
    In a smooth straight pipe the flow remains completely laminar downstream of the
    control. Furthermore, we show that transient (temporary) relaminarization in a
    spatially confined region right downstream the devices occurs also at much higher
    Reynolds numbers, accompanied by a significant local skin friction drag reduction.
    The underlying physical mechanism of relaminarization is attributed to a weakening
    of the near-wall turbulence production cycle.
article_processing_charge: Yes (via OA deal)
author:
- first_name: Jakob
  full_name: Kühnen, Jakob
  id: 3A47AE32-F248-11E8-B48F-1D18A9856A87
  last_name: Kühnen
  orcid: 0000-0003-4312-0179
- first_name: Davide
  full_name: Scarselli, Davide
  id: 40315C30-F248-11E8-B48F-1D18A9856A87
  last_name: Scarselli
  orcid: 0000-0001-5227-4271
- first_name: Markus
  full_name: Schaner, Markus
  id: 316CE034-F248-11E8-B48F-1D18A9856A87
  last_name: Schaner
- first_name: Björn
  full_name: Hof, Björn
  id: 3A374330-F248-11E8-B48F-1D18A9856A87
  last_name: Hof
  orcid: 0000-0003-2057-2754
citation:
  ama: Kühnen J, Scarselli D, Schaner M, Hof B. Relaminarization by steady modification
    of the streamwise velocity profile in a pipe. <i>Flow Turbulence and Combustion</i>.
    2018;100(4):919-942. doi:<a href="https://doi.org/10.1007/s10494-018-9896-4">10.1007/s10494-018-9896-4</a>
  apa: Kühnen, J., Scarselli, D., Schaner, M., &#38; Hof, B. (2018). Relaminarization
    by steady modification of the streamwise velocity profile in a pipe. <i>Flow Turbulence
    and Combustion</i>. Springer. <a href="https://doi.org/10.1007/s10494-018-9896-4">https://doi.org/10.1007/s10494-018-9896-4</a>
  chicago: Kühnen, Jakob, Davide Scarselli, Markus Schaner, and Björn Hof. “Relaminarization
    by Steady Modification of the Streamwise Velocity Profile in a Pipe.” <i>Flow
    Turbulence and Combustion</i>. Springer, 2018. <a href="https://doi.org/10.1007/s10494-018-9896-4">https://doi.org/10.1007/s10494-018-9896-4</a>.
  ieee: J. Kühnen, D. Scarselli, M. Schaner, and B. Hof, “Relaminarization by steady
    modification of the streamwise velocity profile in a pipe,” <i>Flow Turbulence
    and Combustion</i>, vol. 100, no. 4. Springer, pp. 919–942, 2018.
  ista: Kühnen J, Scarselli D, Schaner M, Hof B. 2018. Relaminarization by steady
    modification of the streamwise velocity profile in a pipe. Flow Turbulence and
    Combustion. 100(4), 919–942.
  mla: Kühnen, Jakob, et al. “Relaminarization by Steady Modification of the Streamwise
    Velocity Profile in a Pipe.” <i>Flow Turbulence and Combustion</i>, vol. 100,
    no. 4, Springer, 2018, pp. 919–42, doi:<a href="https://doi.org/10.1007/s10494-018-9896-4">10.1007/s10494-018-9896-4</a>.
  short: J. Kühnen, D. Scarselli, M. Schaner, B. Hof, Flow Turbulence and Combustion
    100 (2018) 919–942.
corr_author: '1'
date_created: 2018-12-11T11:46:23Z
date_published: 2018-01-01T00:00:00Z
date_updated: 2026-08-10T22:30:26Z
day: '01'
ddc:
- '530'
department:
- _id: BjHo
doi: 10.1007/s10494-018-9896-4
ec_funded: 1
external_id:
  isi:
  - '000433113900004'
file:
- access_level: open_access
  checksum: d7c0bade150faabca150b0a9986e60ca
  content_type: application/pdf
  creator: dernst
  date_created: 2018-12-17T15:52:37Z
  date_updated: 2020-07-14T12:46:25Z
  file_id: '5717'
  file_name: 2018_FlowTurbulenceCombust_Kuehnen.pdf
  file_size: 2210020
  relation: main_file
file_date_updated: 2020-07-14T12:46:25Z
has_accepted_license: '1'
intvolume: '       100'
isi: 1
issue: '4'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 919 - 942
project:
- _id: 25152F3A-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '306589'
  name: Decoding the complexity of turbulence at its origin
publication: Flow Turbulence and Combustion
publication_status: published
publisher: Springer
publist_id: '7401'
quality_controlled: '1'
related_material:
  record:
  - id: '7258'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Relaminarization by steady modification of the streamwise velocity profile
  in a pipe
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 100
year: '2018'
...
---
_id: '461'
abstract:
- lang: eng
  text: Turbulence is the major cause of friction losses in transport processes and
    it is responsible for a drastic drag increase in flows over bounding surfaces.
    While much effort is invested into developing ways to control and reduce turbulence
    intensities, so far no methods exist to altogether eliminate turbulence if velocities
    are sufficiently large. We demonstrate for pipe flow that appropriate distortions
    to the velocity profile lead to a complete collapse of turbulence and subsequently
    friction losses are reduced by as much as 90%. Counterintuitively, the return
    to laminar motion is accomplished by initially increasing turbulence intensities
    or by transiently amplifying wall shear. Since neither the Reynolds number nor
    the shear stresses decrease (the latter often increase), these measures are not
    indicative of turbulence collapse. Instead, an amplification mechanism                      measuring
    the interaction between eddies and the mean shear is found to set a threshold
    below which turbulence is suppressed beyond recovery.
acknowledgement: We acknowledge the European Research Council under the European Union’s
  Seventh Framework Programme (FP/2007-2013)/ERC Grant Agreement 306589, the European
  Research Council (ERC) under the European Union’s Horizon 2020 research and innovation
  programme (grant agreement no. 737549) and the Deutsche Forschungsgemeinschaft (Project
  No. FOR 1182) for financial support. We thank our technician P. Maier for providing
  highly valuable ideas and greatly supporting us in all technical aspects. We thank
  M. Schaner for technical drawings, construction and design. We thank M. Schwegel
  for a Matlab code to post-process experimental data.
article_processing_charge: No
arxiv: 1
author:
- first_name: Jakob
  full_name: Kühnen, Jakob
  id: 3A47AE32-F248-11E8-B48F-1D18A9856A87
  last_name: Kühnen
  orcid: 0000-0003-4312-0179
- first_name: Baofang
  full_name: Song, Baofang
  last_name: Song
- first_name: Davide
  full_name: Scarselli, Davide
  id: 40315C30-F248-11E8-B48F-1D18A9856A87
  last_name: Scarselli
  orcid: 0000-0001-5227-4271
- first_name: Nazmi B
  full_name: Budanur, Nazmi B
  id: 3EA1010E-F248-11E8-B48F-1D18A9856A87
  last_name: Budanur
  orcid: 0000-0003-0423-5010
- first_name: Michael
  full_name: Riedl, Michael
  id: 3BE60946-F248-11E8-B48F-1D18A9856A87
  last_name: Riedl
  orcid: 0000-0003-4844-6311
- first_name: Ashley
  full_name: Willis, Ashley
  last_name: Willis
- first_name: Marc
  full_name: Avila, Marc
  last_name: Avila
- first_name: Björn
  full_name: Hof, Björn
  id: 3A374330-F248-11E8-B48F-1D18A9856A87
  last_name: Hof
  orcid: 0000-0003-2057-2754
citation:
  ama: Kühnen J, Song B, Scarselli D, et al. Destabilizing turbulence in pipe flow.
    <i>Nature Physics</i>. 2018;14:386-390. doi:<a href="https://doi.org/10.1038/s41567-017-0018-3">10.1038/s41567-017-0018-3</a>
  apa: Kühnen, J., Song, B., Scarselli, D., Budanur, N. B., Riedl, M., Willis, A.,
    … Hof, B. (2018). Destabilizing turbulence in pipe flow. <i>Nature Physics</i>.
    Nature Publishing Group. <a href="https://doi.org/10.1038/s41567-017-0018-3">https://doi.org/10.1038/s41567-017-0018-3</a>
  chicago: Kühnen, Jakob, Baofang Song, Davide Scarselli, Nazmi B Budanur, Michael
    Riedl, Ashley Willis, Marc Avila, and Björn Hof. “Destabilizing Turbulence in
    Pipe Flow.” <i>Nature Physics</i>. Nature Publishing Group, 2018. <a href="https://doi.org/10.1038/s41567-017-0018-3">https://doi.org/10.1038/s41567-017-0018-3</a>.
  ieee: J. Kühnen <i>et al.</i>, “Destabilizing turbulence in pipe flow,” <i>Nature
    Physics</i>, vol. 14. Nature Publishing Group, pp. 386–390, 2018.
  ista: Kühnen J, Song B, Scarselli D, Budanur NB, Riedl M, Willis A, Avila M, Hof
    B. 2018. Destabilizing turbulence in pipe flow. Nature Physics. 14, 386–390.
  mla: Kühnen, Jakob, et al. “Destabilizing Turbulence in Pipe Flow.” <i>Nature Physics</i>,
    vol. 14, Nature Publishing Group, 2018, pp. 386–90, doi:<a href="https://doi.org/10.1038/s41567-017-0018-3">10.1038/s41567-017-0018-3</a>.
  short: J. Kühnen, B. Song, D. Scarselli, N.B. Budanur, M. Riedl, A. Willis, M. Avila,
    B. Hof, Nature Physics 14 (2018) 386–390.
corr_author: '1'
date_created: 2018-12-11T11:46:36Z
date_published: 2018-01-08T00:00:00Z
date_updated: 2026-08-10T22:30:26Z
day: '08'
department:
- _id: BjHo
doi: 10.1038/s41567-017-0018-3
ec_funded: 1
external_id:
  arxiv:
  - '1711.06543'
  isi:
  - '000429434100020'
intvolume: '        14'
isi: 1
language:
- iso: eng
main_file_link:
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  url: https://arxiv.org/abs/1711.06543
month: '01'
oa: 1
oa_version: Preprint
page: 386-390
project:
- _id: 25152F3A-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '306589'
  name: Decoding the complexity of turbulence at its origin
- _id: 25104D44-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '737549'
  name: Eliminating turbulence in oil pipelines
publication: Nature Physics
publication_status: published
publisher: Nature Publishing Group
publist_id: '7360'
quality_controlled: '1'
related_material:
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    status: public
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    relation: dissertation_contains
    status: public
  - id: '7258'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Destabilizing turbulence in pipe flow
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 14
year: '2018'
...
---
_id: '542'
abstract:
- lang: eng
  text: The t-haplotype, a mouse meiotic driver found on chromosome 17, has been a
    model for autosomal segregation distortion for close to a century, but several
    questions remain regarding its biology and evolutionary history. A recently published
    set of population genomics resources for wild mice includes several individuals
    heterozygous for the t-haplotype, which we use to characterize this selfish element
    at the genomic and transcriptomic level. Our results show that large sections
    of the t-haplotype have been replaced by standard homologous sequences, possibly
    due to occasional events of recombination, and that this complicates the inference
    of its history. As expected for a long genomic segment of very low recombination,
    the t-haplotype carries an excess of fixed nonsynonymous mutations compared to
    the standard chromosome. This excess is stronger for regions that have not undergone
    recent recombination, suggesting that occasional gene flow between the t and the
    standard chromosome may provide a mechanism to regenerate coding sequences that
    have accumulated deleterious mutations. Finally, we find that t-complex genes
    with altered expression largely overlap with deleted or amplified regions, and
    that carrying a t-haplotype alters the testis expression of genes outside of the
    t-complex, providing new leads into the pathways involved in the biology of this
    segregation distorter.
article_processing_charge: No
article_type: original
author:
- first_name: Réka K
  full_name: Kelemen, Réka K
  id: 48D3F8DE-F248-11E8-B48F-1D18A9856A87
  last_name: Kelemen
  orcid: 0000-0002-8489-9281
- first_name: Beatriz
  full_name: Vicoso, Beatriz
  id: 49E1C5C6-F248-11E8-B48F-1D18A9856A87
  last_name: Vicoso
  orcid: 0000-0002-4579-8306
citation:
  ama: Kelemen RK, Vicoso B. Complex history and differentiation patterns of the t-haplotype,
    a mouse meiotic driver. <i>Genetics</i>. 2018;208(1):365-375. doi:<a href="https://doi.org/10.1534/genetics.117.300513">10.1534/genetics.117.300513</a>
  apa: Kelemen, R. K., &#38; Vicoso, B. (2018). Complex history and differentiation
    patterns of the t-haplotype, a mouse meiotic driver. <i>Genetics</i>. Genetics
    Society of America. <a href="https://doi.org/10.1534/genetics.117.300513">https://doi.org/10.1534/genetics.117.300513</a>
  chicago: Kelemen, Réka K, and Beatriz Vicoso. “Complex History and Differentiation
    Patterns of the T-Haplotype, a Mouse Meiotic Driver.” <i>Genetics</i>. Genetics
    Society of America, 2018. <a href="https://doi.org/10.1534/genetics.117.300513">https://doi.org/10.1534/genetics.117.300513</a>.
  ieee: R. K. Kelemen and B. Vicoso, “Complex history and differentiation patterns
    of the t-haplotype, a mouse meiotic driver,” <i>Genetics</i>, vol. 208, no. 1.
    Genetics Society of America, pp. 365–375, 2018.
  ista: Kelemen RK, Vicoso B. 2018. Complex history and differentiation patterns of
    the t-haplotype, a mouse meiotic driver. Genetics. 208(1), 365–375.
  mla: Kelemen, Réka K., and Beatriz Vicoso. “Complex History and Differentiation
    Patterns of the T-Haplotype, a Mouse Meiotic Driver.” <i>Genetics</i>, vol. 208,
    no. 1, Genetics Society of America, 2018, pp. 365–75, doi:<a href="https://doi.org/10.1534/genetics.117.300513">10.1534/genetics.117.300513</a>.
  short: R.K. Kelemen, B. Vicoso, Genetics 208 (2018) 365–375.
corr_author: '1'
date_created: 2018-12-11T11:47:04Z
date_published: 2018-01-01T00:00:00Z
date_updated: 2026-08-10T22:30:31Z
day: '01'
ddc:
- '576'
department:
- _id: BeVi
doi: 10.1534/genetics.117.300513
ec_funded: 1
external_id:
  isi:
  - '000419356300024'
file:
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intvolume: '       208'
isi: 1
issue: '1'
language:
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month: '01'
oa: 1
oa_version: Published Version
page: 365 - 375
project:
- _id: 250BDE62-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '715257'
  name: Prevalence and Influence of Sexual Antagonism on Genome Evolution
publication: Genetics
publication_status: published
publisher: Genetics Society of America
publist_id: '7274'
pubrep_id: '1058'
quality_controlled: '1'
related_material:
  record:
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    relation: popular_science
    status: public
  - id: '17119'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Complex history and differentiation patterns of the t-haplotype, a mouse meiotic
  driver
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 208
year: '2018'
...
---
_id: '412'
abstract:
- lang: eng
  text: Clathrin-mediated endocytosis (CME) is a cellular trafficking process in which
    cargoes and lipids are internalized from the plasma membrane into vesicles coated
    with clathrin and adaptor proteins. CME is essential for many developmental and
    physiological processes in plants, but its underlying mechanism is not well characterised
    compared to that in yeast and animal systems. Here, we searched for new factors
    involved in CME in Arabidopsis thaliana by performing Tandem Affinity Purification
    of proteins that interact with clathrin light chain, a principal component of
    the clathrin coat. Among the confirmed interactors, we found two putative homologues
    of the clathrin-coat uncoating factor auxilin previously described in non-plant
    systems. Overexpression of AUXILIN-LIKE1 and AUXILIN-LIKE2 in A. thaliana caused
    an arrest of seedling growth and development. This was concomitant with inhibited
    endocytosis due to blocking of clathrin recruitment after the initial step of
    adaptor protein binding to the plasma membrane. By contrast, auxilin-like(1/2)
    loss-of-function lines did not present endocytosis-related developmental or cellular
    phenotypes under normal growth conditions. This work contributes to the on-going
    characterization of the endocytotic machinery in plants and provides a robust
    tool for conditionally and specifically interfering with CME in A. thaliana.
acknowledgement: We thank James Matthew Watson, Monika Borowska, and Peggy Stolt-Bergner
  at ProTech Facility of the Vienna Biocenter Core Facilities for the CRISPR/CAS9
  construct; Anna Müller for assistance with molecular cloning; Sebastian Bednarek,
  Liwen Jiang, and Daniël Van Damme for sharing published material; Matyáš Fendrych,
  Daniël Van Damme, and Lindy Abas for valuable discussions; and Martine De Cock for
  help with correcting the manuscript. This work was supported by the European Research
  Council under the European Union Seventh Framework Programme (FP7/2007-2013)/ERC
  Grant 282300 and by the Ministry of Education of the Czech Republic/MŠMT project
  NPUI-LO1417.
article_processing_charge: No
article_type: original
author:
- first_name: Maciek
  full_name: Adamowski, Maciek
  id: 45F536D2-F248-11E8-B48F-1D18A9856A87
  last_name: Adamowski
  orcid: 0000-0001-6463-5257
- first_name: Madhumitha
  full_name: Narasimhan, Madhumitha
  id: 44BF24D0-F248-11E8-B48F-1D18A9856A87
  last_name: Narasimhan
  orcid: 0000-0002-8600-0671
- first_name: Urszula
  full_name: Kania, Urszula
  id: 4AE5C486-F248-11E8-B48F-1D18A9856A87
  last_name: Kania
- first_name: Matous
  full_name: Glanc, Matous
  id: 1AE1EA24-02D0-11E9-9BAA-DAF4881429F2
  last_name: Glanc
  orcid: 0000-0003-0619-7783
- first_name: Geert
  full_name: De Jaeger, Geert
  last_name: De Jaeger
- first_name: Jirí
  full_name: Friml, Jirí
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
citation:
  ama: Adamowski M, Narasimhan M, Kania U, Glanc M, De Jaeger G, Friml J. A functional
    study of AUXILIN LIKE1 and 2 two putative clathrin uncoating factors in Arabidopsis.
    <i>The Plant Cell</i>. 2018;30(3):700-716. doi:<a href="https://doi.org/10.1105/tpc.17.00785">10.1105/tpc.17.00785</a>
  apa: Adamowski, M., Narasimhan, M., Kania, U., Glanc, M., De Jaeger, G., &#38; Friml,
    J. (2018). A functional study of AUXILIN LIKE1 and 2 two putative clathrin uncoating
    factors in Arabidopsis. <i>The Plant Cell</i>. American Society of Plant Biologists.
    <a href="https://doi.org/10.1105/tpc.17.00785">https://doi.org/10.1105/tpc.17.00785</a>
  chicago: Adamowski, Maciek, Madhumitha Narasimhan, Urszula Kania, Matous Glanc,
    Geert De Jaeger, and Jiří Friml. “A Functional Study of AUXILIN LIKE1 and 2 Two
    Putative Clathrin Uncoating Factors in Arabidopsis.” <i>The Plant Cell</i>. American
    Society of Plant Biologists, 2018. <a href="https://doi.org/10.1105/tpc.17.00785">https://doi.org/10.1105/tpc.17.00785</a>.
  ieee: M. Adamowski, M. Narasimhan, U. Kania, M. Glanc, G. De Jaeger, and J. Friml,
    “A functional study of AUXILIN LIKE1 and 2 two putative clathrin uncoating factors
    in Arabidopsis,” <i>The Plant Cell</i>, vol. 30, no. 3. American Society of Plant
    Biologists, pp. 700–716, 2018.
  ista: Adamowski M, Narasimhan M, Kania U, Glanc M, De Jaeger G, Friml J. 2018. A
    functional study of AUXILIN LIKE1 and 2 two putative clathrin uncoating factors
    in Arabidopsis. The Plant Cell. 30(3), 700–716.
  mla: Adamowski, Maciek, et al. “A Functional Study of AUXILIN LIKE1 and 2 Two Putative
    Clathrin Uncoating Factors in Arabidopsis.” <i>The Plant Cell</i>, vol. 30, no.
    3, American Society of Plant Biologists, 2018, pp. 700–16, doi:<a href="https://doi.org/10.1105/tpc.17.00785">10.1105/tpc.17.00785</a>.
  short: M. Adamowski, M. Narasimhan, U. Kania, M. Glanc, G. De Jaeger, J. Friml,
    The Plant Cell 30 (2018) 700–716.
corr_author: '1'
date_created: 2018-12-11T11:46:20Z
date_published: 2018-04-09T00:00:00Z
date_updated: 2026-08-10T22:30:38Z
day: '09'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.1105/tpc.17.00785
ec_funded: 1
external_id:
  isi:
  - '000429441400018'
  pmid:
  - '29511054'
file:
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  date_created: 2022-05-23T09:12:38Z
  date_updated: 2022-05-23T09:12:38Z
  file_id: '11406'
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intvolume: '        30'
isi: 1
issue: '3'
language:
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month: '04'
oa: 1
oa_version: Published Version
page: 700 - 716
pmid: 1
project:
- _id: 25716A02-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '282300'
  name: Polarity and subcellular dynamics in plants
publication: The Plant Cell
publication_identifier:
  eissn:
  - 1532-298X
  issn:
  - 1040-4651
publication_status: published
publisher: American Society of Plant Biologists
publist_id: '7417'
quality_controlled: '1'
related_material:
  record:
  - id: '6269'
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scopus_import: '1'
status: public
title: A functional study of AUXILIN LIKE1 and 2 two putative clathrin uncoating factors
  in Arabidopsis
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 30
year: '2018'
...
---
OA_place: publisher
_id: '48'
abstract:
- lang: eng
  text: 'The hippocampus is a key brain region for spatial memory and navigation and
    is needed at all stages of memory, including encoding, consolidation, and recall.
    Hippocampal place cells selectively discharge at specific locations of the environment
    to form a cognitive map of the space. During the rest period and sleep following
    spatial navigation and/or learning, the waking activity of the place cells is
    reactivated within high synchrony events. This reactivation is thought to be important
    for memory consolidation and stabilization of the spatial representations. The
    aim of my thesis was to directly test whether the reactivation content encoded
    in firing patterns of place cells is important for consolidation of spatial memories.
    In particular, I aimed to test whether, in cases when multiple spatial memory
    traces are acquired during learning, the specific disruption of the reactivation
    of a subset of these memories leads to the selective disruption of the corresponding
    memory traces or through memory interference the other learned memories are disrupted
    as well. In this thesis, using a modified cheeseboard paradigm and a closed-loop
    recording setup with feedback optogenetic stimulation, I examined how the disruption
    of the reactivation of specific spiking patterns affects consolidation of the
    corresponding memory traces. To obtain multiple distinctive memories, animals
    had to perform a spatial task in two distinct cheeseboard environments and the
    reactivation of spiking patterns associated with one of the environments (target)
    was disrupted after learning during four hours rest period using a real-time decoding
    method. This real-time decoding method was capable of selectively affecting the
    firing rates and cofiring correlations of the target environment-encoding cells.
    The selective disruption led to behavioural impairment in the memory tests after
    the rest periods in the target environment but not in the other undisrupted control
    environment. In addition, the map of the target environment was less stable in
    the impaired memory tests compared to the learning session before than the map
    of the control environment. However, when the animal relearned the task, the same
    map recurred in the target environment that was present during learning before
    the disruption. Altogether my work demonstrated that the reactivation content
    is important: assembly-related disruption of reactivation can lead to a selective
    memory impairment and deficiency in map stability. These findings indeed suggest
    that reactivated assembly patterns reflect processes associated with the consolidation
    of memory traces. '
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Igor
  full_name: Gridchyn, Igor
  id: 4B60654C-F248-11E8-B48F-1D18A9856A87
  last_name: Gridchyn
  orcid: 0000-0002-1807-1929
citation:
  ama: Gridchyn I. Reactivation content is important for consolidation of spatial
    memory. 2018. doi:<a href="https://doi.org/10.15479/AT:ISTA:th_1042">10.15479/AT:ISTA:th_1042</a>
  apa: Gridchyn, I. (2018). <i>Reactivation content is important for consolidation
    of spatial memory</i>. Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:th_1042">https://doi.org/10.15479/AT:ISTA:th_1042</a>
  chicago: Gridchyn, Igor. “Reactivation Content Is Important for Consolidation of
    Spatial Memory.” Institute of Science and Technology Austria, 2018. <a href="https://doi.org/10.15479/AT:ISTA:th_1042">https://doi.org/10.15479/AT:ISTA:th_1042</a>.
  ieee: I. Gridchyn, “Reactivation content is important for consolidation of spatial
    memory,” Institute of Science and Technology Austria, 2018.
  ista: Gridchyn I. 2018. Reactivation content is important for consolidation of spatial
    memory. Institute of Science and Technology Austria.
  mla: Gridchyn, Igor. <i>Reactivation Content Is Important for Consolidation of Spatial
    Memory</i>. Institute of Science and Technology Austria, 2018, doi:<a href="https://doi.org/10.15479/AT:ISTA:th_1042">10.15479/AT:ISTA:th_1042</a>.
  short: I. Gridchyn, Reactivation Content Is Important for Consolidation of Spatial
    Memory, Institute of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2018-12-11T11:44:21Z
date_published: 2018-08-27T00:00:00Z
date_updated: 2026-04-08T14:13:15Z
day: '27'
ddc:
- '573'
degree_awarded: PhD
department:
- _id: JoCs
doi: 10.15479/AT:ISTA:th_1042
file:
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file_date_updated: 2021-02-11T23:30:22Z
has_accepted_license: '1'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
page: '104'
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '8006'
pubrep_id: '1042'
status: public
supervisor:
- first_name: Jozsef L
  full_name: Csicsvari, Jozsef L
  id: 3FA14672-F248-11E8-B48F-1D18A9856A87
  last_name: Csicsvari
  orcid: 0000-0002-5193-4036
title: Reactivation content is important for consolidation of spatial memory
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: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2018'
...
---
_id: '21'
abstract:
- lang: eng
  text: Parvalbumin-positive (PV+) GABAergic interneurons in hippocampal microcircuits
    are thought to play a key role in several higher network functions, such as feedforward
    and feedback inhibition, network oscillations, and pattern separation. Fast lateral
    inhibition mediated by GABAergic interneurons may implement a winner-takes-all
    mechanism in the hippocampal input layer. However, it is not clear whether the
    functional connectivity rules of granule cells (GCs) and interneurons in the dentate
    gyrus are consistent with such a mechanism. Using simultaneous patch-clamp recordings
    from up to seven GCs and up to four PV+ interneurons in the dentate gyrus, we
    find that connectivity is structured in space, synapse-specific, and enriched
    in specific disynaptic motifs. In contrast to the neocortex, lateral inhibition
    in the dentate gyrus (in which a GC inhibits neighboring GCs via a PV+ interneuron)
    is ~ 10-times more abundant than recurrent inhibition (in which a GC inhibits
    itself). Thus, unique connectivity rules may enable the dentate gyrus to perform
    specific higher-order computations
acknowledgement: This project received funding from the European Research Council
  (ERC) under the European Union’s Horizon 2020 research and innovation programme
  (grant agreement No 692692) and the Fond zur Förderung der Wissenschaftlichen Forschung
  (Z 312-B27, Wittgenstein award), both to P.J..
article_number: '4605'
article_processing_charge: No
article_type: original
author:
- first_name: 'Claudia '
  full_name: 'Espinoza Martinez, Claudia '
  id: 31FFEE2E-F248-11E8-B48F-1D18A9856A87
  last_name: Espinoza Martinez
  orcid: 0000-0003-4710-2082
- first_name: José
  full_name: Guzmán, José
  id: 30CC5506-F248-11E8-B48F-1D18A9856A87
  last_name: Guzmán
  orcid: 0000-0003-2209-5242
- first_name: Xiaomin
  full_name: Zhang, Xiaomin
  id: 423EC9C2-F248-11E8-B48F-1D18A9856A87
  last_name: Zhang
  orcid: 0000-0003-0256-6529
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Espinoza Martinez C, Guzmán J, Zhang X, Jonas PM. Parvalbumin+ interneurons
    obey unique connectivity rules and establish a powerful lateral-inhibition microcircuit
    in dentate gyrus. <i>Nature Communications</i>. 2018;9(1). doi:<a href="https://doi.org/10.1038/s41467-018-06899-3">10.1038/s41467-018-06899-3</a>
  apa: Espinoza Martinez, C., Guzmán, J., Zhang, X., &#38; Jonas, P. M. (2018). Parvalbumin+
    interneurons obey unique connectivity rules and establish a powerful lateral-inhibition
    microcircuit in dentate gyrus. <i>Nature Communications</i>. Nature Publishing
    Group. <a href="https://doi.org/10.1038/s41467-018-06899-3">https://doi.org/10.1038/s41467-018-06899-3</a>
  chicago: Espinoza Martinez, Claudia , José Guzmán, Xiaomin Zhang, and Peter M Jonas.
    “Parvalbumin+ Interneurons Obey Unique Connectivity Rules and Establish a Powerful
    Lateral-Inhibition Microcircuit in Dentate Gyrus.” <i>Nature Communications</i>.
    Nature Publishing Group, 2018. <a href="https://doi.org/10.1038/s41467-018-06899-3">https://doi.org/10.1038/s41467-018-06899-3</a>.
  ieee: C. Espinoza Martinez, J. Guzmán, X. Zhang, and P. M. Jonas, “Parvalbumin+
    interneurons obey unique connectivity rules and establish a powerful lateral-inhibition
    microcircuit in dentate gyrus,” <i>Nature Communications</i>, vol. 9, no. 1. Nature
    Publishing Group, 2018.
  ista: Espinoza Martinez C, Guzmán J, Zhang X, Jonas PM. 2018. Parvalbumin+ interneurons
    obey unique connectivity rules and establish a powerful lateral-inhibition microcircuit
    in dentate gyrus. Nature Communications. 9(1), 4605.
  mla: Espinoza Martinez, Claudia, et al. “Parvalbumin+ Interneurons Obey Unique Connectivity
    Rules and Establish a Powerful Lateral-Inhibition Microcircuit in Dentate Gyrus.”
    <i>Nature Communications</i>, vol. 9, no. 1, 4605, Nature Publishing Group, 2018,
    doi:<a href="https://doi.org/10.1038/s41467-018-06899-3">10.1038/s41467-018-06899-3</a>.
  short: C. Espinoza Martinez, J. Guzmán, X. Zhang, P.M. Jonas, Nature Communications
    9 (2018).
date_created: 2018-12-11T11:44:12Z
date_published: 2018-11-02T00:00:00Z
date_updated: 2026-08-10T22:30:42Z
day: '02'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1038/s41467-018-06899-3
ec_funded: 1
external_id:
  isi:
  - '000449069700009'
file:
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intvolume: '         9'
isi: 1
issue: '1'
language:
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month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '692692'
  name: Biophysics and circuit function of a giant cortical glutamatergic synapse
- _id: 25C5A090-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: Z00312
  name: Synaptic communication in neuronal microcircuits
publication: Nature Communications
publication_status: published
publisher: Nature Publishing Group
publist_id: '8034'
quality_controlled: '1'
related_material:
  link:
  - description: News on IST Homepage
    relation: press_release
    url: https://ist.ac.at/en/news/lateral-inhibition-keeps-similar-memories-apart/
  record:
  - id: '6363'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Parvalbumin+ interneurons obey unique connectivity rules and establish a powerful
  lateral-inhibition microcircuit in dentate gyrus
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 9
year: '2018'
...
---
_id: '67'
abstract:
- lang: eng
  text: 'Gene regulatory networks evolve through rewiring of individual components—that
    is, through changes in regulatory connections. However, the mechanistic basis
    of regulatory rewiring is poorly understood. Using a canonical gene regulatory
    system, we quantify the properties of transcription factors that determine the
    evolutionary potential for rewiring of regulatory connections: robustness, tunability
    and evolvability. In vivo repression measurements of two repressors at mutated
    operator sites reveal their contrasting evolutionary potential: while robustness
    and evolvability were positively correlated, both were in trade-off with tunability.
    Epistatic interactions between adjacent operators alleviated this trade-off. A
    thermodynamic model explains how the differences in robustness, tunability and
    evolvability arise from biophysical characteristics of repressor–DNA binding.
    The model also uncovers that the energy matrix, which describes how mutations
    affect repressor–DNA binding, encodes crucial information about the evolutionary
    potential of a repressor. The biophysical determinants of evolutionary potential
    for regulatory rewiring constitute a mechanistic framework for understanding network
    evolution.'
article_processing_charge: No
article_type: original
author:
- first_name: Claudia
  full_name: Igler, Claudia
  id: 46613666-F248-11E8-B48F-1D18A9856A87
  last_name: Igler
  orcid: 0000-0001-7777-546X
- first_name: Mato
  full_name: Lagator, Mato
  id: 345D25EC-F248-11E8-B48F-1D18A9856A87
  last_name: Lagator
- first_name: Gasper
  full_name: Tkacik, Gasper
  id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
  last_name: Tkacik
  orcid: 0000-0002-6699-1455
- first_name: Jonathan P
  full_name: Bollback, Jonathan P
  id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
  last_name: Bollback
  orcid: 0000-0002-4624-4612
- 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: Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. Evolutionary potential
    of transcription factors for gene regulatory rewiring. <i>Nature Ecology and Evolution</i>.
    2018;2(10):1633-1643. doi:<a href="https://doi.org/10.1038/s41559-018-0651-y">10.1038/s41559-018-0651-y</a>
  apa: Igler, C., Lagator, M., Tkačik, G., Bollback, J. P., &#38; Guet, C. C. (2018).
    Evolutionary potential of transcription factors for gene regulatory rewiring.
    <i>Nature Ecology and Evolution</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/s41559-018-0651-y">https://doi.org/10.1038/s41559-018-0651-y</a>
  chicago: Igler, Claudia, Mato Lagator, Gašper Tkačik, Jonathan P Bollback, and Calin
    C Guet. “Evolutionary Potential of Transcription Factors for Gene Regulatory Rewiring.”
    <i>Nature Ecology and Evolution</i>. Nature Publishing Group, 2018. <a href="https://doi.org/10.1038/s41559-018-0651-y">https://doi.org/10.1038/s41559-018-0651-y</a>.
  ieee: C. Igler, M. Lagator, G. Tkačik, J. P. Bollback, and C. C. Guet, “Evolutionary
    potential of transcription factors for gene regulatory rewiring,” <i>Nature Ecology
    and Evolution</i>, vol. 2, no. 10. Nature Publishing Group, pp. 1633–1643, 2018.
  ista: Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. 2018. Evolutionary potential
    of transcription factors for gene regulatory rewiring. Nature Ecology and Evolution.
    2(10), 1633–1643.
  mla: Igler, Claudia, et al. “Evolutionary Potential of Transcription Factors for
    Gene Regulatory Rewiring.” <i>Nature Ecology and Evolution</i>, vol. 2, no. 10,
    Nature Publishing Group, 2018, pp. 1633–43, doi:<a href="https://doi.org/10.1038/s41559-018-0651-y">10.1038/s41559-018-0651-y</a>.
  short: C. Igler, M. Lagator, G. Tkačik, J.P. Bollback, C.C. Guet, Nature Ecology
    and Evolution 2 (2018) 1633–1643.
date_created: 2018-12-11T11:44:27Z
date_published: 2018-09-10T00:00:00Z
date_updated: 2026-08-10T22:30:42Z
day: '10'
ddc:
- '570'
department:
- _id: CaGu
- _id: GaTk
- _id: JoBo
doi: 10.1038/s41559-018-0651-y
ec_funded: 1
external_id:
  isi:
  - '000447947600021'
file:
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  checksum: 383a2e2c944a856e2e821ec8e7bf71b6
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  date_created: 2020-05-14T11:28:52Z
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  file_id: '7830'
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  file_size: 1135973
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file_date_updated: 2020-07-14T12:47:37Z
has_accepted_license: '1'
intvolume: '         2'
isi: 1
issue: '10'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Submitted Version
page: 1633 - 1643
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
- _id: 2578D616-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '648440'
  name: Selective Barriers to Horizontal Gene Transfer
- _id: 251EE76E-B435-11E9-9278-68D0E5697425
  grant_number: '24573'
  name: Design principles underlying genetic switch architecture
publication: Nature Ecology and Evolution
publication_status: published
publisher: Nature Publishing Group
publist_id: '7987'
quality_controlled: '1'
related_material:
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    status: public
  - id: '6371'
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    status: public
scopus_import: '1'
status: public
title: Evolutionary potential of transcription factors for gene regulatory rewiring
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 2
year: '2018'
...
---
OA_place: publisher
_id: '50'
abstract:
- lang: eng
  text: The Wnt/planar cell polarity (Wnt/PCP) pathway determines planar polarity
    of epithelial cells in both vertebrates and invertebrates. The role that Wnt/PCP
    signaling plays in mesenchymal contexts, however, is only poorly understood. While
    previous studies have demonstrated the capacity of Wnt/PCP signaling to polarize
    and guide directed migration of mesenchymal cells, it remains unclear whether
    endogenous Wnt/PCP signaling performs these functions instructively, as it does
    in epithelial cells. Here we developed a light-switchable version of the Wnt/PCP
    receptor Frizzled 7 (Fz7) to unambiguously distinguish between an instructive
    and a permissive role of Wnt/PCP signaling for the directional collective migration
    of mesendoderm progenitor cells during zebrafish gastrulation. We show that prechordal
    plate (ppl) cell migration is defective in maternal-zygotic fz7a and fz7b (MZ
    fz7a,b) double mutant embryos, and that Fz7 functions cell-autonomously in this
    process by promoting ppl cell protrusion formation and directed migration. We
    further show that local activation of Fz7 can direct ppl cell migration both in
    vitro and in vivo. Surprisingly, however, uniform Fz7 activation is sufficient
    to fully rescue the ppl cell migration defect in MZ fz7a,b mutant embryos, indicating
    that Wnt/PCP signaling functions permissively rather than instructively in directed
    mesendoderm cell migration during zebrafish gastrulation.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Daniel
  full_name: Capek, Daniel
  id: 31C42484-F248-11E8-B48F-1D18A9856A87
  last_name: Capek
  orcid: 0000-0001-5199-9940
citation:
  ama: Capek D. Optogenetic Frizzled 7 reveals a permissive function of Wnt/PCP signaling
    in directed mesenchymal cell migration. 2018. doi:<a href="https://doi.org/10.15479/AT:ISTA:TH_1031">10.15479/AT:ISTA:TH_1031</a>
  apa: Capek, D. (2018). <i>Optogenetic Frizzled 7 reveals a permissive function of
    Wnt/PCP signaling in directed mesenchymal cell migration</i>. Institute of Science
    and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:TH_1031">https://doi.org/10.15479/AT:ISTA:TH_1031</a>
  chicago: Capek, Daniel. “Optogenetic Frizzled 7 Reveals a Permissive Function of
    Wnt/PCP Signaling in Directed Mesenchymal Cell Migration.” Institute of Science
    and Technology Austria, 2018. <a href="https://doi.org/10.15479/AT:ISTA:TH_1031">https://doi.org/10.15479/AT:ISTA:TH_1031</a>.
  ieee: D. Capek, “Optogenetic Frizzled 7 reveals a permissive function of Wnt/PCP
    signaling in directed mesenchymal cell migration,” Institute of Science and Technology
    Austria, 2018.
  ista: Capek D. 2018. Optogenetic Frizzled 7 reveals a permissive function of Wnt/PCP
    signaling in directed mesenchymal cell migration. Institute of Science and Technology
    Austria.
  mla: Capek, Daniel. <i>Optogenetic Frizzled 7 Reveals a Permissive Function of Wnt/PCP
    Signaling in Directed Mesenchymal Cell Migration</i>. Institute of Science and
    Technology Austria, 2018, doi:<a href="https://doi.org/10.15479/AT:ISTA:TH_1031">10.15479/AT:ISTA:TH_1031</a>.
  short: D. Capek, Optogenetic Frizzled 7 Reveals a Permissive Function of Wnt/PCP
    Signaling in Directed Mesenchymal Cell Migration, Institute of Science and Technology
    Austria, 2018.
corr_author: '1'
date_created: 2018-12-11T11:44:21Z
date_published: 2018-06-22T00:00:00Z
date_updated: 2026-04-16T10:07:33Z
day: '22'
ddc:
- '570'
- '591'
- '596'
degree_awarded: PhD
department:
- _id: CaHe
doi: 10.15479/AT:ISTA:TH_1031
file:
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  checksum: d3eca3dcacb67bffdde6e6609c31cdd0
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  creator: dernst
  date_created: 2019-04-08T13:42:26Z
  date_updated: 2021-02-11T11:17:17Z
  embargo: 2019-06-25
  file_id: '6238'
  file_name: 2018_Thesis_Capek.pdf
  file_size: 31576521
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  date_created: 2019-04-08T13:42:27Z
  date_updated: 2021-02-11T23:30:21Z
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  file_id: '6239'
  file_name: 2018_Thesis_Capek_source.docx
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file_date_updated: 2021-02-11T23:30:21Z
has_accepted_license: '1'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: '95'
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '8004'
pubrep_id: '1031'
related_material:
  record:
  - id: '661'
    relation: part_of_dissertation
    status: public
  - id: '1100'
    relation: part_of_dissertation
    status: public
  - id: '676'
    relation: part_of_dissertation
    status: public
status: public
supervisor:
- 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
title: Optogenetic Frizzled 7 reveals a permissive function of Wnt/PCP signaling in
  directed mesenchymal cell migration
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2018'
...
---
_id: '5585'
abstract:
- lang: eng
  text: Mean repression values and standard error of the mean are given for all operator
    mutant libraries.
article_processing_charge: No
author:
- first_name: Claudia
  full_name: Igler, Claudia
  id: 46613666-F248-11E8-B48F-1D18A9856A87
  last_name: Igler
  orcid: 0000-0001-7777-546X
- first_name: Mato
  full_name: Lagator, Mato
  id: 345D25EC-F248-11E8-B48F-1D18A9856A87
  last_name: Lagator
- first_name: Gasper
  full_name: Tkacik, Gasper
  id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
  last_name: Tkacik
  orcid: 0000-0002-6699-1455
- first_name: Jonathan P
  full_name: Bollback, Jonathan P
  id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
  last_name: Bollback
  orcid: 0000-0002-4624-4612
- 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: Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. Data for the paper Evolutionary
    potential of transcription factors for gene regulatory rewiring. 2018. doi:<a
    href="https://doi.org/10.15479/AT:ISTA:108">10.15479/AT:ISTA:108</a>
  apa: Igler, C., Lagator, M., Tkačik, G., Bollback, J. P., &#38; Guet, C. C. (2018).
    Data for the paper Evolutionary potential of transcription factors for gene regulatory
    rewiring. Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:108">https://doi.org/10.15479/AT:ISTA:108</a>
  chicago: Igler, Claudia, Mato Lagator, Gašper Tkačik, Jonathan P Bollback, and Calin
    C Guet. “Data for the Paper Evolutionary Potential of Transcription Factors for
    Gene Regulatory Rewiring.” Institute of Science and Technology Austria, 2018.
    <a href="https://doi.org/10.15479/AT:ISTA:108">https://doi.org/10.15479/AT:ISTA:108</a>.
  ieee: C. Igler, M. Lagator, G. Tkačik, J. P. Bollback, and C. C. Guet, “Data for
    the paper Evolutionary potential of transcription factors for gene regulatory
    rewiring.” Institute of Science and Technology Austria, 2018.
  ista: Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. 2018. Data for the paper
    Evolutionary potential of transcription factors for gene regulatory rewiring,
    Institute of Science and Technology Austria, <a href="https://doi.org/10.15479/AT:ISTA:108">10.15479/AT:ISTA:108</a>.
  mla: Igler, Claudia, et al. <i>Data for the Paper Evolutionary Potential of Transcription
    Factors for Gene Regulatory Rewiring</i>. Institute of Science and Technology
    Austria, 2018, doi:<a href="https://doi.org/10.15479/AT:ISTA:108">10.15479/AT:ISTA:108</a>.
  short: C. Igler, M. Lagator, G. Tkačik, J.P. Bollback, C.C. Guet, (2018).
datarep_id: '108'
date_created: 2018-12-12T12:31:40Z
date_published: 2018-07-20T00:00:00Z
date_updated: 2026-08-10T22:30:42Z
day: '20'
ddc:
- '576'
department:
- _id: CaGu
- _id: GaTk
doi: 10.15479/AT:ISTA:108
ec_funded: 1
file:
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  checksum: 1435781526c77413802adee0d4583cce
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  date_created: 2018-12-12T13:02:45Z
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  file_id: '5611'
  file_name: IST-2018-108-v1+1_data_figures.xlsx
  file_size: 16507
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file_date_updated: 2020-07-14T12:47:07Z
has_accepted_license: '1'
license: https://creativecommons.org/publicdomain/zero/1.0/
month: '07'
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
- _id: 2578D616-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '648440'
  name: Selective Barriers to Horizontal Gene Transfer
- _id: 251EE76E-B435-11E9-9278-68D0E5697425
  grant_number: '24573'
  name: Design principles underlying genetic switch architecture
publisher: Institute of Science and Technology Austria
related_material:
  record:
  - id: '67'
    relation: research_paper
    status: public
  - id: '6371'
    relation: research_paper
    status: public
status: public
title: Data for the paper Evolutionary potential of transcription factors for gene
  regulatory rewiring
tmp:
  image: /images/cc_0.png
  legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
  name: Creative Commons Public Domain Dedication (CC0 1.0)
  short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2018'
...
---
OA_place: publisher
_id: '6266'
abstract:
- lang: eng
  text: 'A major challenge in neuroscience research is to dissect the circuits that
    orchestrate behavior in health and disease. Proteins from a wide range of non-mammalian
    species, such as microbial opsins, have been successfully transplanted to specific
    neuronal targets to override their natural communication patterns. The goal of
    our work is to manipulate synaptic communication in a manner that closely incorporates
    the functional intricacies of synapses by preserving temporal encoding (i.e. the
    firing pattern of the presynaptic neuron) and connectivity (i.e. target specific
    synapses rather than specific neurons). Our strategy to achieve this goal builds
    on the use of non-mammalian transplants to create a synthetic synapse. The mode
    of modulation comes from pre-synaptic uptake of a synthetic neurotransmitter (SN)
    into synaptic vesicles by means of a genetically targeted transporter selective
    for the SN. Upon natural vesicular release, exposure of the SN to the synaptic
    cleft will modify the post-synaptic potential through an orthogonal ligand gated
    ion channel. To achieve this goal we have functionally characterized a mixed cationic
    methionine-gated ion channel from Arabidopsis thaliana, designed a method to functionally
    characterize a synthetic transporter in isolated synaptic vesicles without the
    need for transgenic animals, identified and extracted multiple prokaryotic uptake
    systems that are substrate specific for methionine (Met), and established a primary/cell
    line co-culture system that would allow future combinatorial testing of this orthogonal
    transmitter-transporter-channel trifecta. Synthetic synapses will provide a unique
    opportunity to manipulate synaptic communication while maintaining the electrophysiological
    integrity of the pre-synaptic cell. In this way, information may be preserved
    that was generated in upstream circuits and that could be essential for concerted
    function and information processing. '
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Catherine
  full_name: Mckenzie, Catherine
  id: 3EEDE19A-F248-11E8-B48F-1D18A9856A87
  last_name: Mckenzie
citation:
  ama: Mckenzie C. Design and characterization of methods and biological components
    to realize synthetic neurotransmission . 2018. doi:<a href="https://doi.org/10.15479/at:ista:th_1055">10.15479/at:ista:th_1055</a>
  apa: Mckenzie, C. (2018). <i>Design and characterization of methods and biological
    components to realize synthetic neurotransmission </i>. Institute of Science and
    Technology Austria. <a href="https://doi.org/10.15479/at:ista:th_1055">https://doi.org/10.15479/at:ista:th_1055</a>
  chicago: Mckenzie, Catherine. “Design and Characterization of Methods and Biological
    Components to Realize Synthetic Neurotransmission .” Institute of Science and
    Technology Austria, 2018. <a href="https://doi.org/10.15479/at:ista:th_1055">https://doi.org/10.15479/at:ista:th_1055</a>.
  ieee: C. Mckenzie, “Design and characterization of methods and biological components
    to realize synthetic neurotransmission ,” Institute of Science and Technology
    Austria, 2018.
  ista: Mckenzie C. 2018. Design and characterization of methods and biological components
    to realize synthetic neurotransmission . Institute of Science and Technology Austria.
  mla: Mckenzie, Catherine. <i>Design and Characterization of Methods and Biological
    Components to Realize Synthetic Neurotransmission </i>. Institute of Science and
    Technology Austria, 2018, doi:<a href="https://doi.org/10.15479/at:ista:th_1055">10.15479/at:ista:th_1055</a>.
  short: C. Mckenzie, Design and Characterization of Methods and Biological Components
    to Realize Synthetic Neurotransmission , Institute of Science and Technology Austria,
    2018.
corr_author: '1'
date_created: 2019-04-09T14:13:39Z
date_published: 2018-10-31T00:00:00Z
date_updated: 2026-04-08T14:14:05Z
day: '31'
ddc:
- '571'
- '573'
degree_awarded: PhD
department:
- _id: HaJa
doi: 10.15479/at:ista:th_1055
file:
- access_level: open_access
  checksum: 9d2c2dca04b00e485470c28b262af59a
  content_type: application/pdf
  creator: dernst
  date_created: 2019-04-09T14:12:40Z
  date_updated: 2021-02-11T11:17:16Z
  embargo: 2019-11-24
  file_id: '6267'
  file_name: 2018_Thesis_McKenzie.pdf
  file_size: 4906420
  relation: main_file
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  checksum: 50b58c272899601bc6fd9642c4dc97f1
  content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
  creator: dernst
  date_created: 2019-04-09T14:12:40Z
  date_updated: 2020-07-14T12:47:25Z
  embargo_to: open_access
  file_id: '6268'
  file_name: 2018_Thesis_McKenzie_source.docx
  file_size: 5053545
  relation: source_file
file_date_updated: 2021-02-11T11:17:16Z
has_accepted_license: '1'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: '95'
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
pubrep_id: '1055'
related_material:
  record:
  - id: '7132'
    relation: new_edition
    status: public
status: public
supervisor:
- first_name: Harald L
  full_name: Janovjak, Harald L
  id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
  last_name: Janovjak
  orcid: 0000-0002-8023-9315
title: 'Design and characterization of methods and biological components to realize
  synthetic neurotransmission '
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2018'
...
---
_id: '5816'
abstract:
- lang: eng
  text: Solid-state qubit manipulation and read-out fidelities are reaching fault-tolerance,
    but quantum error correction requires millions of physical qubits and therefore
    a scalable quantum computer architecture. To solve signal-line bandwidth and fan-out
    problems, microwave sources required for qubit manipulation might be embedded
    close to the qubit chip, typically operating at temperatures below 4 K. Here,
    we perform the first low temperature measurements of a 130 nm BiCMOS based SiGe
    voltage controlled oscillator at cryogenic temperature. We determined the frequency
    and output power dependence on temperature and magnetic field up to 5 T and measured
    the temperature influence on its noise performance. The device maintains its full
    functionality from 300 K to 4 K. The carrier frequency at 4 K increases by 3%
    with respect to the carrier frequency at 300 K, and the output power at 4 K increases
    by 10 dB relative to the output power at 300 K. The frequency tuning range of
    approximately 20% remains unchanged between 300 K and 4 K. In an in-plane magnetic
    field of 5 T, the carrier frequency shifts by only 0.02% compared to the frequency
    at zero magnetic field.
article_number: '114701'
article_processing_charge: No
arxiv: 1
author:
- first_name: Arne
  full_name: Hollmann, Arne
  last_name: Hollmann
- first_name: Daniel
  full_name: Jirovec, Daniel
  id: 4C473F58-F248-11E8-B48F-1D18A9856A87
  last_name: Jirovec
  orcid: 0000-0002-7197-4801
- first_name: Maciej
  full_name: Kucharski, Maciej
  last_name: Kucharski
- first_name: Dietmar
  full_name: Kissinger, Dietmar
  last_name: Kissinger
- first_name: Gunter
  full_name: Fischer, Gunter
  last_name: Fischer
- first_name: Lars R.
  full_name: Schreiber, Lars R.
  last_name: Schreiber
citation:
  ama: Hollmann A, Jirovec D, Kucharski M, Kissinger D, Fischer G, Schreiber LR. 30
    GHz-voltage controlled oscillator operating at 4 K. <i>Review of Scientific Instruments</i>.
    2018;89(11). doi:<a href="https://doi.org/10.1063/1.5038258">10.1063/1.5038258</a>
  apa: Hollmann, A., Jirovec, D., Kucharski, M., Kissinger, D., Fischer, G., &#38;
    Schreiber, L. R. (2018). 30 GHz-voltage controlled oscillator operating at 4 K.
    <i>Review of Scientific Instruments</i>. AIP Publishing. <a href="https://doi.org/10.1063/1.5038258">https://doi.org/10.1063/1.5038258</a>
  chicago: Hollmann, Arne, Daniel Jirovec, Maciej Kucharski, Dietmar Kissinger, Gunter
    Fischer, and Lars R. Schreiber. “30 GHz-Voltage Controlled Oscillator Operating
    at 4 K.” <i>Review of Scientific Instruments</i>. AIP Publishing, 2018. <a href="https://doi.org/10.1063/1.5038258">https://doi.org/10.1063/1.5038258</a>.
  ieee: A. Hollmann, D. Jirovec, M. Kucharski, D. Kissinger, G. Fischer, and L. R.
    Schreiber, “30 GHz-voltage controlled oscillator operating at 4 K,” <i>Review
    of Scientific Instruments</i>, vol. 89, no. 11. AIP Publishing, 2018.
  ista: Hollmann A, Jirovec D, Kucharski M, Kissinger D, Fischer G, Schreiber LR.
    2018. 30 GHz-voltage controlled oscillator operating at 4 K. Review of Scientific
    Instruments. 89(11), 114701.
  mla: Hollmann, Arne, et al. “30 GHz-Voltage Controlled Oscillator Operating at 4
    K.” <i>Review of Scientific Instruments</i>, vol. 89, no. 11, 114701, AIP Publishing,
    2018, doi:<a href="https://doi.org/10.1063/1.5038258">10.1063/1.5038258</a>.
  short: A. Hollmann, D. Jirovec, M. Kucharski, D. Kissinger, G. Fischer, L.R. Schreiber,
    Review of Scientific Instruments 89 (2018).
date_created: 2019-01-10T14:22:23Z
date_published: 2018-11-01T00:00:00Z
date_updated: 2026-08-10T22:30:46Z
day: '01'
department:
- _id: GeKa
doi: 10.1063/1.5038258
external_id:
  arxiv:
  - '1804.09522'
  isi:
  - '000451735700054'
intvolume: '        89'
isi: 1
issue: '11'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1804.09522
month: '11'
oa: 1
oa_version: Preprint
publication: Review of Scientific Instruments
publication_identifier:
  issn:
  - 0034-6748
publication_status: published
publisher: AIP Publishing
quality_controlled: '1'
related_material:
  record:
  - id: '10058'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: 30 GHz-voltage controlled oscillator operating at 4 K
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 89
year: '2018'
...
---
_id: '2'
abstract:
- lang: eng
  text: Indirect reciprocity explores how humans act when their reputation is at stake,
    and which social norms they use to assess the actions of others. A crucial question
    in indirect reciprocity is which social norms can maintain stable cooperation
    in a society. Past research has highlighted eight such norms, called “leading-eight”
    strategies. This past research, however, is based on the assumption that all relevant
    information about other population members is publicly available and that everyone
    agrees on who is good or bad. Instead, here we explore the reputation dynamics
    when information is private and noisy. We show that under these conditions, most
    leading-eight strategies fail to evolve. Those leading-eight strategies that do
    evolve are unable to sustain full cooperation.Indirect reciprocity is a mechanism
    for cooperation based on shared moral systems and individual reputations. It assumes
    that members of a community routinely observe and assess each other and that they
    use this information to decide who is good or bad, and who deserves cooperation.
    When information is transmitted publicly, such that all community members agree
    on each other’s reputation, previous research has highlighted eight crucial moral
    systems. These “leading-eight” strategies can maintain cooperation and resist
    invasion by defectors. However, in real populations individuals often hold their
    own private views of others. Once two individuals disagree about their opinion
    of some third party, they may also see its subsequent actions in a different light.
    Their opinions may further diverge over time. Herein, we explore indirect reciprocity
    when information transmission is private and noisy. We find that in the presence
    of perception errors, most leading-eight strategies cease to be stable. Even if
    a leading-eight strategy evolves, cooperation rates may drop considerably when
    errors are common. Our research highlights the role of reliable information and
    synchronized reputations to maintain stable moral systems.
article_processing_charge: No
author:
- first_name: Christian
  full_name: Hilbe, Christian
  id: 2FDF8F3C-F248-11E8-B48F-1D18A9856A87
  last_name: Hilbe
  orcid: 0000-0001-5116-955X
- first_name: Laura
  full_name: Schmid, Laura
  id: 38B437DE-F248-11E8-B48F-1D18A9856A87
  last_name: Schmid
  orcid: 0000-0002-6978-7329
- first_name: Josef
  full_name: Tkadlec, Josef
  id: 3F24CCC8-F248-11E8-B48F-1D18A9856A87
  last_name: Tkadlec
  orcid: 0000-0002-1097-9684
- 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, Schmid L, Tkadlec J, Chatterjee K, Nowak M. Indirect reciprocity with
    private, noisy, and incomplete information. <i>PNAS</i>. 2018;115(48):12241-12246.
    doi:<a href="https://doi.org/10.1073/pnas.1810565115">10.1073/pnas.1810565115</a>
  apa: Hilbe, C., Schmid, L., Tkadlec, J., Chatterjee, K., &#38; Nowak, M. (2018).
    Indirect reciprocity with private, noisy, and incomplete information. <i>PNAS</i>.
    National Academy of Sciences. <a href="https://doi.org/10.1073/pnas.1810565115">https://doi.org/10.1073/pnas.1810565115</a>
  chicago: Hilbe, Christian, Laura Schmid, Josef Tkadlec, Krishnendu Chatterjee, and
    Martin Nowak. “Indirect Reciprocity with Private, Noisy, and Incomplete Information.”
    <i>PNAS</i>. National Academy of Sciences, 2018. <a href="https://doi.org/10.1073/pnas.1810565115">https://doi.org/10.1073/pnas.1810565115</a>.
  ieee: C. Hilbe, L. Schmid, J. Tkadlec, K. Chatterjee, and M. Nowak, “Indirect reciprocity
    with private, noisy, and incomplete information,” <i>PNAS</i>, vol. 115, no. 48.
    National Academy of Sciences, pp. 12241–12246, 2018.
  ista: Hilbe C, Schmid L, Tkadlec J, Chatterjee K, Nowak M. 2018. Indirect reciprocity
    with private, noisy, and incomplete information. PNAS. 115(48), 12241–12246.
  mla: Hilbe, Christian, et al. “Indirect Reciprocity with Private, Noisy, and Incomplete
    Information.” <i>PNAS</i>, vol. 115, no. 48, National Academy of Sciences, 2018,
    pp. 12241–46, doi:<a href="https://doi.org/10.1073/pnas.1810565115">10.1073/pnas.1810565115</a>.
  short: C. Hilbe, L. Schmid, J. Tkadlec, K. Chatterjee, M. Nowak, PNAS 115 (2018)
    12241–12246.
date_created: 2018-12-11T11:44:05Z
date_published: 2018-11-27T00:00:00Z
date_updated: 2026-08-10T22:30:49Z
day: '27'
department:
- _id: KrCh
doi: 10.1073/pnas.1810565115
ec_funded: 1
external_id:
  isi:
  - '000451351000063'
  pmid:
  - '30429320'
intvolume: '       115'
isi: 1
issue: '48'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pubmed/30429320
month: '11'
oa: 1
oa_version: Submitted Version
page: 12241-12246
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: 25832EC2-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: S 11407_N23
  name: Rigorous Systems Engineering
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
related_material:
  link:
  - description: News on IST Homepage
    relation: press_release
    url: https://ist.ac.at/en/news/no-cooperation-without-open-communication/
  record:
  - id: '10293'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Indirect reciprocity with private, noisy, and incomplete information
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 115
year: '2018'
...
---
_id: '442'
abstract:
- lang: eng
  text: The rapid auxin-triggered growth of the Arabidopsis hypocotyls involves the
    nuclear TIR1/AFB-Aux/IAA signaling and is accompanied by acidification of the
    apoplast and cell walls (Fendrych et al., 2016). Here, we describe in detail the
    method for analysis of the elongation and the TIR1/AFB-Aux/IAA-dependent auxin
    response in hypocotyl segments as well as the determination of relative values
    of the cell wall pH.
acknowledgement: 'This protocol was adapted from Fendrych et al., 2016. This project
  has received funding from the European Union’s Horizon 2020 research and innovation
  programme under the Marie Skłodowska-Curie Grant Agreement No. 665385, and Austrian
  Science Fund (FWF) [M 2128-B21]. '
article_processing_charge: No
article_type: original
author:
- first_name: Lanxin
  full_name: Li, Lanxin
  id: 367EF8FA-F248-11E8-B48F-1D18A9856A87
  last_name: Li
  orcid: 0000-0002-5607-272X
- first_name: Gabriel
  full_name: Krens, Gabriel
  id: 2B819732-F248-11E8-B48F-1D18A9856A87
  last_name: Krens
  orcid: 0000-0003-4761-5996
- first_name: Matyas
  full_name: Fendrych, Matyas
  id: 43905548-F248-11E8-B48F-1D18A9856A87
  last_name: Fendrych
  orcid: 0000-0002-9767-8699
- first_name: Jirí
  full_name: Friml, Jirí
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
citation:
  ama: Li L, Krens G, Fendrych M, Friml J. Real-time analysis of auxin response, cell
    wall pH and elongation in Arabidopsis thaliana Hypocotyls. <i>Bio-protocol</i>.
    2018;8(1). doi:<a href="https://doi.org/10.21769/BioProtoc.2685">10.21769/BioProtoc.2685</a>
  apa: Li, L., Krens, G., Fendrych, M., &#38; Friml, J. (2018). Real-time analysis
    of auxin response, cell wall pH and elongation in Arabidopsis thaliana Hypocotyls.
    <i>Bio-Protocol</i>. Bio-protocol. <a href="https://doi.org/10.21769/BioProtoc.2685">https://doi.org/10.21769/BioProtoc.2685</a>
  chicago: Li, Lanxin, Gabriel Krens, Matyas Fendrych, and Jiří Friml. “Real-Time
    Analysis of Auxin Response, Cell Wall PH and Elongation in Arabidopsis Thaliana
    Hypocotyls.” <i>Bio-Protocol</i>. Bio-protocol, 2018. <a href="https://doi.org/10.21769/BioProtoc.2685">https://doi.org/10.21769/BioProtoc.2685</a>.
  ieee: L. Li, G. Krens, M. Fendrych, and J. Friml, “Real-time analysis of auxin response,
    cell wall pH and elongation in Arabidopsis thaliana Hypocotyls,” <i>Bio-protocol</i>,
    vol. 8, no. 1. Bio-protocol, 2018.
  ista: Li L, Krens G, Fendrych M, Friml J. 2018. Real-time analysis of auxin response,
    cell wall pH and elongation in Arabidopsis thaliana Hypocotyls. Bio-protocol.
    8(1).
  mla: Li, Lanxin, et al. “Real-Time Analysis of Auxin Response, Cell Wall PH and
    Elongation in Arabidopsis Thaliana Hypocotyls.” <i>Bio-Protocol</i>, vol. 8, no.
    1, Bio-protocol, 2018, doi:<a href="https://doi.org/10.21769/BioProtoc.2685">10.21769/BioProtoc.2685</a>.
  short: L. Li, G. Krens, M. Fendrych, J. Friml, Bio-Protocol 8 (2018).
corr_author: '1'
date_created: 2018-12-11T11:46:30Z
date_published: 2018-01-05T00:00:00Z
date_updated: 2026-08-10T22:30:47Z
day: '05'
ddc:
- '576'
- '581'
department:
- _id: JiFr
- _id: Bio
doi: 10.21769/BioProtoc.2685
ec_funded: 1
file:
- access_level: open_access
  checksum: 6644ba698206eda32b0abf09128e63e3
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:17:43Z
  date_updated: 2020-07-14T12:46:29Z
  file_id: '5299'
  file_name: IST-2018-970-v1+1_2018_Lanxin_Real-time_analysis.pdf
  file_size: 11352389
  relation: main_file
file_date_updated: 2020-07-14T12:46:29Z
has_accepted_license: '1'
intvolume: '         8'
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
project:
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '665385'
  name: International IST Doctoral Program
publication: Bio-protocol
publication_identifier:
  eissn:
  - 2331-8325
publication_status: published
publisher: Bio-protocol
publist_id: '7381'
pubrep_id: '970'
quality_controlled: '1'
related_material:
  record:
  - id: '10083'
    relation: dissertation_contains
    status: public
status: public
title: Real-time analysis of auxin response, cell wall pH and elongation in Arabidopsis
  thaliana Hypocotyls
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: 8
year: '2018'
...
---
OA_place: publisher
_id: '395'
abstract:
- lang: eng
  text: 'Autism spectrum disorders (ASD) are a group of genetic disorders often overlapping
    with other neurological conditions. Despite the remarkable number of scientific
    breakthroughs of the last 100 years, the treatment of neurodevelopmental disorders
    (e.g. autism spectrum disorder, intellectual disability, epilepsy) remains a great
    challenge. Recent advancements in geno mics, like whole-exome or whole-genome
    sequencing, have enabled scientists to identify numerous mutations underlying
    neurodevelopmental disorders. Given the few hundred risk genes that were discovered,
    the etiological variability and the heterogeneous phenotypic outcomes, the need
    for genotype -along with phenotype- based diagnosis of individual patients becomes
    a requisite. Driven by this rationale, in a previous study our group described
    mutations, identified via whole - exome sequencing, in the gene BCKDK – encoding
    for a key regulator of branched chain amin o acid (BCAA) catabolism - as a cause
    of ASD. Following up on the role of BCAAs, in the study described here we show
    that the solute carrier transporter 7a5 (SLC7A5), a large neutral amino acid transporter
    localized mainly at the blood brain barrier (BBB), has an essential role in maintaining
    normal levels of brain BCAAs. In mice, deletion of Slc7a5 from the endothelial
    cells of the BBB leads to atypical brain amino acid profile, abnormal mRNA translation
    and severe neurolo gical abnormalities. Additionally, deletion of Slc7a5 from
    the neural progenitor cell population leads to microcephaly. Interestingly, we
    demonstrate that BCAA intracerebroventricular administration ameliorates abnormal
    behaviors in adult mutant mice. Furthermore, whole - exome sequencing of patients
    diagnosed with neurological dis o r ders helped us identify several patients with
    autistic traits, microcephaly and motor delay carrying deleterious homozygous
    mutations in the SLC7A5 gene. In conclusion, our data elucidate a neurological
    syndrome defined by SLC7A5 mutations and support an essential role for t he BCAA
    s in human bra in function. Together with r ecent studies (described in chapter
    two) that have successfully made the transition into clinical practice, our findings
    on the role of B CAAs might have a crucial impact on the development of novel
    individualized therapeutic strategies for ASD. '
acknowledged_ssus:
- _id: PreCl
- _id: EM-Fac
- _id: Bio
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Dora-Clara
  full_name: Tarlungeanu, Dora-Clara
  id: 2ABCE612-F248-11E8-B48F-1D18A9856A87
  last_name: Tarlungeanu
citation:
  ama: Tarlungeanu D-C. The branched chain amino acids in autism spectrum disorders
    . 2018. doi:<a href="https://doi.org/10.15479/AT:ISTA:th_992">10.15479/AT:ISTA:th_992</a>
  apa: Tarlungeanu, D.-C. (2018). <i>The branched chain amino acids in autism spectrum
    disorders </i>. Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:th_992">https://doi.org/10.15479/AT:ISTA:th_992</a>
  chicago: Tarlungeanu, Dora-Clara. “The Branched Chain Amino Acids in Autism Spectrum
    Disorders .” Institute of Science and Technology Austria, 2018. <a href="https://doi.org/10.15479/AT:ISTA:th_992">https://doi.org/10.15479/AT:ISTA:th_992</a>.
  ieee: D.-C. Tarlungeanu, “The branched chain amino acids in autism spectrum disorders
    ,” Institute of Science and Technology Austria, 2018.
  ista: Tarlungeanu D-C. 2018. The branched chain amino acids in autism spectrum disorders
    . Institute of Science and Technology Austria.
  mla: Tarlungeanu, Dora-Clara. <i>The Branched Chain Amino Acids in Autism Spectrum
    Disorders </i>. Institute of Science and Technology Austria, 2018, doi:<a href="https://doi.org/10.15479/AT:ISTA:th_992">10.15479/AT:ISTA:th_992</a>.
  short: D.-C. Tarlungeanu, The Branched Chain Amino Acids in Autism Spectrum Disorders
    , Institute of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2018-12-11T11:46:14Z
date_published: 2018-03-01T00:00:00Z
date_updated: 2026-04-08T14:15:20Z
day: '01'
ddc:
- '570'
- '616'
degree_awarded: PhD
department:
- _id: GaNo
doi: 10.15479/AT:ISTA:th_992
file:
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file_date_updated: 2021-02-11T23:30:15Z
has_accepted_license: '1'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: '88'
project:
- _id: 25473368-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: F03523
  name: Transmembrane Transporters in Health and Disease
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '7434'
pubrep_id: '992'
related_material:
  record:
  - id: '1183'
    relation: part_of_dissertation
    status: public
status: public
supervisor:
- first_name: Gaia
  full_name: Novarino, Gaia
  id: 3E57A680-F248-11E8-B48F-1D18A9856A87
  last_name: Novarino
  orcid: 0000-0002-7673-7178
title: 'The branched chain amino acids in autism spectrum disorders '
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: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2018'
...
---
_id: '47'
abstract:
- lang: eng
  text: Plant hormones as signalling molecules play an essential role in the control
    of plant growth and development. Typically, sites of hormonal action are usually
    distant from the site of biosynthesis thus relying on efficient transport mechanisms.
    Over the last decades, molecular identification of proteins and protein complexes
    involved in hormonal transport has started. Advanced screens for genes involved
    in hormonal transport in combination with transport assays using heterologous
    systems such as yeast, insect, or tobacco BY2 cells or Xenopus oocytes provided
    important insights into mechanisms underlying distribution of hormones in plant
    body and led to identification of principal transporters for each hormone. This
    review gives a short overview of the mechanisms of hormonal transport and transporters
    identified in Arabidopsis thaliana.
article_processing_charge: No
author:
- first_name: Rashed
  full_name: Abualia, Rashed
  id: 4827E134-F248-11E8-B48F-1D18A9856A87
  last_name: Abualia
  orcid: 0000-0002-9357-9415
- first_name: Eva
  full_name: Benková, Eva
  id: 38F4F166-F248-11E8-B48F-1D18A9856A87
  last_name: Benková
  orcid: 0000-0002-8510-9739
- first_name: Benoît
  full_name: Lacombe, Benoît
  last_name: Lacombe
citation:
  ama: Abualia R, Benková E, Lacombe B. Transporters and mechanisms of hormone transport
    in arabidopsis. <i>Advances in Botanical Research</i>. 2018;87:115-138. doi:<a
    href="https://doi.org/10.1016/bs.abr.2018.09.007">10.1016/bs.abr.2018.09.007</a>
  apa: Abualia, R., Benková, E., &#38; Lacombe, B. (2018). Transporters and mechanisms
    of hormone transport in arabidopsis. <i>Advances in Botanical Research</i>. Elsevier.
    <a href="https://doi.org/10.1016/bs.abr.2018.09.007">https://doi.org/10.1016/bs.abr.2018.09.007</a>
  chicago: Abualia, Rashed, Eva Benková, and Benoît Lacombe. “Transporters and Mechanisms
    of Hormone Transport in Arabidopsis.” <i>Advances in Botanical Research</i>. Elsevier,
    2018. <a href="https://doi.org/10.1016/bs.abr.2018.09.007">https://doi.org/10.1016/bs.abr.2018.09.007</a>.
  ieee: R. Abualia, E. Benková, and B. Lacombe, “Transporters and mechanisms of hormone
    transport in arabidopsis,” <i>Advances in Botanical Research</i>, vol. 87. Elsevier,
    pp. 115–138, 2018.
  ista: Abualia R, Benková E, Lacombe B. 2018. Transporters and mechanisms of hormone
    transport in arabidopsis. Advances in Botanical Research. 87, 115–138.
  mla: Abualia, Rashed, et al. “Transporters and Mechanisms of Hormone Transport in
    Arabidopsis.” <i>Advances in Botanical Research</i>, vol. 87, Elsevier, 2018,
    pp. 115–38, doi:<a href="https://doi.org/10.1016/bs.abr.2018.09.007">10.1016/bs.abr.2018.09.007</a>.
  short: R. Abualia, E. Benková, B. Lacombe, Advances in Botanical Research 87 (2018)
    115–138.
date_created: 2018-12-11T11:44:20Z
date_published: 2018-01-01T00:00:00Z
date_updated: 2026-08-10T22:30:52Z
day: '01'
department:
- _id: EvBe
doi: 10.1016/bs.abr.2018.09.007
external_id:
  isi:
  - '000453657800006'
intvolume: '        87'
isi: 1
language:
- iso: eng
month: '01'
oa_version: None
page: 115 - 138
publication: Advances in Botanical Research
publication_status: published
publisher: Elsevier
publist_id: '8007'
quality_controlled: '1'
related_material:
  record:
  - id: '10303'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Transporters and mechanisms of hormone transport in arabidopsis
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 87
year: '2018'
...
---
_id: '323'
abstract:
- lang: eng
  text: 'In the here presented thesis, we explore the role of branched actin networks
    in cell migration and antigen presentation, the two most relevant processes in
    dendritic cell biology. Branched actin networks construct lamellipodial protrusions
    at the leading edge of migrating cells. These are typically seen as adhesive structures,
    which mediate force transduction to the extracellular matrix that leads to forward
    locomotion. We ablated Arp2/3 nucleation promoting factor WAVE in DCs and found
    that the resulting cells lack lamellipodial protrusions. Instead, depending on
    the maturation state, one or multiple filopodia were formed. By challenging these
    cells in a variety of migration assays we found that lamellipodial protrusions
    are dispensable for the locomotion of leukocytes and actually dampen the speed
    of migration. However, lamellipodia are critically required to negotiate complex
    environments that DCs experience while they travel to the next draining lymph
    node. Taken together our results suggest that leukocyte lamellipodia have rather
    a sensory- than a force transducing function. Furthermore, we show for the first
    time structure and dynamics of dendritic cell F-actin at the immunological synapse
    with naïve T cells. Dendritic cell F-actin appears as dynamic foci that are nucleated
    by the Arp2/3 complex. WAVE ablated dendritic cells show increased membrane tension,
    leading to an altered ultrastructure of the immunological synapse and severe T
    cell priming defects. These results point towards a previously unappreciated role
    of the cellular mechanics of dendritic cells in T cell activation. Additionally,
    we present a novel cell culture based system for the differentiation of dendritic
    cells from conditionally immortalized hematopoietic precursors. These precursor
    cells are genetically tractable via the CRISPR/Cas9 system while they retain their
    ability to differentiate into highly migratory dendritic cells and other immune
    cells. This will foster the study of all aspects of dendritic cell biology and
    beyond. '
acknowledged_ssus:
- _id: NanoFab
- _id: Bio
- _id: PreCl
- _id: EM-Fac
acknowledgement: "First of all I would like to thank Michael Sixt for giving me the
  opportunity to work in \r\nhis group and for his support throughout the years. He
  is a truly inspiring person and \r\nthe  best  boss  one  can  imagine.  I  would
  \ also  like  to  thank  all  current  and  past \r\nmembers of the Sixt group for
  their help and the great working atmosphere in the lab. \r\nIt is a true privilege
  to work with such a bright, funny and friendly group of people and \r\nI’m  proud
  \ that  I  could  be  part  of  it.  Furthermore,  I  would  like  to  say  ‘thank
  \ you’  to Daria Siekhaus for all the meetings and discussion we had throughout
  the years \r\nand to  Federica  Benvenuti  for  being  part  of  my  committee.
  \ I  am  also  grateful  to  Jack \r\nMerrin  in  the  nanofabrication  facility
  \ and  all  the  people  working  in  the  bioimaging-\r\n, the electron microscopy-
  and the preclinical facilities."
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Alexander F
  full_name: Leithner, Alexander F
  id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
  last_name: Leithner
  orcid: 0000-0002-1073-744X
citation:
  ama: Leithner AF. Branched actin networks in dendritic cell biology. 2018. doi:<a
    href="https://doi.org/10.15479/AT:ISTA:th_998">10.15479/AT:ISTA:th_998</a>
  apa: Leithner, A. F. (2018). <i>Branched actin networks in dendritic cell biology</i>.
    Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:th_998">https://doi.org/10.15479/AT:ISTA:th_998</a>
  chicago: Leithner, Alexander F. “Branched Actin Networks in Dendritic Cell Biology.”
    Institute of Science and Technology Austria, 2018. <a href="https://doi.org/10.15479/AT:ISTA:th_998">https://doi.org/10.15479/AT:ISTA:th_998</a>.
  ieee: A. F. Leithner, “Branched actin networks in dendritic cell biology,” Institute
    of Science and Technology Austria, 2018.
  ista: Leithner AF. 2018. Branched actin networks in dendritic cell biology. Institute
    of Science and Technology Austria.
  mla: Leithner, Alexander F. <i>Branched Actin Networks in Dendritic Cell Biology</i>.
    Institute of Science and Technology Austria, 2018, doi:<a href="https://doi.org/10.15479/AT:ISTA:th_998">10.15479/AT:ISTA:th_998</a>.
  short: A.F. Leithner, Branched Actin Networks in Dendritic Cell Biology, Institute
    of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2018-12-11T11:45:49Z
date_published: 2018-04-12T00:00:00Z
date_updated: 2025-09-22T08:27:34Z
day: '12'
ddc:
- '571'
- '599'
- '610'
degree_awarded: PhD
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:th_998
file:
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  date_created: 2019-04-05T09:23:11Z
  date_updated: 2021-02-11T23:30:17Z
  embargo_to: open_access
  file_id: '6219'
  file_name: PhD_thesis_AlexLeithner_final_version.docx
  file_size: 29027671
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  checksum: 071f7476db29e41146824ebd0697cb10
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  creator: dernst
  date_created: 2019-04-05T09:23:11Z
  date_updated: 2021-02-11T11:17:16Z
  embargo: 2019-04-15
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  relation: main_file
file_date_updated: 2021-02-11T23:30:17Z
has_accepted_license: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: '99'
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '7542'
pubrep_id: '998'
related_material:
  record:
  - id: '1321'
    relation: part_of_dissertation
    status: public
status: public
supervisor:
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
title: Branched actin networks in dendritic cell biology
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: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2018'
...
---
_id: '449'
abstract:
- lang: eng
  text: Auxin is unique among plant hormones due to its directional transport that
    is mediated by the polarly distributed PIN auxin transporters at the plasma membrane.
    The canalization hypothesis proposes that the auxin feedback on its polar flow
    is a crucial, plant-specific mechanism mediating multiple self-organizing developmental
    processes. Here, we used the auxin effect on the PIN polar localization in Arabidopsis
    thaliana roots as a proxy for the auxin feedback on the PIN polarity during canalization.
    We performed microarray experiments to find regulators of this process that act
    downstream of auxin. We identified genes that were transcriptionally regulated
    by auxin in an AXR3/IAA17- and ARF7/ARF19-dependent manner. Besides the known
    components of the PIN polarity, such as PID and PIP5K kinases, a number of potential
    new regulators were detected, among which the WRKY23 transcription factor, which
    was characterized in more detail. Gain- and loss-of-function mutants confirmed
    a role for WRKY23 in mediating the auxin effect on the PIN polarity. Accordingly,
    processes requiring auxin-mediated PIN polarity rearrangements, such as vascular
    tissue development during leaf venation, showed a higher WRKY23 expression and
    required the WRKY23 activity. Our results provide initial insights into the auxin
    transcriptional network acting upstream of PIN polarization and, potentially,
    canalization-mediated plant development.
article_processing_charge: Yes
author:
- first_name: Tomas
  full_name: Prat, Tomas
  id: 3DA3BFEE-F248-11E8-B48F-1D18A9856A87
  last_name: Prat
- first_name: Jakub
  full_name: Hajny, Jakub
  id: 4800CC20-F248-11E8-B48F-1D18A9856A87
  last_name: Hajny
  orcid: 0000-0003-2140-7195
- first_name: Wim
  full_name: Grunewald, Wim
  last_name: Grunewald
- first_name: Mina K
  full_name: Vasileva, Mina K
  id: 3407EB18-F248-11E8-B48F-1D18A9856A87
  last_name: Vasileva
- first_name: Gergely
  full_name: Molnar, Gergely
  id: 34F1AF46-F248-11E8-B48F-1D18A9856A87
  last_name: Molnar
- first_name: Ricardo
  full_name: Tejos, Ricardo
  last_name: Tejos
- first_name: Markus
  full_name: Schmid, Markus
  last_name: Schmid
- first_name: Michael
  full_name: Sauer, Michael
  last_name: Sauer
- first_name: Jirí
  full_name: Friml, Jirí
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
citation:
  ama: Prat T, Hajny J, Grunewald W, et al. WRKY23 is a component of the transcriptional
    network mediating auxin feedback on PIN polarity. <i>PLoS Genetics</i>. 2018;14(1).
    doi:<a href="https://doi.org/10.1371/journal.pgen.1007177">10.1371/journal.pgen.1007177</a>
  apa: Prat, T., Hajny, J., Grunewald, W., Vasileva, M. K., Molnar, G., Tejos, R.,
    … Friml, J. (2018). WRKY23 is a component of the transcriptional network mediating
    auxin feedback on PIN polarity. <i>PLoS Genetics</i>. Public Library of Science.
    <a href="https://doi.org/10.1371/journal.pgen.1007177">https://doi.org/10.1371/journal.pgen.1007177</a>
  chicago: Prat, Tomas, Jakub Hajny, Wim Grunewald, Mina K Vasileva, Gergely Molnar,
    Ricardo Tejos, Markus Schmid, Michael Sauer, and Jiří Friml. “WRKY23 Is a Component
    of the Transcriptional Network Mediating Auxin Feedback on PIN Polarity.” <i>PLoS
    Genetics</i>. Public Library of Science, 2018. <a href="https://doi.org/10.1371/journal.pgen.1007177">https://doi.org/10.1371/journal.pgen.1007177</a>.
  ieee: T. Prat <i>et al.</i>, “WRKY23 is a component of the transcriptional network
    mediating auxin feedback on PIN polarity,” <i>PLoS Genetics</i>, vol. 14, no.
    1. Public Library of Science, 2018.
  ista: Prat T, Hajny J, Grunewald W, Vasileva MK, Molnar G, Tejos R, Schmid M, Sauer
    M, Friml J. 2018. WRKY23 is a component of the transcriptional network mediating
    auxin feedback on PIN polarity. PLoS Genetics. 14(1).
  mla: Prat, Tomas, et al. “WRKY23 Is a Component of the Transcriptional Network Mediating
    Auxin Feedback on PIN Polarity.” <i>PLoS Genetics</i>, vol. 14, no. 1, Public
    Library of Science, 2018, doi:<a href="https://doi.org/10.1371/journal.pgen.1007177">10.1371/journal.pgen.1007177</a>.
  short: T. Prat, J. Hajny, W. Grunewald, M.K. Vasileva, G. Molnar, R. Tejos, M. Schmid,
    M. Sauer, J. Friml, PLoS Genetics 14 (2018).
corr_author: '1'
date_created: 2018-12-11T11:46:32Z
date_published: 2018-01-29T00:00:00Z
date_updated: 2026-08-10T22:30:57Z
day: '29'
ddc:
- '581'
department:
- _id: JiFr
doi: 10.1371/journal.pgen.1007177
ec_funded: 1
external_id:
  isi:
  - '000423718600034'
file:
- access_level: open_access
  checksum: 0276d66788ec076f4924164a39e6a712
  content_type: application/pdf
  creator: system
  date_created: 2018-12-12T10:10:52Z
  date_updated: 2020-07-14T12:46:30Z
  file_id: '4843'
  file_name: IST-2018-967-v1+1_journal.pgen.1007177.pdf
  file_size: 24709062
  relation: main_file
file_date_updated: 2020-07-14T12:46:30Z
has_accepted_license: '1'
intvolume: '        14'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
project:
- _id: 25716A02-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '282300'
  name: Polarity and subcellular dynamics in plants
publication: PLoS Genetics
publication_status: published
publisher: Public Library of Science
publist_id: '7373'
pubrep_id: '967'
quality_controlled: '1'
related_material:
  record:
  - id: '7172'
    relation: dissertation_contains
    status: public
  - id: '1127'
    relation: dissertation_contains
    status: public
  - id: '8822'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: WRKY23 is a component of the transcriptional network mediating auxin feedback
  on PIN polarity
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 14
year: '2018'
...
---
_id: '191'
abstract:
- lang: eng
  text: Intercellular distribution of the plant hormone auxin largely depends on the
    polar subcellular distribution of the plasma membrane PIN-FORMED (PIN) auxin transporters.
    PIN polarity switches in response to different developmental and environmental
    signals have been shown to redirect auxin fluxes mediating certain developmental
    responses. PIN phosphorylation at different sites and by different kinases is
    crucial for PIN function. Here we investigate the role of PIN phosphorylation
    during gravitropic response. Loss- and gain-of-function mutants in PINOID and
    related kinases but not in D6PK kinase as well as mutations mimicking constitutive
    dephosphorylated or phosphorylated status of two clusters of predicted phosphorylation
    sites partially disrupted PIN3 phosphorylation and caused defects in gravitropic
    bending in roots and hypocotyls. In particular, they impacted PIN3 polarity rearrangements
    in response to gravity and during feed-back regulation by auxin itself. Thus PIN
    phosphorylation, besides regulating transport activity and apical-basal targeting,
    is also important for the rapid polarity switches in response to environmental
    and endogenous signals.
article_number: '10279'
article_processing_charge: No
author:
- first_name: Peter
  full_name: Grones, Peter
  id: 399876EC-F248-11E8-B48F-1D18A9856A87
  last_name: Grones
- first_name: Melinda F
  full_name: Abas, Melinda F
  id: 3CFB3B1C-F248-11E8-B48F-1D18A9856A87
  last_name: Abas
- first_name: Jakub
  full_name: Hajny, Jakub
  id: 4800CC20-F248-11E8-B48F-1D18A9856A87
  last_name: Hajny
  orcid: 0000-0003-2140-7195
- first_name: Angharad
  full_name: Jones, Angharad
  last_name: Jones
- first_name: Sascha
  full_name: Waidmann, Sascha
  last_name: Waidmann
- first_name: Jürgen
  full_name: Kleine Vehn, Jürgen
  last_name: Kleine Vehn
- first_name: Jirí
  full_name: Friml, Jirí
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
citation:
  ama: Grones P, Abas MF, Hajny J, et al. PID/WAG-mediated phosphorylation of the
    Arabidopsis PIN3 auxin transporter mediates polarity switches during gravitropism.
    <i>Scientific Reports</i>. 2018;8(1). doi:<a href="https://doi.org/10.1038/s41598-018-28188-1">10.1038/s41598-018-28188-1</a>
  apa: Grones, P., Abas, M. F., Hajny, J., Jones, A., Waidmann, S., Kleine Vehn, J.,
    &#38; Friml, J. (2018). PID/WAG-mediated phosphorylation of the Arabidopsis PIN3
    auxin transporter mediates polarity switches during gravitropism. <i>Scientific
    Reports</i>. Springer. <a href="https://doi.org/10.1038/s41598-018-28188-1">https://doi.org/10.1038/s41598-018-28188-1</a>
  chicago: Grones, Peter, Melinda F Abas, Jakub Hajny, Angharad Jones, Sascha Waidmann,
    Jürgen Kleine Vehn, and Jiří Friml. “PID/WAG-Mediated Phosphorylation of the Arabidopsis
    PIN3 Auxin Transporter Mediates Polarity Switches during Gravitropism.” <i>Scientific
    Reports</i>. Springer, 2018. <a href="https://doi.org/10.1038/s41598-018-28188-1">https://doi.org/10.1038/s41598-018-28188-1</a>.
  ieee: P. Grones <i>et al.</i>, “PID/WAG-mediated phosphorylation of the Arabidopsis
    PIN3 auxin transporter mediates polarity switches during gravitropism,” <i>Scientific
    Reports</i>, vol. 8, no. 1. Springer, 2018.
  ista: Grones P, Abas MF, Hajny J, Jones A, Waidmann S, Kleine Vehn J, Friml J. 2018.
    PID/WAG-mediated phosphorylation of the Arabidopsis PIN3 auxin transporter mediates
    polarity switches during gravitropism. Scientific Reports. 8(1), 10279.
  mla: Grones, Peter, et al. “PID/WAG-Mediated Phosphorylation of the Arabidopsis
    PIN3 Auxin Transporter Mediates Polarity Switches during Gravitropism.” <i>Scientific
    Reports</i>, vol. 8, no. 1, 10279, Springer, 2018, doi:<a href="https://doi.org/10.1038/s41598-018-28188-1">10.1038/s41598-018-28188-1</a>.
  short: P. Grones, M.F. Abas, J. Hajny, A. Jones, S. Waidmann, J. Kleine Vehn, J.
    Friml, Scientific Reports 8 (2018).
date_created: 2018-12-11T11:45:06Z
date_published: 2018-07-06T00:00:00Z
date_updated: 2026-08-10T22:30:57Z
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title: PID/WAG-mediated phosphorylation of the Arabidopsis PIN3 auxin transporter
  mediates polarity switches during gravitropism
tmp:
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...
