---
_id: '612'
abstract:
- lang: eng
text: Metabotropic GABAB receptors mediate slow inhibitory effects presynaptically
and postsynaptically through the modulation of different effector signalling pathways.
Here, we analysed the distribution of GABAB receptors using highly sensitive SDS-digested
freeze-fracture replica labelling in mouse cerebellar Purkinje cells. Immunoreactivity
for GABAB1 was observed on presynaptic and, more abundantly, on postsynaptic compartments,
showing both scattered and clustered distribution patterns. Quantitative analysis
of immunoparticles revealed a somato-dendritic gradient, with the density of immunoparticles
increasing 26-fold from somata to dendritic spines. To understand the spatial
relationship of GABAB receptors with two key effector ion channels, the G protein-gated
inwardly rectifying K+ (GIRK/Kir3) channel and the voltage-dependent Ca2+ channel,
biochemical and immunohistochemical approaches were performed. Co-immunoprecipitation
analysis demonstrated that GABAB receptors co-assembled with GIRK and CaV2.1 channels
in the cerebellum. Using double-labelling immunoelectron microscopic techniques,
co-clustering between GABAB1 and GIRK2 was detected in dendritic spines, whereas
they were mainly segregated in the dendritic shafts. In contrast, co-clustering
of GABAB1 and CaV2.1 was detected in dendritic shafts but not spines. Presynaptically,
although no significant co-clustering of GABAB1 and GIRK2 or CaV2.1 channels was
detected, inter-cluster distance for GABAB1 and GIRK2 was significantly smaller
in the active zone than in the dendritic shafts, and that for GABAB1 and CaV2.1
was significantly smaller in the active zone than in the dendritic shafts and
spines. Thus, GABAB receptors are associated with GIRK and CaV2.1 channels in
different subcellular compartments. These data provide a better framework for
understanding the different roles played by GABAB receptors and their effector
ion channels in the cerebellar network.
article_processing_charge: No
article_type: original
author:
- first_name: Rafael
full_name: Luján, Rafael
last_name: Luján
- first_name: Carolina
full_name: Aguado, Carolina
last_name: Aguado
- first_name: Francisco
full_name: Ciruela, Francisco
last_name: Ciruela
- first_name: Javier
full_name: Cózar, Javier
last_name: Cózar
- first_name: David
full_name: Kleindienst, David
id: 42E121A4-F248-11E8-B48F-1D18A9856A87
last_name: Kleindienst
- first_name: Luis
full_name: De La Ossa, Luis
last_name: De La Ossa
- first_name: Bernhard
full_name: Bettler, Bernhard
last_name: Bettler
- first_name: Kevin
full_name: Wickman, Kevin
last_name: Wickman
- first_name: Masahiko
full_name: Watanabe, Masahiko
last_name: Watanabe
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
citation:
ama: Luján R, Aguado C, Ciruela F, et al. Differential association of GABAB receptors
with their effector ion channels in Purkinje cells. Brain Structure and Function.
2018;223(3):1565-1587. doi:10.1007/s00429-017-1568-y
apa: Luján, R., Aguado, C., Ciruela, F., Cózar, J., Kleindienst, D., De La Ossa,
L., … Fukazawa, Y. (2018). Differential association of GABAB receptors with their
effector ion channels in Purkinje cells. Brain Structure and Function.
Springer. https://doi.org/10.1007/s00429-017-1568-y
chicago: Luján, Rafael, Carolina Aguado, Francisco Ciruela, Javier Cózar, David
Kleindienst, Luis De La Ossa, Bernhard Bettler, et al. “Differential Association
of GABAB Receptors with Their Effector Ion Channels in Purkinje Cells.” Brain
Structure and Function. Springer, 2018. https://doi.org/10.1007/s00429-017-1568-y.
ieee: R. Luján et al., “Differential association of GABAB receptors with
their effector ion channels in Purkinje cells,” Brain Structure and Function,
vol. 223, no. 3. Springer, pp. 1565–1587, 2018.
ista: Luján R, Aguado C, Ciruela F, Cózar J, Kleindienst D, De La Ossa L, Bettler
B, Wickman K, Watanabe M, Shigemoto R, Fukazawa Y. 2018. Differential association
of GABAB receptors with their effector ion channels in Purkinje cells. Brain Structure
and Function. 223(3), 1565–1587.
mla: Luján, Rafael, et al. “Differential Association of GABAB Receptors with Their
Effector Ion Channels in Purkinje Cells.” Brain Structure and Function,
vol. 223, no. 3, Springer, 2018, pp. 1565–87, doi:10.1007/s00429-017-1568-y.
short: R. Luján, C. Aguado, F. Ciruela, J. Cózar, D. Kleindienst, L. De La Ossa,
B. Bettler, K. Wickman, M. Watanabe, R. Shigemoto, Y. Fukazawa, Brain Structure
and Function 223 (2018) 1565–1587.
date_created: 2018-12-11T11:47:29Z
date_published: 2018-04-01T00:00:00Z
date_updated: 2026-04-25T22:31:09Z
day: '01'
ddc:
- '571'
department:
- _id: RySh
doi: 10.1007/s00429-017-1568-y
ec_funded: 1
external_id:
isi:
- '000428419500030'
file:
- access_level: open_access
checksum: a55b3103476ecb5f4f983d8801807e8b
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:36Z
date_updated: 2020-07-14T12:47:20Z
file_id: '5157'
file_name: IST-2018-1013-v1+1_2018_Kleindienst_Differential.pdf
file_size: 5542926
relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
has_accepted_license: '1'
intvolume: ' 223'
isi: 1
issue: '3'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 1565 - 1587
project:
- _id: 25CBA828-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '720270'
name: Human Brain Project Specific Grant Agreement 1
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: Brain Structure and Function
publication_status: published
publisher: Springer
publist_id: '7192'
pubrep_id: '1013'
quality_controlled: '1'
related_material:
record:
- id: '9562'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Differential association of GABAB receptors with their effector ion channels
in Purkinje cells
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: 223
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. Flow Turbulence and Combustion.
2018;100(4):919-942. doi:10.1007/s10494-018-9896-4
apa: 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. Springer. https://doi.org/10.1007/s10494-018-9896-4
chicago: Kühnen, Jakob, Davide Scarselli, Markus Schaner, and Björn Hof. “Relaminarization
by Steady Modification of the Streamwise Velocity Profile in a Pipe.” Flow
Turbulence and Combustion. Springer, 2018. https://doi.org/10.1007/s10494-018-9896-4.
ieee: J. Kühnen, D. Scarselli, M. Schaner, and B. Hof, “Relaminarization by steady
modification of the streamwise velocity profile in a pipe,” Flow Turbulence
and Combustion, 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.” Flow Turbulence and Combustion, vol. 100,
no. 4, Springer, 2018, pp. 919–42, doi:10.1007/s10494-018-9896-4.
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: 2026-04-25T22:31:13Z
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.
Nature Physics. 2018;14:386-390. doi:10.1038/s41567-017-0018-3
apa: Kühnen, J., Song, B., Scarselli, D., Budanur, N. B., Riedl, M., Willis, A.,
… Hof, B. (2018). Destabilizing turbulence in pipe flow. Nature Physics.
Nature Publishing Group. https://doi.org/10.1038/s41567-017-0018-3
chicago: Kühnen, Jakob, Baofang Song, Davide Scarselli, Nazmi B Budanur, Michael
Riedl, Ashley Willis, Marc Avila, and Björn Hof. “Destabilizing Turbulence in
Pipe Flow.” Nature Physics. Nature Publishing Group, 2018. https://doi.org/10.1038/s41567-017-0018-3.
ieee: J. Kühnen et al., “Destabilizing turbulence in pipe flow,” Nature
Physics, 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.” Nature Physics,
vol. 14, Nature Publishing Group, 2018, pp. 386–90, doi:10.1038/s41567-017-0018-3.
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: 2026-04-25T22:31:13Z
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:
- open_access: '1'
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:
record:
- id: '12726'
relation: dissertation_contains
status: public
- id: '14530'
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: '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. Advances in Botanical Research. 2018;87:115-138. doi:10.1016/bs.abr.2018.09.007
apa: Abualia, R., Benková, E., & Lacombe, B. (2018). Transporters and mechanisms
of hormone transport in arabidopsis. Advances in Botanical Research. Elsevier.
https://doi.org/10.1016/bs.abr.2018.09.007
chicago: Abualia, Rashed, Eva Benková, and Benoît Lacombe. “Transporters and Mechanisms
of Hormone Transport in Arabidopsis.” Advances in Botanical Research. Elsevier,
2018. https://doi.org/10.1016/bs.abr.2018.09.007.
ieee: R. Abualia, E. Benková, and B. Lacombe, “Transporters and mechanisms of hormone
transport in arabidopsis,” Advances in Botanical Research, 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.” Advances in Botanical Research, vol. 87, Elsevier, 2018,
pp. 115–38, doi:10.1016/bs.abr.2018.09.007.
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: 2026-04-25T22:31:14Z
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: '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. PLoS Genetics. 2018;14(1).
doi:10.1371/journal.pgen.1007177
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. PLoS Genetics. Public Library of Science.
https://doi.org/10.1371/journal.pgen.1007177
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.” PLoS
Genetics. Public Library of Science, 2018. https://doi.org/10.1371/journal.pgen.1007177.
ieee: T. Prat et al., “WRKY23 is a component of the transcriptional network
mediating auxin feedback on PIN polarity,” PLoS Genetics, 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.” PLoS Genetics, vol. 14, no. 1, Public
Library of Science, 2018, doi:10.1371/journal.pgen.1007177.
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: 2026-04-25T22:31:15Z
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.
Scientific Reports. 2018;8(1). doi:10.1038/s41598-018-28188-1
apa: Grones, P., Abas, M. F., 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. Springer. https://doi.org/10.1038/s41598-018-28188-1
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.” Scientific
Reports. Springer, 2018. https://doi.org/10.1038/s41598-018-28188-1.
ieee: P. Grones et al., “PID/WAG-mediated phosphorylation of the Arabidopsis
PIN3 auxin transporter mediates polarity switches during gravitropism,” Scientific
Reports, 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.” Scientific
Reports, vol. 8, no. 1, 10279, Springer, 2018, doi:10.1038/s41598-018-28188-1.
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: 2026-04-25T22:31:15Z
day: '06'
ddc:
- '581'
department:
- _id: JiFr
- _id: EvBe
doi: 10.1038/s41598-018-28188-1
ec_funded: 1
external_id:
isi:
- '000437673200053'
file:
- access_level: open_access
checksum: 266b03f4fb8198e83141617aaa99dcab
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T15:38:56Z
date_updated: 2020-07-14T12:45:20Z
file_id: '5714'
file_name: 2018_ScientificReports_Grones.pdf
file_size: 2413876
relation: main_file
file_date_updated: 2020-07-14T12:45:20Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
issue: '1'
language:
- iso: eng
month: '07'
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
- _id: 261099A6-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742985'
name: Tracing Evolution of Auxin Transport and Polarity in Plants
publication: Scientific Reports
publication_status: published
publisher: Springer
publist_id: '7729'
quality_controlled: '1'
related_material:
record:
- id: '8822'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: PID/WAG-mediated phosphorylation of the Arabidopsis PIN3 auxin transporter
mediates polarity switches during gravitropism
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: '5914'
abstract:
- lang: eng
text: With the advent of optogenetics, it became possible to change the activity
of a targeted population of neurons in a temporally controlled manner. To combine
the advantages of 60-channel in vivo tetrode recording and laser-based optogenetics,
we have developed a closed-loop recording system that allows for the actual electrophysiological
signal to be used as a trigger for the laser light mediating the optogenetic intervention.
We have optimized the weight, size, and shape of the corresponding implant to
make it compatible with the size, force, and movements of a behaving mouse, and
we have shown that the system can efficiently block sharp wave ripple (SWR) events
using those events themselves as a trigger. To demonstrate the full potential
of the optogenetic recording system we present a pilot study addressing the contribution
of SWR events to learning in a complex behavioral task.
article_number: e0087
article_processing_charge: No
author:
- first_name: Dámaris K
full_name: Rangel Guerrero, Dámaris K
id: 4871BCE6-F248-11E8-B48F-1D18A9856A87
last_name: Rangel Guerrero
orcid: 0000-0002-8602-4374
- first_name: James G.
full_name: Donnett, James G.
last_name: Donnett
- first_name: Jozsef L
full_name: Csicsvari, Jozsef L
id: 3FA14672-F248-11E8-B48F-1D18A9856A87
last_name: Csicsvari
orcid: 0000-0002-5193-4036
- first_name: Krisztián
full_name: Kovács, Krisztián
id: 2AB5821E-F248-11E8-B48F-1D18A9856A87
last_name: Kovács
orcid: 0000-0001-6251-1007
citation:
ama: 'Rangel Guerrero DK, Donnett JG, Csicsvari JL, Kovács K. Tetrode recording
from the hippocampus of behaving mice coupled with four-point-irradiation closed-loop
optogenetics: A technique to study the contribution of Hippocampal SWR events
to learning. eNeuro. 2018;5(4). doi:10.1523/ENEURO.0087-18.2018'
apa: 'Rangel Guerrero, D. K., Donnett, J. G., Csicsvari, J. L., & Kovács, K.
(2018). Tetrode recording from the hippocampus of behaving mice coupled with four-point-irradiation
closed-loop optogenetics: A technique to study the contribution of Hippocampal
SWR events to learning. ENeuro. Society for Neuroscience. https://doi.org/10.1523/ENEURO.0087-18.2018'
chicago: 'Rangel Guerrero, Dámaris K, James G. Donnett, Jozsef L Csicsvari, and
Krisztián Kovács. “Tetrode Recording from the Hippocampus of Behaving Mice Coupled
with Four-Point-Irradiation Closed-Loop Optogenetics: A Technique to Study the
Contribution of Hippocampal SWR Events to Learning.” ENeuro. Society for
Neuroscience, 2018. https://doi.org/10.1523/ENEURO.0087-18.2018.'
ieee: 'D. K. Rangel Guerrero, J. G. Donnett, J. L. Csicsvari, and K. Kovács, “Tetrode
recording from the hippocampus of behaving mice coupled with four-point-irradiation
closed-loop optogenetics: A technique to study the contribution of Hippocampal
SWR events to learning,” eNeuro, vol. 5, no. 4. Society for Neuroscience,
2018.'
ista: 'Rangel Guerrero DK, Donnett JG, Csicsvari JL, Kovács K. 2018. Tetrode recording
from the hippocampus of behaving mice coupled with four-point-irradiation closed-loop
optogenetics: A technique to study the contribution of Hippocampal SWR events
to learning. eNeuro. 5(4), e0087.'
mla: 'Rangel Guerrero, Dámaris K., et al. “Tetrode Recording from the Hippocampus
of Behaving Mice Coupled with Four-Point-Irradiation Closed-Loop Optogenetics:
A Technique to Study the Contribution of Hippocampal SWR Events to Learning.”
ENeuro, vol. 5, no. 4, e0087, Society for Neuroscience, 2018, doi:10.1523/ENEURO.0087-18.2018.'
short: D.K. Rangel Guerrero, J.G. Donnett, J.L. Csicsvari, K. Kovács, ENeuro 5 (2018).
date_created: 2019-02-03T22:59:16Z
date_published: 2018-07-27T00:00:00Z
date_updated: 2026-04-25T22:31:18Z
day: '27'
ddc:
- '570'
department:
- _id: JoCs
doi: 10.1523/ENEURO.0087-18.2018
ec_funded: 1
external_id:
isi:
- '000443994700007'
file:
- access_level: open_access
checksum: f4915d45fc7ad4648b7b7a13fdecca01
content_type: application/pdf
creator: dernst
date_created: 2019-02-05T12:48:36Z
date_updated: 2020-07-14T12:47:13Z
file_id: '5921'
file_name: 2018_ENeuro_Guerrero.pdf
file_size: 3746884
relation: main_file
file_date_updated: 2020-07-14T12:47:13Z
has_accepted_license: '1'
intvolume: ' 5'
isi: 1
issue: '4'
language:
- iso: eng
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: 257D4372-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I2072-B27
name: Interneuron plasticity during spatial learning
publication: eNeuro
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
related_material:
record:
- id: '6849'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: 'Tetrode recording from the hippocampus of behaving mice coupled with four-point-irradiation
closed-loop optogenetics: A technique to study the contribution of Hippocampal SWR
events to learning'
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: 5
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.
The Plant Cell. 2018;30(3):700-716. doi:10.1105/tpc.17.00785
apa: 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. American Society of Plant Biologists.
https://doi.org/10.1105/tpc.17.00785
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.” The Plant Cell. American
Society of Plant Biologists, 2018. https://doi.org/10.1105/tpc.17.00785.
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,” The Plant Cell, 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.” The Plant Cell, vol. 30, no.
3, American Society of Plant Biologists, 2018, pp. 700–16, doi:10.1105/tpc.17.00785.
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: 2026-04-25T22:31:20Z
day: '09'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.1105/tpc.17.00785
ec_funded: 1
external_id:
isi:
- '000429441400018'
pmid:
- '29511054'
file:
- access_level: open_access
checksum: 4e165e653b67d3f0684697f21aace5a1
content_type: application/pdf
creator: dernst
date_created: 2022-05-23T09:12:38Z
date_updated: 2022-05-23T09:12:38Z
file_id: '11406'
file_name: 2018_PlantCell_Adamowski.pdf
file_size: 4407538
relation: main_file
success: 1
file_date_updated: 2022-05-23T09:12:38Z
has_accepted_license: '1'
intvolume: ' 30'
isi: 1
issue: '3'
language:
- iso: eng
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'
relation: dissertation_contains
status: public
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'
...
---
_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. Nature Ecology and Evolution.
2018;2(10):1633-1643. doi:10.1038/s41559-018-0651-y
apa: Igler, C., Lagator, M., Tkačik, G., Bollback, J. P., & Guet, C. C. (2018).
Evolutionary potential of transcription factors for gene regulatory rewiring.
Nature Ecology and Evolution. Nature Publishing Group. https://doi.org/10.1038/s41559-018-0651-y
chicago: Igler, Claudia, Mato Lagator, Gašper Tkačik, Jonathan P Bollback, and Calin
C Guet. “Evolutionary Potential of Transcription Factors for Gene Regulatory Rewiring.”
Nature Ecology and Evolution. Nature Publishing Group, 2018. https://doi.org/10.1038/s41559-018-0651-y.
ieee: C. Igler, M. Lagator, G. Tkačik, J. P. Bollback, and C. C. Guet, “Evolutionary
potential of transcription factors for gene regulatory rewiring,” Nature Ecology
and Evolution, 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.” Nature Ecology and Evolution, vol. 2, no. 10,
Nature Publishing Group, 2018, pp. 1633–43, doi:10.1038/s41559-018-0651-y.
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: 2026-04-25T22:31:21Z
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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content_type: application/pdf
creator: dernst
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date_updated: 2020-07-14T12:47:37Z
file_id: '7830'
file_name: 2018_NatureEcology_Igler.pdf
file_size: 1135973
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issue: '10'
language:
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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:
record:
- id: '5585'
relation: popular_science
status: public
- id: '6371'
relation: dissertation_contains
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'
...
---
_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:10.15479/AT:ISTA:108
apa: Igler, C., Lagator, M., Tkačik, G., Bollback, J. P., & Guet, C. C. (2018).
Data for the paper Evolutionary potential of transcription factors for gene regulatory
rewiring. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:108
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.
https://doi.org/10.15479/AT:ISTA:108.
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, 10.15479/AT:ISTA:108.
mla: Igler, Claudia, et al. Data for the Paper Evolutionary Potential of Transcription
Factors for Gene Regulatory Rewiring. Institute of Science and Technology
Austria, 2018, doi:10.15479/AT:ISTA:108.
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: 2026-04-25T22:31:21Z
day: '20'
ddc:
- '576'
department:
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- _id: GaTk
doi: 10.15479/AT:ISTA:108
ec_funded: 1
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file_size: 16507
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has_accepted_license: '1'
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'
...
---
_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. G3: Genes, Genomes, Genetics. 2018;8(3):845-857. doi:10.1534/g3.117.300452'
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. G3:
Genes, Genomes, Genetics. Genetics Society of America. https://doi.org/10.1534/g3.117.300452'
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.”
G3: Genes, Genomes, Genetics. Genetics Society of America, 2018. https://doi.org/10.1534/g3.117.300452.'
ieee: 'A. György et al., “Tools allowing independent visualization and genetic
manipulation of Drosophila melanogaster macrophages and surrounding tissues,”
G3: Genes, Genomes, Genetics, 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.”
G3: Genes, Genomes, Genetics, vol. 8, no. 3, Genetics Society of America,
2018, pp. 845–57, doi:10.1534/g3.117.300452.'
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: 2026-04-25T22:31:23Z
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
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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: '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. Nature Communications. 2018;9(1). doi:10.1038/s41467-018-06899-3
apa: Espinoza Martinez, C., Guzmán, J., Zhang, X., & Jonas, P. M. (2018). Parvalbumin+
interneurons obey unique connectivity rules and establish a powerful lateral-inhibition
microcircuit in dentate gyrus. Nature Communications. Nature Publishing
Group. https://doi.org/10.1038/s41467-018-06899-3
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.” Nature Communications.
Nature Publishing Group, 2018. https://doi.org/10.1038/s41467-018-06899-3.
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,” Nature Communications, 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.”
Nature Communications, vol. 9, no. 1, 4605, Nature Publishing Group, 2018,
doi:10.1038/s41467-018-06899-3.
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: 2026-04-25T22:31:23Z
day: '02'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1038/s41467-018-06899-3
ec_funded: 1
external_id:
isi:
- '000449069700009'
file:
- access_level: open_access
checksum: 9fe2a63bd95a5067d896c087d07998f3
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T15:41:57Z
date_updated: 2020-07-14T12:45:28Z
file_id: '5715'
file_name: 2018_NatureComm_Espinoza.pdf
file_size: 4651930
relation: main_file
file_date_updated: 2020-07-14T12:45:28Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
issue: '1'
language:
- iso: eng
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: '402'
abstract:
- lang: eng
text: During metastasis, malignant cells escape the primary tumor, intravasate lymphatic
vessels, and reach draining sentinel lymph nodes before they colonize distant
organs via the blood circulation. Although lymph node metastasis in cancer patients
correlates with poor prognosis, evidence is lacking as to whether and how tumor
cells enter the bloodstream via lymph nodes. To investigate this question, we
delivered carcinoma cells into the lymph nodes of mice by microinfusing the cells
into afferent lymphatic vessels. We found that tumor cells rapidly infiltrated
the lymph node parenchyma, invaded blood vessels, and seeded lung metastases without
involvement of the thoracic duct. These results suggest that the lymph node blood
vessels can serve as an exit route for systemic dissemination of cancer cells
in experimental mouse models. Whether this form of tumor cell spreading occurs
in cancer patients remains to be determined.
acknowledged_ssus:
- _id: Bio
acknowledgement: "M.B. was supported by the Cell Communication in Health and Disease
graduate study program of the Austrian Science Fund (FWF) and the Medical University
of Vienna. M.S. was supported by the European Research Council (grant ERC GA 281556)
and an FWF START award.\r\nWe thank C. Moussion for establishing the intralymphatic
injection at IST Austria and for providing anti-PNAd hybridoma supernatant, R. Förster
and A. Braun for sharing the intralymphatic injection technology, K. Vaahtomeri
for the lentiviral constructs, M. Hons for establishing in vivo multiphoton imaging,
the Sixt lab for intellectual input, M. Schunn for help with the design of the in
vivo experiments, F. Langer for technical assistance with the in vivo experiments,
the bioimaging facility of IST Austria for support, and R. Efferl for providing
the CT26 cell line."
article_processing_charge: No
article_type: original
author:
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Helga
full_name: Schachner, Helga
last_name: Schachner
- first_name: Gabriele
full_name: Asfour, Gabriele
last_name: Asfour
- first_name: Zsuzsanna
full_name: Bagó Horváth, Zsuzsanna
last_name: Bagó Horváth
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- first_name: Pavel
full_name: Uhrin, Pavel
last_name: Uhrin
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
citation:
ama: Brown M, Assen FP, Leithner AF, et al. Lymph node blood vessels provide exit
routes for metastatic tumor cell dissemination in mice. Science. 2018;359(6382):1408-1411.
doi:10.1126/science.aal3662
apa: Brown, M., Assen, F. P., Leithner, A. F., Abe, J., Schachner, H., Asfour, G.,
… Kerjaschki, D. (2018). Lymph node blood vessels provide exit routes for metastatic
tumor cell dissemination in mice. Science. American Association for the
Advancement of Science. https://doi.org/10.1126/science.aal3662
chicago: Brown, Markus, Frank P Assen, Alexander F Leithner, Jun Abe, Helga Schachner,
Gabriele Asfour, Zsuzsanna Bagó Horváth, et al. “Lymph Node Blood Vessels Provide
Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” Science.
American Association for the Advancement of Science, 2018. https://doi.org/10.1126/science.aal3662.
ieee: M. Brown et al., “Lymph node blood vessels provide exit routes for
metastatic tumor cell dissemination in mice,” Science, vol. 359, no. 6382.
American Association for the Advancement of Science, pp. 1408–1411, 2018.
ista: Brown M, Assen FP, Leithner AF, Abe J, Schachner H, Asfour G, Bagó Horváth
Z, Stein J, Uhrin P, Sixt MK, Kerjaschki D. 2018. Lymph node blood vessels provide
exit routes for metastatic tumor cell dissemination in mice. Science. 359(6382),
1408–1411.
mla: Brown, Markus, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic
Tumor Cell Dissemination in Mice.” Science, vol. 359, no. 6382, American
Association for the Advancement of Science, 2018, pp. 1408–11, doi:10.1126/science.aal3662.
short: M. Brown, F.P. Assen, A.F. Leithner, J. Abe, H. Schachner, G. Asfour, Z.
Bagó Horváth, J. Stein, P. Uhrin, M.K. Sixt, D. Kerjaschki, Science 359 (2018)
1408–1411.
corr_author: '1'
date_created: 2018-12-11T11:46:16Z
date_published: 2018-03-23T00:00:00Z
date_updated: 2026-04-25T22:31:22Z
day: '23'
department:
- _id: MiSi
doi: 10.1126/science.aal3662
ec_funded: 1
external_id:
isi:
- '000428043600047'
pmid:
- '29567714'
intvolume: ' 359'
isi: 1
issue: '6382'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1126/science.aal3662
month: '03'
oa: 1
oa_version: Published Version
page: 1408 - 1411
pmid: 1
project:
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and force transduction of migrating leukocytes
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7428'
quality_controlled: '1'
related_material:
record:
- id: '6947'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination
in mice
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 359
year: '2018'
...
---
OA_place: publisher
_id: '6263'
abstract:
- lang: eng
text: 'Antibiotic resistance can emerge spontaneously through genomic mutation and render
treatment ineffective. To counteract this process, in addition to the discovery and
description of resistance mechanisms,a deeper understanding of resistanceevolvabilityand
its determinantsis needed. To address this challenge, this thesisuncoversnew genetic
determinants of resistance evolvability using a customized robotic setup,
exploressystematic ways in which resistance evolution is perturbed due to
dose-responsecharacteristics of drugs and mutation rate differences,and mathematically investigates
the evolutionary fate of one specific type of evolvability modifier -a stress-induced
mutagenesis allele.We find severalgenes which strongly inhibit or potentiate resistance evolution. In order
to identify them, we first developedan automated high-throughput feedback-controlled
protocol whichkeeps the population size and selection pressure approximately constant
for hundreds of cultures by dynamically re-diluting the cultures and adjusting the antibiotic
concentration. We implementedthis protocol on a customized liquid handling robot and
propagated 100 different gene deletion strains of Escherichia coliin triplicate for over 100
generations in tetracycline and in chloramphenicol, and comparedtheir adaptation rates.We find a diminishing returns pattern, where initially sensitive strains adapted more
compared to less sensitive ones. Our data uncover that deletions of certain genes
which do not affect mutation rate,including efflux pump components, a chaperone and
severalstructural and regulatory genes can strongly and reproducibly alterresistance evolution.
Sequencing analysis of evolved populations indicates that epistasis with resistance
mutations is the most likelyexplanation. This work could inspire treatment strategies in
which targeted inhibitors of evolvability mechanisms will be given alongside antibiotics to
slow down resistance evolution and extend theefficacy of antibiotics.We implemented astochasticpopulation genetics model,
toverifyways in which general properties, namely, dose-response characteristics of drugs and mutation rates, influence
evolutionary dynamics. In particular, under the exposure to antibiotics with shallow dose-response curves,bacteria have narrower distributions of fitness effects of new mutations.
We show that in silicothis also leads to slower resistance evolution. We
see and confirm with experiments that increased mutation rates, apart from speeding
up evolution, also leadto high reproducibility of phenotypic adaptation in a context
of continually strong selection pressure.Knowledge of these patterns can aid in predicting the dynamics of antibiotic
resistance evolutionand adapting treatment schemes accordingly.Focusing on a previously described type of evolvability modifier
–a stress-induced mutagenesis allele –we find conditions under which it can persist in a population under
periodic selectionakin to clinical treatment. We set up a deterministic
infinite populationcontinuous time model tracking the frequencies of a mutator and resistance allele and
evaluate various treatment schemes in how well they maintain a stress-induced
mutator allele. In particular,a high diversity of stresses is crucial for the persistence
of the mutator allele. This leads to a general trade-off where exactly those
diversifying treatment schemes which are likely to decrease levels of resistance could lead to stronger selection of highly
evolvable genotypes.In the long run, this work will lead to a deeper understanding of the genetic and cellular
mechanisms involved in antibiotic resistance evolution and could inspire new strategies
for slowing down its rate. '
acknowledged_ssus:
- _id: M-Shop
- _id: LifeSc
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Marta
full_name: Lukacisinova, Marta
id: 4342E402-F248-11E8-B48F-1D18A9856A87
last_name: Lukacisinova
orcid: 0000-0002-2519-8004
citation:
ama: Lukacisinova M. Genetic determinants of antibiotic resistance evolution. 2018.
doi:10.15479/AT:ISTA:th1072
apa: Lukacisinova, M. (2018). Genetic determinants of antibiotic resistance evolution.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th1072
chicago: Lukacisinova, Marta. “Genetic Determinants of Antibiotic Resistance Evolution.”
Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th1072.
ieee: M. Lukacisinova, “Genetic determinants of antibiotic resistance evolution,”
Institute of Science and Technology Austria, 2018.
ista: Lukacisinova M. 2018. Genetic determinants of antibiotic resistance evolution.
Institute of Science and Technology Austria.
mla: Lukacisinova, Marta. Genetic Determinants of Antibiotic Resistance Evolution.
Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th1072.
short: M. Lukacisinova, Genetic Determinants of Antibiotic Resistance Evolution,
Institute of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2019-04-09T13:57:15Z
date_published: 2018-12-28T00:00:00Z
date_updated: 2026-04-08T14:15:06Z
day: '28'
ddc:
- '570'
- '576'
- '579'
degree_awarded: PhD
department:
- _id: ToBo
doi: 10.15479/AT:ISTA:th1072
file:
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content_type: application/pdf
creator: dernst
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file_id: '6265'
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language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: '91'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '1027'
relation: part_of_dissertation
status: public
- id: '696'
relation: part_of_dissertation
status: public
- id: '1619'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Tobias
full_name: Bollenbach, Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
title: Genetic determinants of antibiotic resistance evolution
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2018'
...
---
OA_place: publisher
_id: '51'
abstract:
- lang: eng
text: Asymmetries have long been known about in the central nervous system. From
gross anatomical differences, such as the presence of the parapineal organ in
only one hemisphere of the developing zebrafish, to more subtle differences in
activity between both hemispheres, as seen in freely roaming animals or human
participants under PET and fMRI imaging analysis. The presence of asymmetries
has been demonstrated to have huge behavioural implications, with their disruption
often leading to the generation of neurological disorders, memory problems, changes
in personality, and in an organism's health and well-being. For my Ph.D. work
I aimed to tackle two important avenues of research. The first being the process
of input-side dependency in the hippocampus, with the goal of finding a key gene
responsible for its development (Gene X). The second project was to do with experience-induced
laterality formation in the hippocampus. Specifically, how laterality in the synapse
density of the CA1 stratum radiatum (s.r.) could be induced purely through environmental
enrichment. Through unilateral tracer injections into the CA3, I was able to selectively
measure the properties of synapses within the CA1 and investigate how they differed
based upon which hemisphere the presynaptic neurone originated. Having found the
existence of a previously unreported reversed (left-isomerism) i.v. mutant, through
morpholocal examination of labelled terminals in the CA1 s.r., I aimed to elucidate
a key gene responsible for the process of left or right determination of inputs
to the CA1 s.r.. This work relates to the previous finding of input-side dependent
asymmetry in the wild-type rodent, where the origin of the projecting neurone
to the CA1 will determine the morphology of a synapse, to a greater degree than
the hemisphere in which the projection terminates. Using left- and right-isomerism
i.v. mice, in combination with whole genome sequence analysis, I highlight Ena/VASP-like
(Evl) as a potential target for Gene X. In relation to this topic, I also highlight
my work in the recently published paper of how knockout of PirB can lead to a
lack of input-side dependency in the murine hippocampus. For the second question,
I show that the environmental enrichment paradigm will lead to an asymmetry in
the synapse densities in the hippocampus of mice. I also highlight that the nature
of the enrichment is of less consequence than the process of enrichment itself.
I demonstrate that the CA3 region will dramatically alter its projection targets,
in relation to environmental stimulation, with the asymmetry in synaptic density,
caused by enrichment, relying heavily on commissural fibres. I also highlight
the vital importance of input-side dependent asymmetry, as a necessary component
of experience-dependent laterality formation in the CA1 s.r.. However, my results
suggest that it isn't the only cause, as there appears to be a CA1 dependent mechanism
also at play. Upon further investigation, I highlight the significant, and highly
important, finding that the changes seen in the CA1 s.r. were predominantly caused
through projections from the left-CA3, with the right-CA3 having less involvement
in this mechanism.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Matthew J
full_name: Case, Matthew J
id: 44B7CA5A-F248-11E8-B48F-1D18A9856A87
last_name: Case
citation:
ama: 'Case MJ. From the left to the right: A tale of asymmetries, environments,
and hippocampal development. 2018. doi:10.15479/AT:ISTA:th_1032'
apa: 'Case, M. J. (2018). From the left to the right: A tale of asymmetries,
environments, and hippocampal development. Institute of Science and Technology
Austria. https://doi.org/10.15479/AT:ISTA:th_1032'
chicago: 'Case, Matthew J. “From the Left to the Right: A Tale of Asymmetries, Environments,
and Hippocampal Development.” Institute of Science and Technology Austria, 2018.
https://doi.org/10.15479/AT:ISTA:th_1032.'
ieee: 'M. J. Case, “From the left to the right: A tale of asymmetries, environments,
and hippocampal development,” Institute of Science and Technology Austria, 2018.'
ista: 'Case MJ. 2018. From the left to the right: A tale of asymmetries, environments,
and hippocampal development. Institute of Science and Technology Austria.'
mla: 'Case, Matthew J. From the Left to the Right: A Tale of Asymmetries, Environments,
and Hippocampal Development. Institute of Science and Technology Austria,
2018, doi:10.15479/AT:ISTA:th_1032.'
short: 'M.J. Case, From the Left to the Right: A Tale of Asymmetries, Environments,
and Hippocampal Development, Institute of Science and Technology Austria, 2018.'
corr_author: '1'
date_created: 2018-12-11T11:44:22Z
date_published: 2018-06-27T00:00:00Z
date_updated: 2026-04-08T14:13:44Z
day: '27'
ddc:
- '571'
- '576'
degree_awarded: PhD
department:
- _id: RySh
doi: 10.15479/AT:ISTA:th_1032
file:
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checksum: dcc7b55619d8509dd62b8e99d6cdee44
content_type: application/msword
creator: dernst
date_created: 2019-04-09T07:16:26Z
date_updated: 2021-02-11T23:30:13Z
embargo_to: open_access
file_id: '6251'
file_name: 2018_Thesis_Case_Source.doc
file_size: 141270528
relation: source_file
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checksum: f69fdd5c8709c4e618aa8c1a1221153d
content_type: application/pdf
creator: dernst
date_created: 2019-04-09T07:16:23Z
date_updated: 2021-02-11T11:17:14Z
embargo: 2019-07-05
file_id: '6252'
file_name: 2018_Thesis_Case.pdf
file_size: 15193621
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file_date_updated: 2021-02-11T23:30:13Z
has_accepted_license: '1'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: '186'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '8003'
pubrep_id: '1032'
related_material:
record:
- id: '682'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
title: 'From the left to the right: A tale of asymmetries, environments, and hippocampal
development'
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2018'
...
---
OA_place: publisher
_id: '10'
abstract:
- lang: eng
text: Genomic imprinting is an epigenetic process that leads to parent of origin-specific
gene expression in a subset of genes. Imprinted genes are essential for brain
development, and deregulation of imprinting is associated with neurodevelopmental
diseases and the pathogenesis of psychiatric disorders. However, the cell-type
specificity of imprinting at single cell resolution, and how imprinting and thus
gene dosage regulates neuronal circuit assembly is still largely unknown. Here,
MADM (Mosaic Analysis with Double Markers) technology was employed to assess genomic
imprinting at single cell level. By visualizing MADM-induced uniparental disomies
(UPDs) in distinct colors at single cell level in genetic mosaic animals, this
experimental paradigm provides a unique quantitative platform to systematically
assay the UPD-mediated imbalances in imprinted gene expression at unprecedented
resolution. An experimental pipeline based on FACS, RNA-seq and bioinformatics
analysis was established and applied to systematically map cell-type-specific
‘imprintomes’ in the mouse brain. The results revealed that parental-specific
expression of imprinted genes per se is rarely cell-type-specific even at the
individual cell level. Conversely, when we extended the comparison to downstream
responses resulting from imbalanced imprinted gene expression, we discovered an
unexpectedly high degree of cell-type specificity. Furthermore, we determined
a novel function of genomic imprinting in cortical astrocyte production and in
olfactory bulb (OB) granule cell generation. These results suggest important functional
implication of genomic imprinting for generating cell-type diversity in the brain.
In addition, MADM provides a powerful tool to study candidate genes by concomitant
genetic manipulation and fluorescent labelling of single cells. MADM-based candidate
gene approach was utilized to identify potential imprinted genes involved in the
generation of cortical astrocytes and OB granule cells. We investigated p57Kip2,
a maternally expressed gene and known cell cycle regulator. Although we found
that p57Kip2 does not play a role in these processes, we detected an unexpected
function of the paternal allele previously thought to be silent. Finally, we took
advantage of a key property of MADM which is to allow unambiguous investigation
of environmental impact on single cells. The experimental pipeline based on FACS
and RNA-seq analysis of MADM-labeled cells was established to probe the functional
differences of single cell loss of gene function compared to global loss of function
on a transcriptional level. With this method, both common and distinct responses
were isolated due to cell-autonomous and non-autonomous effects acting on genotypically
identical cells. As a result, transcriptional changes were identified which result
solely from the surrounding environment. Using the MADM technology to study genomic
imprinting at single cell resolution, we have identified cell-type-specific gene
expression, novel gene function and the impact of environment on single cell transcriptomes.
Together, these provide important insights to the understanding of mechanisms
regulating cell-type specificity and thus diversity in the brain.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
citation:
ama: Laukoter S. Role of genomic imprinting in cerebral cortex development. 2018:1-139.
doi:10.15479/AT:ISTA:th1057
apa: Laukoter, S. (2018). Role of genomic imprinting in cerebral cortex development.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th1057
chicago: Laukoter, Susanne. “Role of Genomic Imprinting in Cerebral Cortex Development.”
Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th1057.
ieee: S. Laukoter, “Role of genomic imprinting in cerebral cortex development,”
Institute of Science and Technology Austria, 2018.
ista: Laukoter S. 2018. Role of genomic imprinting in cerebral cortex development.
Institute of Science and Technology Austria.
mla: Laukoter, Susanne. Role of Genomic Imprinting in Cerebral Cortex Development.
Institute of Science and Technology Austria, 2018, pp. 1–139, doi:10.15479/AT:ISTA:th1057.
short: S. Laukoter, Role of Genomic Imprinting in Cerebral Cortex Development, Institute
of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2018-12-11T11:44:08Z
date_published: 2018-11-21T00:00:00Z
date_updated: 2026-04-08T14:12:45Z
day: '21'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: SiHi
doi: 10.15479/AT:ISTA:th1057
file:
- access_level: closed
checksum: 41fdbf5fdce312802935d88a8ad9932c
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: dernst
date_created: 2019-05-10T07:47:04Z
date_updated: 2019-11-23T23:30:03Z
embargo_to: open_access
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file_name: Thesis_LaukoterSusanne_FINAL.docx
file_size: 17949175
relation: source_file
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checksum: 53001a9a0c9e570e598d861bb0af28aa
content_type: application/pdf
creator: dernst
date_created: 2019-05-10T07:47:04Z
date_updated: 2021-02-11T11:17:16Z
embargo: 2019-11-21
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file_name: Thesis_LaukoterSusanne_FINAL.pdf
file_size: 21187245
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file_date_updated: 2021-02-11T11:17:16Z
has_accepted_license: '1'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 1 - 139
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '8046'
pubrep_id: '1057'
status: public
supervisor:
- first_name: Beatriz
full_name: Vicoso, Beatriz
id: 49E1C5C6-F248-11E8-B48F-1D18A9856A87
last_name: Vicoso
orcid: 0000-0002-4579-8306
title: Role of genomic imprinting in cerebral cortex development
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2018'
...
---
OA_place: publisher
_id: '9'
abstract:
- lang: eng
text: 'Immune cells migrating to the sites of infection navigate through diverse
tissue architectures and switch their migratory mechanisms upon demand. However,
little is known about systemic regulators that could allow the acquisition of
these mechanisms. We performed a genetic screen in Drosophila melanogaster to
identify regulators of germband invasion by embryonic macrophages into the confined
space between the ectoderm and mesoderm. We have found that bZIP circadian transcription
factors (TFs) Kayak (dFos) and Vrille (dNFIL3) have opposite effects on macrophage
germband infiltration: Kayak facilitated and Vrille inhibited it. These TFs are
enriched in the macrophages during migration and genetically interact to control
it. Kayak sets a less coordinated mode of migration of the macrophage group and
increases the probability and length of Levy walks. Intriguingly, the motility
of kayak mutant macrophages was also strongly affected during initial germband
invasion but not along another less confined route. Inhibiting Rho1 signaling
within the tail ectoderm partially rescued the Kayak mutant phenotype, strongly
suggesting that migrating macrophages have to overcome a barrier imposed by the
stiffness of the ectoderm. Also, Kayak appeared to be important for the maintenance
of the round cell shape and the rear edge translocation of the macrophages invading
the germband. Complementary to this, the cortical actin cytoskeleton of Kayak-
deficient macrophages was strongly affected. RNA sequencing revealed the filamin
Cheerio and tetraspanin TM4SF to be downstream of Kayak. Chromatin immunoprecipitation
and immunostaining revealed that the formin Diaphanous is another downstream target
of Kayak. Immunostaining revealed that the formin Diaphanous is another downstream
target of Kayak. Indeed, Cheerio, TM4SF and Diaphanous are required within macrophages
for germband invasion, and expression of constitutively active Diaphanous in macrophages
was able to rescue the kayak mutant phenotype. Moreover, Cher and Diaphanous are
also reduced in the macrophages overexpressing Vrille. We hypothesize that Kayak,
through its targets, increases actin polymerization and cortical tension in macrophages
and thus allows extra force generation necessary for macrophage dissemination
and migration through confined stiff tissues, while Vrille counterbalances it.'
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Vera
full_name: Belyaeva, Vera
id: 47F080FE-F248-11E8-B48F-1D18A9856A87
last_name: Belyaeva
citation:
ama: Belyaeva V. Transcriptional regulation of macrophage migration in the Drosophila
melanogaster embryo . 2018. doi:10.15479/AT:ISTA:th1064
apa: Belyaeva, V. (2018). Transcriptional regulation of macrophage migration
in the Drosophila melanogaster embryo . Institute of Science and Technology
Austria. https://doi.org/10.15479/AT:ISTA:th1064
chicago: Belyaeva, Vera. “Transcriptional Regulation of Macrophage Migration in
the Drosophila Melanogaster Embryo .” Institute of Science and Technology Austria,
2018. https://doi.org/10.15479/AT:ISTA:th1064.
ieee: V. Belyaeva, “Transcriptional regulation of macrophage migration in the Drosophila
melanogaster embryo ,” Institute of Science and Technology Austria, 2018.
ista: Belyaeva V. 2018. Transcriptional regulation of macrophage migration in the
Drosophila melanogaster embryo . Institute of Science and Technology Austria.
mla: Belyaeva, Vera. Transcriptional Regulation of Macrophage Migration in the
Drosophila Melanogaster Embryo . Institute of Science and Technology Austria,
2018, doi:10.15479/AT:ISTA:th1064.
short: V. Belyaeva, Transcriptional Regulation of Macrophage Migration in the Drosophila
Melanogaster Embryo , Institute of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2018-12-11T11:44:08Z
date_published: 2018-07-01T00:00:00Z
date_updated: 2026-04-08T14:13:03Z
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issn:
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publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '8047'
pubrep_id: '1064'
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supervisor:
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
title: 'Transcriptional regulation of macrophage migration in the Drosophila melanogaster
embryo '
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
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:10.15479/AT:ISTA:th_1042
apa: Gridchyn, I. (2018). Reactivation content is important for consolidation
of spatial memory. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_1042
chicago: Gridchyn, Igor. “Reactivation Content Is Important for Consolidation of
Spatial Memory.” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_1042.
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. Reactivation Content Is Important for Consolidation of Spatial
Memory. Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_1042.
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
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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
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type: dissertation
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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:10.15479/AT:ISTA:th_992
apa: Tarlungeanu, D.-C. (2018). The branched chain amino acids in autism spectrum
disorders . Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_992
chicago: Tarlungeanu, Dora-Clara. “The Branched Chain Amino Acids in Autism Spectrum
Disorders .” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_992.
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. The Branched Chain Amino Acids in Autism Spectrum
Disorders . Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_992.
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'
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- '570'
- '616'
degree_awarded: PhD
department:
- _id: GaNo
doi: 10.15479/AT:ISTA:th_992
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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:
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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 '
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type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2018'
...
---
OA_place: publisher
_id: '539'
abstract:
- lang: eng
text: The whole life cycle of plants as well as their responses to environmental
stimuli is governed by a complex network of hormonal regulations. A number of
studies have demonstrated an essential role of both auxin and cytokinin in the
regulation of many aspects of plant growth and development including embryogenesis,
postembryonic organogenic processes such as root, and shoot branching, root and
shoot apical meristem activity and phyllotaxis. Over the last decades essential
knowledge on the key molecular factors and pathways that spatio-temporally define
auxin and cytokinin activities in the plant body has accumulated. However, how
both hormonal pathways are interconnected by a complex network of interactions
and feedback circuits that determines the final outcome of the individual hormone
actions is still largely unknown. Root system architecture establishment and in
particular formation of lateral organs is prime example of developmental process
at whose regulation both auxin and cytokinin pathways converge. To dissect convergence
points and pathways that tightly balance auxin - cytokinin antagonistic activities
that determine the root branching pattern transcriptome profiling was applied.
Genome wide expression analyses of the xylem pole pericycle, a tissue giving rise
to lateral roots, led to identification of genes that are highly responsive to
combinatorial auxin and cytokinin treatments and play an essential function in
the auxin-cytokinin regulated root branching. SYNERGISTIC AUXIN CYTOKININ 1 (SYAC1)
gene, which encodes for a protein of unknown function, was detected among the
top candidate genes of which expression was synergistically up-regulated by simultaneous
hormonal treatment. Plants with modulated SYAC1 activity exhibit severe defects
in the root system establishment and attenuate developmental responses to both
auxin and cytokinin. To explore the biological function of the SYAC1, we employed
different strategies including expression pattern analysis, subcellular localization
and phenotypic analyses of the syac1 loss-of-function and gain-of-function transgenic
lines along with the identification of the SYAC1 interaction partners. Detailed
functional characterization revealed that SYAC1 acts as a developmentally specific
regulator of the secretory pathway to control deposition of cell wall components
and thereby rapidly fine tune elongation growth.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Andrej
full_name: Hurny, Andrej
id: 4DC4AF46-F248-11E8-B48F-1D18A9856A87
last_name: Hurny
orcid: 0000-0003-3638-1426
citation:
ama: Hurny A. Identification and characterization of novel auxin-cytokinin cross-talk
components. 2018. doi:10.15479/AT:ISTA:th_930
apa: Hurny, A. (2018). Identification and characterization of novel auxin-cytokinin
cross-talk components. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_930
chicago: Hurny, Andrej. “Identification and Characterization of Novel Auxin-Cytokinin
Cross-Talk Components.” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_930.
ieee: A. Hurny, “Identification and characterization of novel auxin-cytokinin cross-talk
components,” Institute of Science and Technology Austria, 2018.
ista: Hurny A. 2018. Identification and characterization of novel auxin-cytokinin
cross-talk components. Institute of Science and Technology Austria.
mla: Hurny, Andrej. Identification and Characterization of Novel Auxin-Cytokinin
Cross-Talk Components. Institute of Science and Technology Austria, 2018,
doi:10.15479/AT:ISTA:th_930.
short: A. Hurny, Identification and Characterization of Novel Auxin-Cytokinin Cross-Talk
Components, Institute of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2018-12-11T11:47:03Z
date_published: 2018-01-01T00:00:00Z
date_updated: 2026-04-08T14:13:30Z
day: '01'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: EvBe
doi: 10.15479/AT:ISTA:th_930
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issn:
- 2663-337X
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publist_id: '7277'
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related_material:
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status: public
supervisor:
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
title: Identification and characterization of novel auxin-cytokinin cross-talk components
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...