---
_id: '7473'
abstract:
- lang: eng
text: How structural and functional properties of synapses relate to each other
is a fundamental question in neuroscience. Electrophysiology has elucidated mechanisms
of synaptic transmission, and electron microscopy (EM) has provided insight into
morphological properties of synapses. Here we describe an enhanced method for
functional EM (“flash and freeze”), combining optogenetic stimulation with high-pressure
freezing. We demonstrate that the improved method can be applied to intact networks
in acute brain slices and organotypic slice cultures from mice. As a proof of
concept, we probed vesicle pool changes during synaptic transmission at the hippocampal
mossy fiber-CA3 pyramidal neuron synapse. Our findings show overlap of the docked
vesicle pool and the functionally defined readily releasable pool and provide
evidence of fast endocytosis at this synapse. Functional EM with acute slices
and slice cultures has the potential to reveal the structural and functional mechanisms
of transmission in intact, genetically perturbed, and disease-affected synapses.
acknowledgement: This project has received funding from the European Research Council
(ERC) and European Commission (EC), under the European Union’s Horizon 2020 research
and innovation programme (ERC grant agreement No. 692692 and Marie Sklodowska-Curie
708497) and from Fonds zur Förderung der Wissenschaftlichen Forschung (Z 312-B27
Wittgenstein award and DK W1205-B09). We thank Johann Danzl and Ryuichi Shigemoto
for critically reading the manuscript; Walter Kaufmann, Daniel Gutl, and Vanessa
Zheden for extensive EM training, advice, and experimental assistance; Benjamin
Suter for substantial help with light stimulation, ImageJ plugins for analysis,
and manuscript editing; Florian Marr and Christina Altmutter for technical support;
Eleftheria Kralli-Beller for manuscript editing; Julia König and Paul Wurzinger
(Leica Microsystems) for helpful technical discussions; and Taija Makinen for providing
the Prox1-CreERT2 mouse line.
article_processing_charge: No
article_type: original
author:
- first_name: Carolina
full_name: Borges Merjane, Carolina
id: 4305C450-F248-11E8-B48F-1D18A9856A87
last_name: Borges Merjane
orcid: 0000-0003-0005-401X
- first_name: Olena
full_name: Kim, Olena
id: 3F8ABDDA-F248-11E8-B48F-1D18A9856A87
last_name: Kim
orcid: 0000-0003-2344-1039
- 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: Borges Merjane C, Kim O, Jonas PM. Functional electron microscopy (“Flash and
Freeze”) of identified cortical synapses in acute brain slices. Neuron.
2020;105:992-1006. doi:10.1016/j.neuron.2019.12.022
apa: Borges Merjane, C., Kim, O., & Jonas, P. M. (2020). Functional electron
microscopy (“Flash and Freeze”) of identified cortical synapses in acute brain
slices. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2019.12.022
chicago: Borges Merjane, Carolina, Olena Kim, and Peter M Jonas. “Functional Electron
Microscopy (‘Flash and Freeze’) of Identified Cortical Synapses in Acute Brain
Slices.” Neuron. Elsevier, 2020. https://doi.org/10.1016/j.neuron.2019.12.022.
ieee: C. Borges Merjane, O. Kim, and P. M. Jonas, “Functional electron microscopy
(‘Flash and Freeze’) of identified cortical synapses in acute brain slices,” Neuron,
vol. 105. Elsevier, pp. 992–1006, 2020.
ista: Borges Merjane C, Kim O, Jonas PM. 2020. Functional electron microscopy (“Flash
and Freeze”) of identified cortical synapses in acute brain slices. Neuron. 105,
992–1006.
mla: Borges Merjane, Carolina, et al. “Functional Electron Microscopy (‘Flash and
Freeze’) of Identified Cortical Synapses in Acute Brain Slices.” Neuron,
vol. 105, Elsevier, 2020, pp. 992–1006, doi:10.1016/j.neuron.2019.12.022.
short: C. Borges Merjane, O. Kim, P.M. Jonas, Neuron 105 (2020) 992–1006.
corr_author: '1'
date_created: 2020-02-10T15:59:45Z
date_published: 2020-03-18T00:00:00Z
date_updated: 2026-05-15T22:30:34Z
day: '18'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1016/j.neuron.2019.12.022
ec_funded: 1
external_id:
isi:
- '000520854700008'
pmid:
- '31928842'
file:
- access_level: open_access
checksum: 3582664addf26859e86ac5bec3e01416
content_type: application/pdf
creator: dernst
date_created: 2020-11-20T08:58:53Z
date_updated: 2020-11-20T08:58:53Z
file_id: '8778'
file_name: 2020_Neuron_BorgesMerjane.pdf
file_size: 9712957
relation: main_file
success: 1
file_date_updated: 2020-11-20T08:58:53Z
has_accepted_license: '1'
intvolume: ' 105'
isi: 1
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '03'
oa: 1
oa_version: Published Version
page: 992-1006
pmid: 1
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: 25BAF7B2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '708497'
name: Presynaptic calcium channels distribution and impact on coupling at the hippocampal
mossy fiber synapse
- _id: 25C5A090-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z00312
name: Synaptic communication in neuronal microcircuits
- _id: 25C3DBB6-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W01205
name: Zellkommunikation in Gesundheit und Krankheit
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/flash-and-freeze-reveals-dynamics-of-nerve-connections/
record:
- id: '11196'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Functional electron microscopy (“Flash and Freeze”) of identified cortical
synapses in acute brain slices
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 105
year: '2020'
...
---
_id: '8139'
abstract:
- lang: eng
text: 'Clathrin-mediated endocytosis (CME) is a crucial cellular process implicated
in many aspects of plant growth, development, intra- and inter-cellular signaling,
nutrient uptake and pathogen defense. Despite these significant roles, little
is known about the precise molecular details of how it functions in planta. In
order to facilitate the direct quantitative study of plant CME, here we review
current routinely used methods and present refined, standardized quantitative
imaging protocols which allow the detailed characterization of CME at multiple
scales in plant tissues. These include: (i) an efficient electron microscopy protocol
for the imaging of Arabidopsis CME vesicles in situ, thus providing a method for
the detailed characterization of the ultra-structure of clathrin-coated vesicles;
(ii) a detailed protocol and analysis for quantitative live-cell fluorescence
microscopy to precisely examine the temporal interplay of endocytosis components
during single CME events; (iii) a semi-automated analysis to allow the quantitative
characterization of global internalization of cargos in whole plant tissues; and
(iv) an overview and validation of useful genetic and pharmacological tools to
interrogate the molecular mechanisms and function of CME in intact plant samples.'
acknowledged_ssus:
- _id: EM-Fac
- _id: Bio
acknowledgement: "This paper is dedicated to the memory of Christien Merrifield. He
pioneered quantitative\r\nimaging approaches in mammalian CME and his mentorship
inspired the development of all\r\nthe analysis methods presented here. His joy
in research, pure scientific curiosity and\r\nmicroscopy excellence remain a constant
inspiration. We thank Daniel Van Damme for gifting\r\nus the CLC2-GFP x TPLATE-TagRFP
plants used in this manuscript. We further thank the\r\nScientific Service Units
at IST Austria; specifically, the Electron Microscopy Facility for\r\ntechnical
assistance (in particular Vanessa Zheden) and the BioImaging Facility BioImaging\r\nFacility
for access to equipment. "
article_number: jcs248062
article_processing_charge: No
article_type: original
author:
- first_name: Alexander J
full_name: Johnson, Alexander J
id: 46A62C3A-F248-11E8-B48F-1D18A9856A87
last_name: Johnson
orcid: 0000-0002-2739-8843
- first_name: Nataliia
full_name: Gnyliukh, Nataliia
id: 390C1120-F248-11E8-B48F-1D18A9856A87
last_name: Gnyliukh
orcid: 0000-0002-2198-0509
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Madhumitha
full_name: Narasimhan, Madhumitha
id: 44BF24D0-F248-11E8-B48F-1D18A9856A87
last_name: Narasimhan
orcid: 0000-0002-8600-0671
- first_name: G
full_name: Vert, G
last_name: Vert
- first_name: SY
full_name: Bednarek, SY
last_name: Bednarek
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Johnson AJ, Gnyliukh N, Kaufmann W, et al. Experimental toolbox for quantitative
evaluation of clathrin-mediated endocytosis in the plant model Arabidopsis. Journal
of Cell Science. 2020;133(15). doi:10.1242/jcs.248062
apa: Johnson, A. J., Gnyliukh, N., Kaufmann, W., Narasimhan, M., Vert, G., Bednarek,
S., & Friml, J. (2020). Experimental toolbox for quantitative evaluation of
clathrin-mediated endocytosis in the plant model Arabidopsis. Journal of Cell
Science. The Company of Biologists. https://doi.org/10.1242/jcs.248062
chicago: Johnson, Alexander J, Nataliia Gnyliukh, Walter Kaufmann, Madhumitha Narasimhan,
G Vert, SY Bednarek, and Jiří Friml. “Experimental Toolbox for Quantitative Evaluation
of Clathrin-Mediated Endocytosis in the Plant Model Arabidopsis.” Journal of
Cell Science. The Company of Biologists, 2020. https://doi.org/10.1242/jcs.248062.
ieee: A. J. Johnson et al., “Experimental toolbox for quantitative evaluation
of clathrin-mediated endocytosis in the plant model Arabidopsis,” Journal of
Cell Science, vol. 133, no. 15. The Company of Biologists, 2020.
ista: Johnson AJ, Gnyliukh N, Kaufmann W, Narasimhan M, Vert G, Bednarek S, Friml
J. 2020. Experimental toolbox for quantitative evaluation of clathrin-mediated
endocytosis in the plant model Arabidopsis. Journal of Cell Science. 133(15),
jcs248062.
mla: Johnson, Alexander J., et al. “Experimental Toolbox for Quantitative Evaluation
of Clathrin-Mediated Endocytosis in the Plant Model Arabidopsis.” Journal of
Cell Science, vol. 133, no. 15, jcs248062, The Company of Biologists, 2020,
doi:10.1242/jcs.248062.
short: A.J. Johnson, N. Gnyliukh, W. Kaufmann, M. Narasimhan, G. Vert, S. Bednarek,
J. Friml, Journal of Cell Science 133 (2020).
date_created: 2020-07-21T08:58:19Z
date_published: 2020-08-06T00:00:00Z
date_updated: 2026-05-15T22:30:38Z
day: '06'
ddc:
- '575'
department:
- _id: JiFr
- _id: EM-Fac
doi: 10.1242/jcs.248062
ec_funded: 1
external_id:
isi:
- '000561047900021'
pmid:
- '32616560'
file:
- access_level: open_access
checksum: 2d11f79a0b4e0a380fb002b933da331a
content_type: application/pdf
creator: ajohnson
date_created: 2020-11-26T17:12:51Z
date_updated: 2021-08-08T22:30:03Z
embargo: 2021-08-07
file_id: '8815'
file_name: 2020 - Johnson - JSC - plant CME toolbox.pdf
file_size: 15150403
relation: main_file
file_date_updated: 2021-08-08T22:30:03Z
has_accepted_license: '1'
intvolume: ' 133'
isi: 1
issue: '15'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 26538374-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I03630
name: Molecular mechanisms of endocytic cargo recognition in plants
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
publication: Journal of Cell Science
publication_identifier:
eissn:
- 1477-9137
issn:
- 0021-9533
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
related_material:
record:
- id: '14510'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Experimental toolbox for quantitative evaluation of clathrin-mediated endocytosis
in the plant model Arabidopsis
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 133
year: '2020'
...
---
OA_place: publisher
OA_type: hybrid
_id: '8002'
abstract:
- lang: eng
text: Wound healing in plant tissues, consisting of rigid cell wall-encapsulated
cells, represents a considerable challenge and occurs through largely unknown
mechanisms distinct from those in animals. Owing to their inability to migrate,
plant cells rely on targeted cell division and expansion to regenerate wounds.
Strict coordination of these wound-induced responses is essential to ensure efficient,
spatially restricted wound healing. Single-cell tracking by live imaging allowed
us to gain mechanistic insight into the wound perception and coordination of wound
responses after laser-based wounding in Arabidopsis root. We revealed a crucial
contribution of the collapse of damaged cells in wound perception and detected
an auxin increase specific to cells immediately adjacent to the wound. This localized
auxin increase balances wound-induced cell expansion and restorative division
rates in a dose-dependent manner, leading to tumorous overproliferation when the
canonical TIR1 auxin signaling is disrupted. Auxin and wound-induced turgor pressure
changes together also spatially define the activation of key components of regeneration,
such as the transcription regulator ERF115. Our observations suggest that the
wound signaling involves the sensing of collapse of damaged cells and a local
auxin signaling activation to coordinate the downstream transcriptional responses
in the immediate wound vicinity.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
article_number: '202003346'
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Lukas
full_name: Hörmayer, Lukas
id: 2EEE7A2A-F248-11E8-B48F-1D18A9856A87
last_name: Hörmayer
orcid: 0000-0001-8295-2926
- first_name: Juan C
full_name: Montesinos López, Juan C
id: 310A8E3E-F248-11E8-B48F-1D18A9856A87
last_name: Montesinos López
orcid: 0000-0001-9179-6099
- first_name: Petra
full_name: Marhavá, Petra
id: 44E59624-F248-11E8-B48F-1D18A9856A87
last_name: Marhavá
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
- first_name: Saiko
full_name: Yoshida, Saiko
id: 2E46069C-F248-11E8-B48F-1D18A9856A87
last_name: Yoshida
orcid: 0000-0001-6111-9353
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Hörmayer L, Montesinos López JC, Marhavá P, Benková E, Yoshida S, Friml J.
Wounding-induced changes in cellular pressure and localized auxin signalling spatially
coordinate restorative divisions in roots. Proceedings of the National Academy
of Sciences of the United States of America. 2020;117(26). doi:10.1073/pnas.2003346117
apa: Hörmayer, L., Montesinos López, J. C., Marhavá, P., Benková, E., Yoshida, S.,
& Friml, J. (2020). Wounding-induced changes in cellular pressure and localized
auxin signalling spatially coordinate restorative divisions in roots. Proceedings
of the National Academy of Sciences of the United States of America. National
Academy of Sciences. https://doi.org/10.1073/pnas.2003346117
chicago: Hörmayer, Lukas, Juan C Montesinos López, Petra Marhavá, Eva Benková, Saiko
Yoshida, and Jiří Friml. “Wounding-Induced Changes in Cellular Pressure and Localized
Auxin Signalling Spatially Coordinate Restorative Divisions in Roots.” Proceedings
of the National Academy of Sciences of the United States of America. National
Academy of Sciences, 2020. https://doi.org/10.1073/pnas.2003346117.
ieee: L. Hörmayer, J. C. Montesinos López, P. Marhavá, E. Benková, S. Yoshida, and
J. Friml, “Wounding-induced changes in cellular pressure and localized auxin signalling
spatially coordinate restorative divisions in roots,” Proceedings of the National
Academy of Sciences of the United States of America, vol. 117, no. 26. National
Academy of Sciences, 2020.
ista: Hörmayer L, Montesinos López JC, Marhavá P, Benková E, Yoshida S, Friml J.
2020. Wounding-induced changes in cellular pressure and localized auxin signalling
spatially coordinate restorative divisions in roots. Proceedings of the National
Academy of Sciences of the United States of America. 117(26), 202003346.
mla: Hörmayer, Lukas, et al. “Wounding-Induced Changes in Cellular Pressure and
Localized Auxin Signalling Spatially Coordinate Restorative Divisions in Roots.”
Proceedings of the National Academy of Sciences of the United States of America,
vol. 117, no. 26, 202003346, National Academy of Sciences, 2020, doi:10.1073/pnas.2003346117.
short: L. Hörmayer, J.C. Montesinos López, P. Marhavá, E. Benková, S. Yoshida, J.
Friml, Proceedings of the National Academy of Sciences of the United States of
America 117 (2020).
corr_author: '1'
date_created: 2020-06-22T13:33:52Z
date_published: 2020-06-30T00:00:00Z
date_updated: 2026-05-15T22:30:46Z
day: '30'
ddc:
- '580'
department:
- _id: JiFr
- _id: EvBe
doi: 10.1073/pnas.2003346117
ec_funded: 1
external_id:
isi:
- '000565729700033'
pmid:
- '32541049'
file:
- access_level: open_access
checksum: 908b09437680181de9990915f2113aca
content_type: application/pdf
creator: dernst
date_created: 2020-06-23T11:30:53Z
date_updated: 2020-07-14T12:48:07Z
file_id: '8009'
file_name: 2020_PNAS_Hoermayer.pdf
file_size: 2407102
relation: main_file
file_date_updated: 2020-07-14T12:48:07Z
has_accepted_license: '1'
intvolume: ' 117'
isi: 1
issue: '26'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 261099A6-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742985'
name: Tracing Evolution of Auxin Transport and Polarity in Plants
- _id: 262EF96E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29988
name: RNA-directed DNA methylation in plant development
publication: Proceedings of the National Academy of Sciences of the United States
of America
publication_identifier:
eissn:
- 1091-6490
issn:
- 0027-8424
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/how-wounded-plants-coordinate-their-healing/
record:
- id: '9992'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Wounding-induced changes in cellular pressure and localized auxin signalling
spatially coordinate restorative divisions in roots
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 117
year: '2020'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '9160'
abstract:
- lang: eng
text: Auxin is a key hormonal regulator, that governs plant growth and development
in concert with other hormonal pathways. The unique feature of auxin is its polar,
cell-to-cell transport that leads to the formation of local auxin maxima and gradients,
which coordinate initiation and patterning of plant organs. The molecular machinery
mediating polar auxin transport is one of the important points of interaction
with other hormones. Multiple hormonal pathways converge at the regulation of
auxin transport and form a regulatory network that integrates various developmental
and environmental inputs to steer plant development. In this review, we discuss
recent advances in understanding the mechanisms that underlie regulation of polar
auxin transport by multiple hormonal pathways. Specifically, we focus on the post-translational
mechanisms that contribute to fine-tuning of the abundance and polarity of auxin
transporters at the plasma membrane and thereby enable rapid modification of the
auxin flow to coordinate plant growth and development.
acknowledgement: H.S. is the recipient of a DOC Fellowship of the Austrian Academy
of Sciences at the Institute of Science and Technology, Austria. J.C.M. is the recipient
of an EMBO Long-Term Fellowship (ALTF number 710-2016). We would like to thank Jiri
Friml and Carina Baskett for critical reading of the manuscript and Shutang Tan
and Maciek Adamowski for helpful discussions. No conflict of interest declared.
article_number: '100048'
article_processing_charge: No
article_type: original
author:
- first_name: Hana
full_name: Semeradova, Hana
id: 42FE702E-F248-11E8-B48F-1D18A9856A87
last_name: Semeradova
- first_name: Juan C
full_name: Montesinos López, Juan C
id: 310A8E3E-F248-11E8-B48F-1D18A9856A87
last_name: Montesinos López
orcid: 0000-0001-9179-6099
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
citation:
ama: 'Semerádová H, Montesinos López JC, Benková E. All roads lead to auxin: Post-translational
regulation of auxin transport by multiple hormonal pathways. Plant Communications.
2020;1(3). doi:10.1016/j.xplc.2020.100048'
apa: 'Semerádová, H., Montesinos López, J. C., & Benková, E. (2020). All roads
lead to auxin: Post-translational regulation of auxin transport by multiple hormonal
pathways. Plant Communications. Elsevier. https://doi.org/10.1016/j.xplc.2020.100048'
chicago: 'Semerádová, Hana, Juan C Montesinos López, and Eva Benková. “All Roads
Lead to Auxin: Post-Translational Regulation of Auxin Transport by Multiple Hormonal
Pathways.” Plant Communications. Elsevier, 2020. https://doi.org/10.1016/j.xplc.2020.100048.'
ieee: 'H. Semerádová, J. C. Montesinos López, and E. Benková, “All roads lead to
auxin: Post-translational regulation of auxin transport by multiple hormonal pathways,”
Plant Communications, vol. 1, no. 3. Elsevier, 2020.'
ista: 'Semerádová H, Montesinos López JC, Benková E. 2020. All roads lead to auxin:
Post-translational regulation of auxin transport by multiple hormonal pathways.
Plant Communications. 1(3), 100048.'
mla: 'Semerádová, Hana, et al. “All Roads Lead to Auxin: Post-Translational Regulation
of Auxin Transport by Multiple Hormonal Pathways.” Plant Communications,
vol. 1, no. 3, 100048, Elsevier, 2020, doi:10.1016/j.xplc.2020.100048.'
short: H. Semerádová, J.C. Montesinos López, E. Benková, Plant Communications 1
(2020).
corr_author: '1'
date_created: 2021-02-18T10:18:43Z
date_published: 2020-05-11T00:00:00Z
date_updated: 2026-05-15T22:30:47Z
day: '11'
ddc:
- '580'
department:
- _id: EvBe
doi: 10.1016/j.xplc.2020.100048
external_id:
isi:
- '000654052800010'
pmid:
- '33367243'
file:
- access_level: open_access
checksum: 785b266d82a94b007cf40dbbe7c4847e
content_type: application/pdf
creator: dernst
date_created: 2021-02-18T10:23:59Z
date_updated: 2021-02-18T10:23:59Z
file_id: '9161'
file_name: 2020_PlantComm_Semeradova.pdf
file_size: 840289
relation: main_file
success: 1
file_date_updated: 2021-02-18T10:23:59Z
has_accepted_license: '1'
intvolume: ' 1'
isi: 1
issue: '3'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 261821BC-B435-11E9-9278-68D0E5697425
grant_number: '24746'
name: Molecular mechanisms of the cytokinin regulated endomembrane trafficking to
coordinate plant organogenesis
- _id: 253E54C8-B435-11E9-9278-68D0E5697425
grant_number: ALTF710-2016
name: Molecular mechanism of auxindriven formative divisions delineating lateral
root organogenesis in plants
publication: Plant Communications
publication_identifier:
issn:
- 2590-3462
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
record:
- id: '10135'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: 'All roads lead to auxin: Post-translational regulation of auxin transport
by multiple hormonal pathways'
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 0043cee0-e5fc-11ee-9736-f83bc23afbf0
volume: 1
year: '2020'
...
---
_id: '8831'
abstract:
- lang: eng
text: Holes in planar Ge have high mobilities, strong spin-orbit interaction and
electrically tunable g-factors, and are therefore emerging as a promising candidate
for hybrid superconductorsemiconductor devices. This is further motivated by the
observation of supercurrent transport in planar Ge Josephson Field effect transistors
(JoFETs). A key challenge towards hybrid germanium quantum technology is the design
of high quality interfaces and superconducting contacts that are robust against
magnetic fields. By combining the assets of Al, which has a long superconducting
coherence, and Nb, which has a significant superconducting gap, we form low-disordered
JoFETs with large ICRN products that are capable of withstanding high magnetic
fields. We furthermore demonstrate the ability of phase-biasing individual JoFETs
opening up an avenue to explore topological superconductivity in planar Ge. The
persistence of superconductivity in the reported hybrid devices beyond 1.8 T paves
the way towards integrating spin qubits and proximity-induced superconductivity
on the same chip.
acknowledged_ssus:
- _id: M-Shop
- _id: NanoFab
acknowledgement: "This research and related results were made possible with the support
of the NOMIS Foundation. This research was supported by the Scientific Service Units
of IST Austria through resources provided by the MIBA Machine Shop and the nanofabrication
facility, the European Union’s Horizon 2020 research and innovation program under
the Marie Sklodowska-Curie grant agreement #844511 and the Grant Agreement #862046.
ICN2 acknowledge funding from Generalitat de Catalunya 2017 SGR 327. ICN2 is supported
by the Severo Ochoa\r\nprogram from Spanish MINECO (Grant No. SEV2017-0706) and
is funded by the CERCA Programme / Generalitat de Catalunya. Part of the present
work has been performed in the framework of Universitat Aut`onoma de Barcelona Materials
Science PhD program. The HAADF-STEM microscopy was conducted in the Laboratorio
de Microscopias Avanzadas at Instituto de Nanociencia de Aragon-Universidad de Zaragoza.
Authors acknowledge the LMA-INA for offering access to their instruments and expertise.
We acknowledge support from CSIC Research Platform on Quantum Technologies PTI-001.
This project has received funding from\r\nthe European Union’s Horizon 2020 research
and innovation programme under grant agreement No 823717 – ESTEEM3. M.B. acknowledges
support from SUR Generalitat de Catalunya and the EU Social Fund; project ref. 2020
FI 00103. GS and MV acknowledge support through a projectruimte grant associated
with the Netherlands Organization of Scientific Research (NWO)."
article_number: '2012.00322'
article_processing_charge: No
arxiv: 1
author:
- first_name: Kushagra
full_name: Aggarwal, Kushagra
id: b22ab905-3539-11eb-84c3-fc159dcd79cb
last_name: Aggarwal
orcid: 0000-0001-9985-9293
- first_name: Andrea C
full_name: Hofmann, Andrea C
id: 340F461A-F248-11E8-B48F-1D18A9856A87
last_name: Hofmann
- first_name: Daniel
full_name: Jirovec, Daniel
id: 4C473F58-F248-11E8-B48F-1D18A9856A87
last_name: Jirovec
orcid: 0000-0002-7197-4801
- first_name: Ivan
full_name: Prieto Gonzalez, Ivan
id: 2A307FE2-F248-11E8-B48F-1D18A9856A87
last_name: Prieto Gonzalez
orcid: 0000-0002-7370-5357
- first_name: Amir
full_name: Sammak, Amir
last_name: Sammak
- first_name: Marc
full_name: Botifoll, Marc
last_name: Botifoll
- first_name: Sara
full_name: Marti-Sanchez, Sara
last_name: Marti-Sanchez
- first_name: Menno
full_name: Veldhorst, Menno
last_name: Veldhorst
- first_name: Jordi
full_name: Arbiol, Jordi
last_name: Arbiol
- first_name: Giordano
full_name: Scappucci, Giordano
last_name: Scappucci
- first_name: Georgios
full_name: Katsaros, Georgios
id: 38DB5788-F248-11E8-B48F-1D18A9856A87
last_name: Katsaros
orcid: 0000-0001-8342-202X
citation:
ama: Aggarwal K, Hofmann AC, Jirovec D, et al. Enhancement of proximity induced
superconductivity in planar Germanium. arXiv. doi:10.48550/arXiv.2012.00322
apa: Aggarwal, K., Hofmann, A. C., Jirovec, D., Prieto Gonzalez, I., Sammak, A.,
Botifoll, M., … Katsaros, G. (n.d.). Enhancement of proximity induced superconductivity
in planar Germanium. arXiv. https://doi.org/10.48550/arXiv.2012.00322
chicago: Aggarwal, Kushagra, Andrea C Hofmann, Daniel Jirovec, Ivan Prieto Gonzalez,
Amir Sammak, Marc Botifoll, Sara Marti-Sanchez, et al. “Enhancement of Proximity
Induced Superconductivity in Planar Germanium.” ArXiv, n.d. https://doi.org/10.48550/arXiv.2012.00322.
ieee: K. Aggarwal et al., “Enhancement of proximity induced superconductivity
in planar Germanium,” arXiv. .
ista: Aggarwal K, Hofmann AC, Jirovec D, Prieto Gonzalez I, Sammak A, Botifoll M,
Marti-Sanchez S, Veldhorst M, Arbiol J, Scappucci G, Katsaros G. Enhancement of
proximity induced superconductivity in planar Germanium. arXiv, 2012.00322.
mla: Aggarwal, Kushagra, et al. “Enhancement of Proximity Induced Superconductivity
in Planar Germanium.” ArXiv, 2012.00322, doi:10.48550/arXiv.2012.00322.
short: K. Aggarwal, A.C. Hofmann, D. Jirovec, I. Prieto Gonzalez, A. Sammak, M.
Botifoll, S. Marti-Sanchez, M. Veldhorst, J. Arbiol, G. Scappucci, G. Katsaros,
ArXiv (n.d.).
corr_author: '1'
date_created: 2020-12-02T10:42:53Z
date_published: 2020-12-02T00:00:00Z
date_updated: 2026-05-15T22:30:48Z
day: '02'
ddc:
- '530'
department:
- _id: GeKa
doi: 10.48550/arXiv.2012.00322
ec_funded: 1
external_id:
arxiv:
- '2012.00322'
file:
- access_level: open_access
checksum: 22a612e206232fa94b138b2c2f957582
content_type: application/pdf
creator: gkatsaro
date_created: 2020-12-02T10:42:31Z
date_updated: 2020-12-02T10:42:31Z
file_id: '8832'
file_name: Superconducting_2D_Ge.pdf
file_size: 1697939
relation: main_file
file_date_updated: 2020-12-02T10:42:31Z
has_accepted_license: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Submitted Version
project:
- _id: 262116AA-B435-11E9-9278-68D0E5697425
name: Hybrid Semiconductor - Superconductor Quantum Devices
- _id: 26A151DA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '844511'
name: Majorana bound states in Ge/SiGe heterostructures
- _id: 237E5020-32DE-11EA-91FC-C7463DDC885E
call_identifier: H2020
grant_number: '862046'
name: TOPOLOGICALLY PROTECTED AND SCALABLE QUANTUM BITS
publication: arXiv
publication_status: draft
related_material:
record:
- id: '10559'
relation: later_version
status: public
- id: '8834'
relation: research_data
status: public
- id: '10058'
relation: dissertation_contains
status: public
status: public
title: Enhancement of proximity induced superconductivity in planar Germanium
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '8532'
abstract:
- lang: eng
text: The molecular anatomy of synapses defines their characteristics in transmission
and plasticity. Precise measurements of the number and distribution of synaptic
proteins are important for our understanding of synapse heterogeneity within and
between brain regions. Freeze–fracture replica immunogold electron microscopy
enables us to analyze them quantitatively on a two-dimensional membrane surface.
Here, we introduce Darea software, which utilizes deep learning for analysis of
replica images and demonstrate its usefulness for quick measurements of the pre-
and postsynaptic areas, density and distribution of gold particles at synapses
in a reproducible manner. We used Darea for comparing glutamate receptor and calcium
channel distributions between hippocampal CA3-CA1 spine synapses on apical and
basal dendrites, which differ in signaling pathways involved in synaptic plasticity.
We found that apical synapses express a higher density of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic
acid (AMPA) receptors and a stronger increase of AMPA receptors with synaptic
size, while basal synapses show a larger increase in N-methyl-D-aspartate (NMDA)
receptors with size. Interestingly, AMPA and NMDA receptors are segregated within
postsynaptic sites and negatively correlated in density among both apical and
basal synapses. In the presynaptic sites, Cav2.1 voltage-gated calcium channels
show similar densities in apical and basal synapses with distributions consistent
with an exclusion zone model of calcium channel-release site topography.
acknowledgement: "This research was funded by Austrian Academy of Sciences, DOC fellowship
to D.K., European Research\r\nCouncil Advanced Grant 694539 and European Union Human
Brain Project (HBP) SGA2 785907 to R.S.\r\nWe acknowledge Elena Hollergschwandtner
for technical support."
article_number: '6737'
article_processing_charge: No
article_type: original
author:
- first_name: David
full_name: Kleindienst, David
id: 42E121A4-F248-11E8-B48F-1D18A9856A87
last_name: Kleindienst
- first_name: Jacqueline-Claire
full_name: Montanaro-Punzengruber, Jacqueline-Claire
id: 3786AB44-F248-11E8-B48F-1D18A9856A87
last_name: Montanaro-Punzengruber
- first_name: Pradeep
full_name: Bhandari, Pradeep
id: 45EDD1BC-F248-11E8-B48F-1D18A9856A87
last_name: Bhandari
orcid: 0000-0003-0863-4481
- first_name: Matthew J
full_name: Case, Matthew J
id: 44B7CA5A-F248-11E8-B48F-1D18A9856A87
last_name: Case
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Kleindienst D, Montanaro-Punzengruber J-C, Bhandari P, Case MJ, Fukazawa Y,
Shigemoto R. Deep learning-assisted high-throughput analysis of freeze-fracture
replica images applied to glutamate receptors and calcium channels at hippocampal
synapses. International Journal of Molecular Sciences. 2020;21(18). doi:10.3390/ijms21186737
apa: Kleindienst, D., Montanaro-Punzengruber, J.-C., Bhandari, P., Case, M. J.,
Fukazawa, Y., & Shigemoto, R. (2020). Deep learning-assisted high-throughput
analysis of freeze-fracture replica images applied to glutamate receptors and
calcium channels at hippocampal synapses. International Journal of Molecular
Sciences. MDPI. https://doi.org/10.3390/ijms21186737
chicago: Kleindienst, David, Jacqueline-Claire Montanaro-Punzengruber, Pradeep Bhandari,
Matthew J Case, Yugo Fukazawa, and Ryuichi Shigemoto. “Deep Learning-Assisted
High-Throughput Analysis of Freeze-Fracture Replica Images Applied to Glutamate
Receptors and Calcium Channels at Hippocampal Synapses.” International Journal
of Molecular Sciences. MDPI, 2020. https://doi.org/10.3390/ijms21186737.
ieee: D. Kleindienst, J.-C. Montanaro-Punzengruber, P. Bhandari, M. J. Case, Y.
Fukazawa, and R. Shigemoto, “Deep learning-assisted high-throughput analysis of
freeze-fracture replica images applied to glutamate receptors and calcium channels
at hippocampal synapses,” International Journal of Molecular Sciences,
vol. 21, no. 18. MDPI, 2020.
ista: Kleindienst D, Montanaro-Punzengruber J-C, Bhandari P, Case MJ, Fukazawa Y,
Shigemoto R. 2020. Deep learning-assisted high-throughput analysis of freeze-fracture
replica images applied to glutamate receptors and calcium channels at hippocampal
synapses. International Journal of Molecular Sciences. 21(18), 6737.
mla: Kleindienst, David, et al. “Deep Learning-Assisted High-Throughput Analysis
of Freeze-Fracture Replica Images Applied to Glutamate Receptors and Calcium Channels
at Hippocampal Synapses.” International Journal of Molecular Sciences,
vol. 21, no. 18, 6737, MDPI, 2020, doi:10.3390/ijms21186737.
short: D. Kleindienst, J.-C. Montanaro-Punzengruber, P. Bhandari, M.J. Case, Y.
Fukazawa, R. Shigemoto, International Journal of Molecular Sciences 21 (2020).
corr_author: '1'
date_created: 2020-09-20T22:01:35Z
date_published: 2020-09-14T00:00:00Z
date_updated: 2026-05-15T22:30:49Z
day: '14'
ddc:
- '570'
department:
- _id: RySh
doi: 10.3390/ijms21186737
ec_funded: 1
external_id:
isi:
- '000579945300001'
file:
- access_level: open_access
checksum: 2e4f62f3cfe945b7391fc3070e5a289f
content_type: application/pdf
creator: dernst
date_created: 2020-09-21T14:08:58Z
date_updated: 2020-09-21T14:08:58Z
file_id: '8551'
file_name: 2020_JournMolecSciences_Kleindienst.pdf
file_size: 5748456
relation: main_file
success: 1
file_date_updated: 2020-09-21T14:08:58Z
has_accepted_license: '1'
intvolume: ' 21'
isi: 1
issue: '18'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '09'
oa: 1
oa_version: Published Version
project:
- _id: 25CA28EA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '694539'
name: 'In situ analysis of single channel subunit composition in neurons: physiological
implication in synaptic plasticity and behaviour'
- _id: 25D32BC0-B435-11E9-9278-68D0E5697425
name: Mechanism of formation and maintenance of input side-dependent asymmetry in
the hippocampus
- _id: 26436750-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '785907'
name: Human Brain Project Specific Grant Agreement 2
publication: International Journal of Molecular Sciences
publication_identifier:
eissn:
- 1422-0067
issn:
- 1661-6596
publication_status: published
publisher: MDPI
quality_controlled: '1'
related_material:
record:
- id: '9562'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Deep learning-assisted high-throughput analysis of freeze-fracture replica
images applied to glutamate receptors and calcium channels at hippocampal synapses
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: 21
year: '2020'
...
---
OA_place: publisher
_id: '8657'
abstract:
- lang: eng
text: "Synthesis of proteins – translation – is a fundamental process of life. Quantitative
studies anchor translation into the context of bacterial physiology and reveal
several mathematical relationships, called “growth laws,” which capture physiological
feedbacks between protein synthesis and cell growth. Growth laws describe the
dependency of the ribosome abundance as a function of growth rate, which can change
depending on the growth conditions. Perturbations of translation reveal that bacteria
employ a compensatory strategy in which the reduced translation capability results
in increased expression of the translation machinery.\r\nPerturbations of translation
are achieved in various ways; clinically interesting is the application of translation-targeting
antibiotics – translation inhibitors. The antibiotic effects on bacterial physiology
are often poorly understood. Bacterial responses to two or more simultaneously
applied antibiotics are even more puzzling. The combined antibiotic effect determines
the type of drug interaction, which ranges from synergy (the effect is stronger
than expected) to antagonism (the effect is weaker) and suppression (one of the
drugs loses its potency).\r\nIn the first part of this work, we systematically
measure the pairwise interaction network for translation inhibitors that interfere
with different steps in translation. We find that the interactions are surprisingly
diverse and tend to be more antagonistic. To explore the underlying mechanisms,
we begin with a minimal biophysical model of combined antibiotic action. We base
this model on the kinetics of antibiotic uptake and binding together with the
physiological response described by the growth laws. The biophysical model explains
some drug interactions, but not all; it specifically fails to predict suppression.\r\nIn
the second part of this work, we hypothesize that elusive suppressive drug interactions
result from the interplay between ribosomes halted in different stages of translation.
To elucidate this putative mechanism of drug interactions between translation
inhibitors, we generate translation bottlenecks genetically using in- ducible
control of translation factors that regulate well-defined translation cycle steps.
These perturbations accurately mimic antibiotic action and drug interactions,
supporting that the interplay of different translation bottlenecks partially causes
these interactions.\r\nWe extend this approach by varying two translation bottlenecks
simultaneously. This approach reveals the suppression of translocation inhibition
by inhibited translation. We rationalize this effect by modeling dense traffic
of ribosomes that move on transcripts in a translation factor-mediated manner.
This model predicts a dissolution of traffic jams caused by inhibited translocation
when the density of ribosome traffic is reduced by lowered initiation. We base
this model on the growth laws and quantitative relationships between different
translation and growth parameters.\r\nIn the final part of this work, we describe
a set of tools aimed at quantification of physiological and translation parameters.
We further develop a simple model that directly connects the abundance of a translation
factor with the growth rate, which allows us to extract physiological parameters
describing initiation. We demonstrate the development of tools for measuring translation
rate.\r\nThis thesis showcases how a combination of high-throughput growth rate
mea- surements, genetics, and modeling can reveal mechanisms of drug interactions.
Furthermore, by a gradual transition from combinations of antibiotics to precise
genetic interventions, we demonstrated the equivalency between genetic and chemi-
cal perturbations of translation. These findings tile the path for quantitative
studies of antibiotic combinations and illustrate future approaches towards the
quantitative description of translation."
acknowledged_ssus:
- _id: LifeSc
- _id: M-Shop
acknowledgement: I thank Life Science Facilities for their continuous support with
providing top-notch laboratory materials, keeping the devices humming, and coordinating
the repairs and building of custom-designed laboratory equipment with the MIBA Machine
shop.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Bor
full_name: Kavcic, Bor
id: 350F91D2-F248-11E8-B48F-1D18A9856A87
last_name: Kavcic
orcid: 0000-0001-6041-254X
citation:
ama: 'Kavcic B. Perturbations of protein synthesis: from antibiotics to genetics
and physiology. 2020. doi:10.15479/AT:ISTA:8657'
apa: 'Kavcic, B. (2020). Perturbations of protein synthesis: from antibiotics
to genetics and physiology. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8657'
chicago: 'Kavcic, Bor. “Perturbations of Protein Synthesis: From Antibiotics to
Genetics and Physiology.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8657.'
ieee: 'B. Kavcic, “Perturbations of protein synthesis: from antibiotics to genetics
and physiology,” Institute of Science and Technology Austria, 2020.'
ista: 'Kavcic B. 2020. Perturbations of protein synthesis: from antibiotics to genetics
and physiology. Institute of Science and Technology Austria.'
mla: 'Kavcic, Bor. Perturbations of Protein Synthesis: From Antibiotics to Genetics
and Physiology. Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8657.'
short: 'B. Kavcic, Perturbations of Protein Synthesis: From Antibiotics to Genetics
and Physiology, Institute of Science and Technology Austria, 2020.'
corr_author: '1'
date_created: 2020-10-13T16:46:14Z
date_published: 2020-10-14T00:00:00Z
date_updated: 2026-04-08T07:27:48Z
day: '14'
ddc:
- '571'
- '530'
- '570'
degree_awarded: PhD
department:
- _id: GaTk
doi: 10.15479/AT:ISTA:8657
file:
- access_level: open_access
checksum: d708ecd62b6fcc3bc1feb483b8dbe9eb
content_type: application/pdf
creator: bkavcic
date_created: 2020-10-15T06:41:20Z
date_updated: 2021-10-07T22:30:03Z
embargo: 2021-10-06
file_id: '8663'
file_name: kavcicB_thesis202009.pdf
file_size: 52636162
relation: main_file
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checksum: bb35f2352a04db19164da609f00501f3
content_type: application/zip
creator: bkavcic
date_created: 2020-10-15T06:41:53Z
date_updated: 2021-10-07T22:30:03Z
embargo_to: open_access
file_id: '8664'
file_name: 2020b.zip
file_size: 321681247
relation: source_file
file_date_updated: 2021-10-07T22:30:03Z
has_accepted_license: '1'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: '271'
publication_identifier:
isbn:
- 978-3-99078-011-4
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '7673'
relation: part_of_dissertation
status: public
- id: '8250'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
title: 'Perturbations of protein synthesis: from antibiotics to genetics and physiology'
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2020'
...
---
_id: '8569'
abstract:
- lang: eng
text: Concerted radial migration of newly born cortical projection neurons, from
their birthplace to their final target lamina, is a key step in the assembly of
the cerebral cortex. The cellular and molecular mechanisms regulating the specific
sequential steps of radial neuronal migration in vivo are however still unclear,
let alone the effects and interactions with the extracellular environment. In
any in vivo context, cells will always be exposed to a complex extracellular environment
consisting of (1) secreted factors acting as potential signaling cues, (2) the
extracellular matrix, and (3) other cells providing cell–cell interaction through
receptors and/or direct physical stimuli. Most studies so far have described and
focused mainly on intrinsic cell-autonomous gene functions in neuronal migration
but there is accumulating evidence that non-cell-autonomous-, local-, systemic-,
and/or whole tissue-wide effects substantially contribute to the regulation of
radial neuronal migration. These non-cell-autonomous effects may differentially
affect cortical neuron migration in distinct cellular environments. However, the
cellular and molecular natures of such non-cell-autonomous mechanisms are mostly
unknown. Furthermore, physical forces due to collective migration and/or community
effects (i.e., interactions with surrounding cells) may play important roles in
neocortical projection neuron migration. In this concise review, we first outline
distinct models of non-cell-autonomous interactions of cortical projection neurons
along their radial migration trajectory during development. We then summarize
experimental assays and platforms that can be utilized to visualize and potentially
probe non-cell-autonomous mechanisms. Lastly, we define key questions to address
in the future.
acknowledgement: AH was a recipient of a DOC Fellowship (24812) of the Austrian Academy
of Sciences. This work also received support from IST Austria institutional funds;
the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework
Programme (FP7/2007–2013) under REA Grant Agreement No. 618444 to SH.
article_number: '574382'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Hansen AH, Hippenmeyer S. Non-cell-autonomous mechanisms in radial projection
neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental
Biology. 2020;8(9). doi:10.3389/fcell.2020.574382
apa: Hansen, A. H., & Hippenmeyer, S. (2020). Non-cell-autonomous mechanisms
in radial projection neuron migration in the developing cerebral cortex. Frontiers
in Cell and Developmental Biology. Frontiers. https://doi.org/10.3389/fcell.2020.574382
chicago: Hansen, Andi H, and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms
in Radial Projection Neuron Migration in the Developing Cerebral Cortex.” Frontiers
in Cell and Developmental Biology. Frontiers, 2020. https://doi.org/10.3389/fcell.2020.574382.
ieee: A. H. Hansen and S. Hippenmeyer, “Non-cell-autonomous mechanisms in radial
projection neuron migration in the developing cerebral cortex,” Frontiers in
Cell and Developmental Biology, vol. 8, no. 9. Frontiers, 2020.
ista: Hansen AH, Hippenmeyer S. 2020. Non-cell-autonomous mechanisms in radial projection
neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental
Biology. 8(9), 574382.
mla: Hansen, Andi H., and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms in
Radial Projection Neuron Migration in the Developing Cerebral Cortex.” Frontiers
in Cell and Developmental Biology, vol. 8, no. 9, 574382, Frontiers, 2020,
doi:10.3389/fcell.2020.574382.
short: A.H. Hansen, S. Hippenmeyer, Frontiers in Cell and Developmental Biology
8 (2020).
corr_author: '1'
date_created: 2020-09-26T06:11:07Z
date_published: 2020-09-25T00:00:00Z
date_updated: 2026-05-15T22:30:52Z
day: '25'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3389/fcell.2020.574382
ec_funded: 1
external_id:
isi:
- '000577915900001'
pmid:
- '33102480'
file:
- access_level: open_access
checksum: 01f731824194c94c81a5da360d997073
content_type: application/pdf
creator: dernst
date_created: 2020-09-28T13:11:17Z
date_updated: 2020-09-28T13:11:17Z
file_id: '8584'
file_name: 2020_Frontiers_Hansen.pdf
file_size: 5527139
relation: main_file
success: 1
file_date_updated: 2020-09-28T13:11:17Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular mechanisms of radial neuronal migration
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
publication: Frontiers in Cell and Developmental Biology
publication_identifier:
issn:
- 2296-634X
publication_status: published
publisher: Frontiers
quality_controlled: '1'
related_material:
record:
- id: '9962'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Non-cell-autonomous mechanisms in radial projection neuron migration in the
developing cerebral cortex
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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 8
year: '2020'
...
---
_id: '8250'
abstract:
- lang: eng
text: 'Antibiotics that interfere with translation, when combined, interact in diverse
and difficult-to-predict ways. Here, we explain these interactions by “translation
bottlenecks”: points in the translation cycle where antibiotics block ribosomal
progression. To elucidate the underlying mechanisms of drug interactions between
translation inhibitors, we generate translation bottlenecks genetically using
inducible control of translation factors that regulate well-defined translation
cycle steps. These perturbations accurately mimic antibiotic action and drug interactions,
supporting that the interplay of different translation bottlenecks causes these
interactions. We further show that growth laws, combined with drug uptake and
binding kinetics, enable the direct prediction of a large fraction of observed
interactions, yet fail to predict suppression. However, varying two translation
bottlenecks simultaneously supports that dense traffic of ribosomes and competition
for translation factors account for the previously unexplained suppression. These
results highlight the importance of “continuous epistasis” in bacterial physiology.'
acknowledgement: "We thank M. Hennessey-Wesen, I. Tomanek, K. Jain, A. Staron, K.
Tomasek, M. Scott,\r\nK.C. Huang, and Z. Gitai for reading the manuscript and constructive
comments. B.K. is\r\nindebted to C. Guet for additional guidance and generous support,
which rendered this\r\nwork possible. B.K. thanks all members of Guet group for
many helpful discussions and\r\nsharing of resources. B.K. additionally acknowledges
the tremendous support from A.\r\nAngermayr and K. Mitosch with experimental work.
We further thank E. Brown for\r\nhelpful comments regarding lamotrigine, and A.
Buskirk for valuable suggestions\r\nregarding the ribosome footprint size. This
work was supported in part by Austrian\r\nScience Fund (FWF) standalone grants P
27201-B22 (to T.B.) and P 28844 (to G.T.),\r\nHFSP program Grant RGP0042/2013 (to
T.B.), German Research Foundation (DFG)\r\nstandalone grant BO 3502/2-1 (to T.B.),
and German Research Foundation (DFG)\r\nCollaborative Research Centre (SFB) 1310
(to T.B.). Open access funding provided by\r\nProjekt DEAL."
article_number: '4013'
article_processing_charge: No
article_type: original
author:
- first_name: Bor
full_name: Kavcic, Bor
id: 350F91D2-F248-11E8-B48F-1D18A9856A87
last_name: Kavcic
orcid: 0000-0001-6041-254X
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
- first_name: Tobias
full_name: Bollenbach, Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Kavcic B, Tkačik G, Bollenbach MT. Mechanisms of drug interactions between
translation-inhibiting antibiotics. Nature Communications. 2020;11. doi:10.1038/s41467-020-17734-z
apa: Kavcic, B., Tkačik, G., & Bollenbach, M. T. (2020). Mechanisms of drug
interactions between translation-inhibiting antibiotics. Nature Communications.
Springer Nature. https://doi.org/10.1038/s41467-020-17734-z
chicago: Kavcic, Bor, Gašper Tkačik, and Mark Tobias Bollenbach. “Mechanisms of
Drug Interactions between Translation-Inhibiting Antibiotics.” Nature Communications.
Springer Nature, 2020. https://doi.org/10.1038/s41467-020-17734-z.
ieee: B. Kavcic, G. Tkačik, and M. T. Bollenbach, “Mechanisms of drug interactions
between translation-inhibiting antibiotics,” Nature Communications, vol.
11. Springer Nature, 2020.
ista: Kavcic B, Tkačik G, Bollenbach MT. 2020. Mechanisms of drug interactions between
translation-inhibiting antibiotics. Nature Communications. 11, 4013.
mla: Kavcic, Bor, et al. “Mechanisms of Drug Interactions between Translation-Inhibiting
Antibiotics.” Nature Communications, vol. 11, 4013, Springer Nature, 2020,
doi:10.1038/s41467-020-17734-z.
short: B. Kavcic, G. Tkačik, M.T. Bollenbach, Nature Communications 11 (2020).
date_created: 2020-08-12T09:13:50Z
date_published: 2020-08-11T00:00:00Z
date_updated: 2026-05-15T22:30:51Z
day: '11'
ddc:
- '570'
department:
- _id: GaTk
doi: 10.1038/s41467-020-17734-z
external_id:
isi:
- '000562769300008'
pmid:
- '32782250'
file:
- access_level: open_access
checksum: 986bebb308850a55850028d3d2b5b664
content_type: application/pdf
creator: dernst
date_created: 2020-08-17T07:36:57Z
date_updated: 2020-08-17T07:36:57Z
file_id: '8275'
file_name: 2020_NatureComm_Kavcic.pdf
file_size: 1965672
relation: main_file
success: 1
file_date_updated: 2020-08-17T07:36:57Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
- _id: 254E9036-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P28844-B27
name: Biophysics of information processing in gene regulation
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
record:
- id: '8657'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Mechanisms of drug interactions between translation-inhibiting antibiotics
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: 11
year: '2020'
...
---
_id: '9750'
abstract:
- lang: eng
text: Tension of the actomyosin cell cortex plays a key role in determining cell-cell
contact growth and size. The level of cortical tension outside of the cell-cell
contact, when pulling at the contact edge, scales with the total size to which
a cell-cell contact can grow1,2. Here we show in zebrafish primary germ layer
progenitor cells that this monotonic relationship only applies to a narrow range
of cortical tension increase, and that above a critical threshold, contact size
inversely scales with cortical tension. This switch from cortical tension increasing
to decreasing progenitor cell-cell contact size is caused by cortical tension
promoting E-cadherin anchoring to the actomyosin cytoskeleton, thereby increasing
clustering and stability of E-cadherin at the contact. Once tension-mediated E-cadherin
stabilization at the contact exceeds a critical threshold level, the rate by which
the contact expands in response to pulling forces from the cortex sharply drops,
leading to smaller contacts at physiologically relevant timescales of contact
formation. Thus, the activity of cortical tension in expanding cell-cell contact
size is limited by tension stabilizing E-cadherin-actin complexes at the contact.
acknowledged_ssus:
- _id: Bio
- _id: EM-Fac
- _id: SSU
acknowledgement: We would like to thank Edouard Hannezo for discussions, Shayan Shami
Pour and Daniel Capek for help with data analysis, Vanessa Barone and other members
of the Heisenberg laboratory for thoughtful discussions and comments on the manuscript.
We also thank Jack Merrin for preparing the microwells, and the Scientific Service
Units at IST Austria, specifically Bioimaging and Electron Microscopy, and the Zebrafish
Facility for continuous support. We acknowledge Hitoshi Morita for the kind gift
of VinculinB-GFP plasmid. This research was supported by an ERC Advanced Grant (MECSPEC)
to C.-P.H, EMBO Long Term grant (ALTF 187-2013) to M.S and IST Fellow Marie-Curie
COFUND No. P_IST_EU01 to J.S.
article_processing_charge: No
author:
- first_name: Jana
full_name: Slovakova, Jana
id: 30F3F2F0-F248-11E8-B48F-1D18A9856A87
last_name: Slovakova
- first_name: Mateusz K
full_name: Sikora, Mateusz K
id: 2F74BCDE-F248-11E8-B48F-1D18A9856A87
last_name: Sikora
- first_name: Silvia
full_name: Caballero Mancebo, Silvia
id: 2F1E1758-F248-11E8-B48F-1D18A9856A87
last_name: Caballero Mancebo
orcid: 0000-0002-5223-3346
- first_name: Gabriel
full_name: Krens, Gabriel
id: 2B819732-F248-11E8-B48F-1D18A9856A87
last_name: Krens
orcid: 0000-0003-4761-5996
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Karla
full_name: Huljev, Karla
id: 44C6F6A6-F248-11E8-B48F-1D18A9856A87
last_name: Huljev
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Slovakova J, Sikora MK, Caballero Mancebo S, et al. Tension-dependent stabilization
of E-cadherin limits cell-cell contact expansion. bioRxiv. 2020. doi:10.1101/2020.11.20.391284
apa: Slovakova, J., Sikora, M. K., Caballero Mancebo, S., Krens, G., Kaufmann, W.,
Huljev, K., & Heisenberg, C.-P. J. (2020). Tension-dependent stabilization
of E-cadherin limits cell-cell contact expansion. bioRxiv. Cold Spring
Harbor Laboratory. https://doi.org/10.1101/2020.11.20.391284
chicago: Slovakova, Jana, Mateusz K Sikora, Silvia Caballero Mancebo, Gabriel Krens,
Walter Kaufmann, Karla Huljev, and Carl-Philipp J Heisenberg. “Tension-Dependent
Stabilization of E-Cadherin Limits Cell-Cell Contact Expansion.” BioRxiv.
Cold Spring Harbor Laboratory, 2020. https://doi.org/10.1101/2020.11.20.391284.
ieee: J. Slovakova et al., “Tension-dependent stabilization of E-cadherin
limits cell-cell contact expansion,” bioRxiv. Cold Spring Harbor Laboratory,
2020.
ista: Slovakova J, Sikora MK, Caballero Mancebo S, Krens G, Kaufmann W, Huljev K,
Heisenberg C-PJ. 2020. Tension-dependent stabilization of E-cadherin limits cell-cell
contact expansion. bioRxiv, 10.1101/2020.11.20.391284.
mla: Slovakova, Jana, et al. “Tension-Dependent Stabilization of E-Cadherin Limits
Cell-Cell Contact Expansion.” BioRxiv, Cold Spring Harbor Laboratory, 2020,
doi:10.1101/2020.11.20.391284.
short: J. Slovakova, M.K. Sikora, S. Caballero Mancebo, G. Krens, W. Kaufmann, K.
Huljev, C.-P.J. Heisenberg, BioRxiv (2020).
date_created: 2021-07-29T11:29:50Z
date_published: 2020-11-20T00:00:00Z
date_updated: 2026-05-15T22:30:52Z
day: '20'
department:
- _id: CaHe
- _id: EM-Fac
- _id: Bio
doi: 10.1101/2020.11.20.391284
ec_funded: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2020.11.20.391284
month: '11'
oa: 1
oa_version: Preprint
page: '41'
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
- _id: 2521E28E-B435-11E9-9278-68D0E5697425
grant_number: 187-2013
name: Modulation of adhesion function in cell-cell contact formation by cortical
tension
publication: bioRxiv
publication_status: published
publisher: Cold Spring Harbor Laboratory
related_material:
record:
- id: '10766'
relation: later_version
status: public
- id: '9623'
relation: dissertation_contains
status: public
status: public
title: Tension-dependent stabilization of E-cadherin limits cell-cell contact expansion
type: preprint
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2020'
...
---
_id: '7673'
abstract:
- lang: eng
text: Combining drugs can improve the efficacy of treatments. However, predicting
the effect of drug combinations is still challenging. The combined potency of
drugs determines the drug interaction, which is classified as synergistic, additive,
antagonistic, or suppressive. While probabilistic, non-mechanistic models exist,
there is currently no biophysical model that can predict antibiotic interactions.
Here, we present a physiologically relevant model of the combined action of antibiotics
that inhibit protein synthesis by targeting the ribosome. This model captures
the kinetics of antibiotic binding and transport, and uses bacterial growth laws
to predict growth in the presence of antibiotic combinations. We find that this
biophysical model can produce all drug interaction types except suppression. We
show analytically that antibiotics which cannot bind to the ribosome simultaneously
generally act as substitutes for one another, leading to additive drug interactions.
Previously proposed null expectations for higher-order drug interactions follow
as a limiting case of our model. We further extend the model to include the effects
of direct physical or allosteric interactions between individual drugs on the
ribosome. Notably, such direct interactions profoundly change the combined drug
effect, depending on the kinetic parameters of the drugs used. The model makes
additional predictions for the effects of resistance genes on drug interactions
and for interactions between ribosome-targeting antibiotics and antibiotics with
other targets. These findings enhance our understanding of the interplay between
drug action and cell physiology and are a key step toward a general framework
for predicting drug interactions.
article_processing_charge: No
author:
- first_name: Bor
full_name: Kavcic, Bor
id: 350F91D2-F248-11E8-B48F-1D18A9856A87
last_name: Kavcic
orcid: 0000-0001-6041-254X
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
- first_name: Tobias
full_name: Bollenbach, Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Kavcic B, Tkačik G, Bollenbach MT. A minimal biophysical model of combined
antibiotic action. bioRxiv. 2020. doi:10.1101/2020.04.18.047886
apa: Kavcic, B., Tkačik, G., & Bollenbach, M. T. (2020). A minimal biophysical
model of combined antibiotic action. bioRxiv. Cold Spring Harbor Laboratory.
https://doi.org/10.1101/2020.04.18.047886
chicago: Kavcic, Bor, Gašper Tkačik, and Mark Tobias Bollenbach. “A Minimal Biophysical
Model of Combined Antibiotic Action.” BioRxiv. Cold Spring Harbor Laboratory,
2020. https://doi.org/10.1101/2020.04.18.047886.
ieee: B. Kavcic, G. Tkačik, and M. T. Bollenbach, “A minimal biophysical model of
combined antibiotic action,” bioRxiv. Cold Spring Harbor Laboratory, 2020.
ista: Kavcic B, Tkačik G, Bollenbach MT. 2020. A minimal biophysical model of combined
antibiotic action. bioRxiv, 10.1101/2020.04.18.047886.
mla: Kavcic, Bor, et al. “A Minimal Biophysical Model of Combined Antibiotic Action.”
BioRxiv, Cold Spring Harbor Laboratory, 2020, doi:10.1101/2020.04.18.047886.
short: B. Kavcic, G. Tkačik, M.T. Bollenbach, BioRxiv (2020).
date_created: 2020-04-22T08:27:56Z
date_published: 2020-04-18T00:00:00Z
date_updated: 2026-05-15T22:30:51Z
day: '18'
department:
- _id: GaTk
doi: 10.1101/2020.04.18.047886
language:
- iso: eng
main_file_link:
- open_access: '1'
url: 'https://doi.org/10.1101/2020.04.18.047886 '
month: '04'
oa: 1
oa_version: Preprint
project:
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
- _id: 254E9036-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P28844-B27
name: Biophysics of information processing in gene regulation
publication: bioRxiv
publication_status: published
publisher: Cold Spring Harbor Laboratory
related_material:
record:
- id: '8997'
relation: later_version
status: public
- id: '8657'
relation: dissertation_contains
status: public
status: public
title: A minimal biophysical model of combined antibiotic action
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
OA_place: publisher
_id: '7258'
abstract:
- lang: eng
text: Many flows encountered in nature and applications are characterized by a chaotic
motion known as turbulence. Turbulent flows generate intense friction with pipe
walls and are responsible for considerable amounts of energy losses at world scale.
The nature of turbulent friction and techniques aimed at reducing it have been
subject of extensive research over the last century, but no definite answer has
been found yet. In this thesis we show that in pipes at moderate turbulent Reynolds
numbers friction is better described by the power law first introduced by Blasius
and not by the Prandtl–von Kármán formula. At higher Reynolds numbers, large scale
motions gradually become more important in the flow and can be related to the
change in scaling of friction. Next, we present a series of new techniques that
can relaminarize turbulence by suppressing a key mechanism that regenerates it
at walls, the lift–up effect. In addition, we investigate the process of turbulence
decay in several experiments and discuss the drag reduction potential. Finally,
we examine the behavior of friction under pulsating conditions inspired by the
human heart cycle and we show that under such circumstances turbulent friction
can be reduced to produce energy savings.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Davide
full_name: Scarselli, Davide
id: 40315C30-F248-11E8-B48F-1D18A9856A87
last_name: Scarselli
orcid: 0000-0001-5227-4271
citation:
ama: Scarselli D. New approaches to reduce friction in turbulent pipe flow. 2020.
doi:10.15479/AT:ISTA:7258
apa: Scarselli, D. (2020). New approaches to reduce friction in turbulent pipe
flow. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:7258
chicago: Scarselli, Davide. “New Approaches to Reduce Friction in Turbulent Pipe
Flow.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:7258.
ieee: D. Scarselli, “New approaches to reduce friction in turbulent pipe flow,”
Institute of Science and Technology Austria, 2020.
ista: Scarselli D. 2020. New approaches to reduce friction in turbulent pipe flow.
Institute of Science and Technology Austria.
mla: Scarselli, Davide. New Approaches to Reduce Friction in Turbulent Pipe Flow.
Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:7258.
short: D. Scarselli, New Approaches to Reduce Friction in Turbulent Pipe Flow, Institute
of Science and Technology Austria, 2020.
corr_author: '1'
date_created: 2020-01-12T16:07:26Z
date_published: 2020-01-13T00:00:00Z
date_updated: 2026-04-08T07:28:22Z
day: '13'
ddc:
- '532'
degree_awarded: PhD
department:
- _id: BjHo
doi: 10.15479/AT:ISTA:7258
ec_funded: 1
file:
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checksum: 4df1ab24e9896635106adde5a54615bf
content_type: application/zip
creator: dscarsel
date_created: 2020-01-12T15:57:14Z
date_updated: 2021-01-13T23:30:05Z
embargo_to: open_access
file_id: '7259'
file_name: 2020_Scarselli_Thesis.zip
file_size: 26640830
relation: source_file
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checksum: 48659ab98e3414293c7a721385c2fd1c
content_type: application/pdf
creator: dscarsel
date_created: 2020-01-12T15:56:14Z
date_updated: 2021-01-13T23:30:05Z
embargo: 2021-01-12
file_id: '7260'
file_name: 2020_Scarselli_Thesis.pdf
file_size: 8515844
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file_date_updated: 2021-01-13T23:30:05Z
has_accepted_license: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: None
page: '174'
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
- _id: 25136C54-B435-11E9-9278-68D0E5697425
grant_number: HO 4393/1-2
name: Experimental studies of the turbulence transition and transport processes
in turbulent Taylor-Couette currents
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '422'
relation: part_of_dissertation
status: public
- id: '461'
relation: part_of_dissertation
status: public
- id: '6228'
relation: part_of_dissertation
status: public
- id: '6486'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Björn
full_name: Hof, Björn
id: 3A374330-F248-11E8-B48F-1D18A9856A87
last_name: Hof
orcid: 0000-0003-2057-2754
title: New approaches to reduce friction in turbulent pipe flow
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2020'
...
---
_id: '7427'
abstract:
- lang: eng
text: Plants, like other multicellular organisms, survive through a delicate balance
between growth and defense against pathogens. Salicylic acid (SA) is a major defense
signal in plants, and the perception mechanism as well as downstream signaling
activating the immune response are known. Here, we identify a parallel SA signaling
that mediates growth attenuation. SA directly binds to A subunits of protein phosphatase
2A (PP2A), inhibiting activity of this complex. Among PP2A targets, the PIN2 auxin
transporter is hyperphosphorylated in response to SA, leading to changed activity
of this important growth regulator. Accordingly, auxin transport and auxin-mediated
root development, including growth, gravitropic response, and lateral root organogenesis,
are inhibited. This study reveals how SA, besides activating immunity, concomitantly
attenuates growth through crosstalk with the auxin distribution network. Further
analysis of this dual role of SA and characterization of additional SA-regulated
PP2A targets will provide further insights into mechanisms maintaining a balance
between growth and defense.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
acknowledgement: "We thank Shigeyuki Betsuyaku (University of Tsukuba), Alison Delong
(Brown University), Xinnian Dong (Duke University), Dolf Weijers (Wageningen University),
Yuelin Zhang (UBC), and Martine Pastuglia (Institut Jean-Pierre Bourgin) for sharing
published materials; Jana Riederer for help with cantharidin physiological analysis;
David Domjan for help with cloning pET28a-PIN2HL; Qing Lu for help with DARTS; Hana
Kozubı´kova´ for technical support on SA derivative synthesis; Zuzana Vondra´ kova´
for technical support with tobacco cells; Lucia Strader (Washington University),
Bert De Rybel (Ghent University), Bartel Vanholme (Ghent University), and Lukas
Mach (BOKU) for helpful discussions; and bioimaging and life science facilities
of IST Austria for continuous support. We gratefully acknowledge the Nottingham
Arabidopsis Stock Center (NASC) for providing T-DNA insertional mutants. The DSC
and SPR instruments were provided by the EQ-BOKU VIBT GmbH and the BOKU Core Facility
for Biomolecular and Cellular Analysis, with help of Irene Schaffner. The research
leading to these results has received funding from the European Union’s Horizon
2020 program (ERC grant agreement no. 742985 to J.F.) and the People Programme (Marie
Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013)
under REA grant agreement no. 291734. S.T. was supported by a European Molecular
Biology Organization (EMBO) long-term postdoctoral fellowship (ALTF 723-2015). O.N.
was supported by the Ministry of Education, Youth and Sports of the Czech Republic
(European Regional Development Fund-Project ‘‘Centre for Experimental Plant Biology’’
no. CZ.02.1.01/0.0/0.0/16_019/0000738). J. Pospısil was supported by European Regional
Development Fund Project ‘‘Centre for Experimental Plant Biology’’\r\n(no. CZ.02.1.01/0.0/0.0/16_019/0000738).
J. Petrasek was supported by EU Operational Programme Prague-Competitiveness (no.
CZ.2.16/3.1.00/21519). "
article_processing_charge: No
article_type: original
author:
- first_name: Shutang
full_name: Tan, Shutang
id: 2DE75584-F248-11E8-B48F-1D18A9856A87
last_name: Tan
orcid: 0000-0002-0471-8285
- first_name: Melinda F
full_name: Abas, Melinda F
id: 3CFB3B1C-F248-11E8-B48F-1D18A9856A87
last_name: Abas
- first_name: Inge
full_name: Verstraeten, Inge
id: 362BF7FE-F248-11E8-B48F-1D18A9856A87
last_name: Verstraeten
orcid: 0000-0001-7241-2328
- first_name: Matous
full_name: Glanc, Matous
id: 1AE1EA24-02D0-11E9-9BAA-DAF4881429F2
last_name: Glanc
orcid: 0000-0003-0619-7783
- first_name: Gergely
full_name: Molnar, Gergely
id: 34F1AF46-F248-11E8-B48F-1D18A9856A87
last_name: Molnar
- first_name: Jakub
full_name: Hajny, Jakub
id: 4800CC20-F248-11E8-B48F-1D18A9856A87
last_name: Hajny
orcid: 0000-0003-2140-7195
- first_name: Pavel
full_name: Lasák, Pavel
last_name: Lasák
- first_name: Ivan
full_name: Petřík, Ivan
last_name: Petřík
- first_name: Eugenia
full_name: Russinova, Eugenia
last_name: Russinova
- first_name: Jan
full_name: Petrášek, Jan
last_name: Petrášek
- first_name: Ondřej
full_name: Novák, Ondřej
last_name: Novák
- first_name: Jiří
full_name: Pospíšil, Jiří
last_name: Pospíšil
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Tan S, Abas MF, Verstraeten I, et al. Salicylic acid targets protein phosphatase
2A to attenuate growth in plants. Current Biology. 2020;30(3):381-395.e8.
doi:10.1016/j.cub.2019.11.058
apa: Tan, S., Abas, M. F., Verstraeten, I., Glanc, M., Molnar, G., Hajny, J., …
Friml, J. (2020). Salicylic acid targets protein phosphatase 2A to attenuate growth
in plants. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2019.11.058
chicago: Tan, Shutang, Melinda F Abas, Inge Verstraeten, Matous Glanc, Gergely Molnar,
Jakub Hajny, Pavel Lasák, et al. “Salicylic Acid Targets Protein Phosphatase 2A
to Attenuate Growth in Plants.” Current Biology. Cell Press, 2020. https://doi.org/10.1016/j.cub.2019.11.058.
ieee: S. Tan et al., “Salicylic acid targets protein phosphatase 2A to attenuate
growth in plants,” Current Biology, vol. 30, no. 3. Cell Press, p. 381–395.e8,
2020.
ista: Tan S, Abas MF, Verstraeten I, Glanc M, Molnar G, Hajny J, Lasák P, Petřík
I, Russinova E, Petrášek J, Novák O, Pospíšil J, Friml J. 2020. Salicylic acid
targets protein phosphatase 2A to attenuate growth in plants. Current Biology.
30(3), 381–395.e8.
mla: Tan, Shutang, et al. “Salicylic Acid Targets Protein Phosphatase 2A to Attenuate
Growth in Plants.” Current Biology, vol. 30, no. 3, Cell Press, 2020, p.
381–395.e8, doi:10.1016/j.cub.2019.11.058.
short: S. Tan, M.F. Abas, I. Verstraeten, M. Glanc, G. Molnar, J. Hajny, P. Lasák,
I. Petřík, E. Russinova, J. Petrášek, O. Novák, J. Pospíšil, J. Friml, Current
Biology 30 (2020) 381–395.e8.
corr_author: '1'
date_created: 2020-02-02T23:01:00Z
date_published: 2020-02-03T00:00:00Z
date_updated: 2026-05-15T22:30:55Z
day: '03'
ddc:
- '580'
department:
- _id: JiFr
- _id: EvBe
doi: 10.1016/j.cub.2019.11.058
ec_funded: 1
external_id:
isi:
- '000511287900018'
pmid:
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page: 381-395.e8
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project:
- _id: 261099A6-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742985'
name: Tracing Evolution of Auxin Transport and Polarity in Plants
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 256FEF10-B435-11E9-9278-68D0E5697425
grant_number: 723-2015
name: Molecular Mechanism underlying Salicylic Acid Regulation of Endocytic Trafficking
in Arabidopsis
publication: Current Biology
publication_identifier:
issn:
- '09609822'
publication_status: published
publisher: Cell Press
quality_controlled: '1'
related_material:
record:
- id: '8822'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Salicylic acid targets protein phosphatase 2A to attenuate growth in plants
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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 30
year: '2020'
...
---
_id: '7500'
abstract:
- lang: eng
text: "Plant survival depends on vascular tissues, which originate in a self‐organizing
manner as strands of cells co‐directionally transporting the plant hormone auxin.
The latter phenomenon (also known as auxin canalization) is classically hypothesized
to be regulated by auxin itself via the effect of this hormone on the polarity
of its own intercellular transport. Correlative observations supported this concept,
but molecular insights remain limited.\r\nIn the current study, we established
an experimental system based on the model Arabidopsis thaliana, which exhibits
auxin transport channels and formation of vasculature strands in response to local
auxin application.\r\nOur methodology permits the genetic analysis of auxin canalization
under controllable experimental conditions. By utilizing this opportunity, we
confirmed the dependence of auxin canalization on a PIN‐dependent auxin transport
and nuclear, TIR1/AFB‐mediated auxin signaling. We also show that leaf venation
and auxin‐mediated PIN repolarization in the root require TIR1/AFB signaling.\r\nFurther
studies based on this experimental system are likely to yield better understanding
of the mechanisms underlying auxin transport polarization in other developmental
contexts."
acknowledgement: We thank Mark Estelle, José M. Alonso and the Arabidopsis Stock Centre
for providing seeds. We acknowledge the core facility CELLIM of CEITEC supported
by the MEYS CR (LM2015062 Czech‐BioImaging) and Plant Sciences Core Facility of
CEITEC Masaryk University for help in generating essential data. This project received
funding from the European Research Council (ERC) under the European Union's Horizon
2020 research and innovation program (grant agreement no. 742985) and the Czech
Science Foundation GAČR (GA13‐40637S and GA18‐26981S) to JF. JH is the recipient
of a DOC Fellowship of the Austrian Academy of Sciences at the Institute of Science
and Technology. The authors declare no competing interests.
article_processing_charge: No
article_type: original
author:
- first_name: E
full_name: Mazur, E
last_name: Mazur
- first_name: Ivan
full_name: Kulik, Ivan
id: F0AB3FCE-02D1-11E9-BD0E-99399A5D3DEB
last_name: Kulik
- first_name: Jakub
full_name: Hajny, Jakub
id: 4800CC20-F248-11E8-B48F-1D18A9856A87
last_name: Hajny
orcid: 0000-0003-2140-7195
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Mazur E, Kulik I, Hajny J, Friml J. Auxin canalization and vascular tissue
formation by TIR1/AFB-mediated auxin signaling in arabidopsis. New Phytologist.
2020;226(5):1375-1383. doi:10.1111/nph.16446
apa: Mazur, E., Kulik, I., Hajny, J., & Friml, J. (2020). Auxin canalization
and vascular tissue formation by TIR1/AFB-mediated auxin signaling in arabidopsis.
New Phytologist. Wiley. https://doi.org/10.1111/nph.16446
chicago: Mazur, E, Ivan Kulik, Jakub Hajny, and Jiří Friml. “Auxin Canalization
and Vascular Tissue Formation by TIR1/AFB-Mediated Auxin Signaling in Arabidopsis.”
New Phytologist. Wiley, 2020. https://doi.org/10.1111/nph.16446.
ieee: E. Mazur, I. Kulik, J. Hajny, and J. Friml, “Auxin canalization and vascular
tissue formation by TIR1/AFB-mediated auxin signaling in arabidopsis,” New
Phytologist, vol. 226, no. 5. Wiley, pp. 1375–1383, 2020.
ista: Mazur E, Kulik I, Hajny J, Friml J. 2020. Auxin canalization and vascular
tissue formation by TIR1/AFB-mediated auxin signaling in arabidopsis. New Phytologist.
226(5), 1375–1383.
mla: Mazur, E., et al. “Auxin Canalization and Vascular Tissue Formation by TIR1/AFB-Mediated
Auxin Signaling in Arabidopsis.” New Phytologist, vol. 226, no. 5, Wiley,
2020, pp. 1375–83, doi:10.1111/nph.16446.
short: E. Mazur, I. Kulik, J. Hajny, J. Friml, New Phytologist 226 (2020) 1375–1383.
corr_author: '1'
date_created: 2020-02-18T10:03:47Z
date_published: 2020-06-01T00:00:00Z
date_updated: 2026-05-15T22:30:55Z
day: '01'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.1111/nph.16446
ec_funded: 1
external_id:
isi:
- '000514939700001'
pmid:
- '31971254'
file:
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checksum: 17de728b0205979feb95ce663ba918c2
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creator: dernst
date_created: 2020-11-20T09:32:10Z
date_updated: 2020-11-20T09:32:10Z
file_id: '8781'
file_name: 2020_NewPhytologist_Mazur.pdf
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file_date_updated: 2020-11-20T09:32:10Z
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intvolume: ' 226'
isi: 1
issue: '5'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 1375-1383
pmid: 1
project:
- _id: 261099A6-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742985'
name: Tracing Evolution of Auxin Transport and Polarity in Plants
- _id: 2699E3D2-B435-11E9-9278-68D0E5697425
grant_number: '25239'
name: Cell surface receptor complexes for PIN polarity and auxin-mediated development
publication: New Phytologist
publication_identifier:
eissn:
- 1469-8137
issn:
- 0028-646x
publication_status: published
publisher: Wiley
quality_controlled: '1'
related_material:
record:
- id: '8822'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Auxin canalization and vascular tissue formation by TIR1/AFB-mediated auxin
signaling 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: 226
year: '2020'
...
---
OA_place: publisher
_id: '8822'
abstract:
- lang: eng
text: "Self-organization is a hallmark of plant development manifested e.g. by intricate
leaf vein patterns, flexible formation of vasculature during organogenesis or
its regeneration following wounding. Spontaneously arising channels transporting
the phytohormone auxin, created by coordinated polar localizations of PIN-FORMED
1 (PIN1) auxin exporter, provide positional cues for these as well as other plant
patterning processes. To find regulators acting downstream of auxin and the TIR1/AFB
auxin signaling pathway essential for PIN1 coordinated polarization during auxin
canalization, we performed microarray experiments. Besides the known components
of general PIN polarity maintenance, such as PID and PIP5K kinases, we identified
and characterized a new regulator of auxin canalization, the transcription factor
WRKY DNA-BINDING PROTEIN 23 (WRKY23).\r\nNext, we designed a subsequent microarray
experiment to further uncover other molecular players, downstream of auxin-TIR1/AFB-WRKY23
involved in the regulation of auxin-mediated PIN repolarization. We identified
a novel and crucial part of the molecular machinery underlying auxin canalization.
The auxin-regulated malectin-type receptor-like kinase CAMEL and the associated
leucine-rich repeat receptor-like kinase CANAR target and directly phosphorylate
PIN auxin transporters. camel and canar mutants are impaired in PIN1 subcellular
trafficking and auxin-mediated repolarization leading to defects in auxin transport,
ultimately to leaf venation and vasculature regeneration defects. Our results
describe the CAMEL-CANAR receptor complex, which is required for auxin feed-back
on its own transport and thus for coordinated tissue polarization during auxin
canalization."
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Jakub
full_name: Hajny, Jakub
id: 4800CC20-F248-11E8-B48F-1D18A9856A87
last_name: Hajny
orcid: 0000-0003-2140-7195
citation:
ama: Hajny J. Identification and characterization of the molecular machinery of
auxin-dependent canalization during vasculature formation and regeneration. 2020.
doi:10.15479/AT:ISTA:8822
apa: Hajny, J. (2020). Identification and characterization of the molecular machinery
of auxin-dependent canalization during vasculature formation and regeneration.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8822
chicago: Hajny, Jakub. “Identification and Characterization of the Molecular Machinery
of Auxin-Dependent Canalization during Vasculature Formation and Regeneration.”
Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8822.
ieee: J. Hajny, “Identification and characterization of the molecular machinery
of auxin-dependent canalization during vasculature formation and regeneration,”
Institute of Science and Technology Austria, 2020.
ista: Hajny J. 2020. Identification and characterization of the molecular machinery
of auxin-dependent canalization during vasculature formation and regeneration.
Institute of Science and Technology Austria.
mla: Hajny, Jakub. Identification and Characterization of the Molecular Machinery
of Auxin-Dependent Canalization during Vasculature Formation and Regeneration.
Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8822.
short: J. Hajny, Identification and Characterization of the Molecular Machinery
of Auxin-Dependent Canalization during Vasculature Formation and Regeneration,
Institute of Science and Technology Austria, 2020.
corr_author: '1'
date_created: 2020-12-01T12:38:18Z
date_published: 2020-12-01T00:00:00Z
date_updated: 2026-04-08T07:28:35Z
day: '01'
ddc:
- '580'
degree_awarded: PhD
department:
- _id: JiFr
doi: 10.15479/AT:ISTA:8822
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creator: jhajny
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file_size: 91279806
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page: '249'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
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status: public
- id: '7500'
relation: part_of_dissertation
status: public
- id: '6260'
relation: part_of_dissertation
status: public
- id: '7427'
relation: part_of_dissertation
status: public
- id: '191'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
title: Identification and characterization of the molecular machinery of auxin-dependent
canalization during vasculature formation and regeneration
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2020'
...
---
OA_place: publisher
_id: '8983'
abstract:
- lang: eng
text: Metabolic adaptation is a critical feature of migrating cells. It tunes the
metabolic programs of migrating cells to allow them to efficiently exert their
crucial roles in development, inflammatory responses and tumor metastasis. Cell
migration through physically challenging contexts requires energy. However, how
the metabolic reprogramming that underlies in vivo cell invasion is controlled
is still unanswered. In my PhD project, I identify a novel conserved metabolic
shift in Drosophila melanogaster immune cells that by modulating their bioenergetic
potential controls developmentally programmed tissue invasion. We show that this
regulation requires a novel conserved nuclear protein, named Atossa. Atossa enhances
the transcription of a set of proteins, including an RNA helicase Porthos and
two metabolic enzymes, each of which increases the tissue invasion of leading
Drosophila macrophages and can rescue the atossa mutant phenotype. Porthos selectively
regulates the translational efficiency of a subset of mRNAs containing a 5’-UTR
cis-regulatory TOP-like sequence. These 5’TOPL mRNA targets encode mitochondrial-related
proteins, including subunits of mitochondrial oxidative phosphorylation (OXPHOS)
components III and V and other metabolic-related proteins. Porthos powers up mitochondrial
OXPHOS to engender a sufficient ATP supply, which is required for tissue invasion
of leading macrophages. Atossa’s two vertebrate orthologs rescue the invasion
defect. In my PhD project, I elucidate that Atossa displays a conserved developmental
metabolic control to modulate metabolic capacities and the cellular energy state,
through altered transcription and translation, to aid the tissue infiltration
of leading cells into energy demanding barriers.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: E-Lib
- _id: CampIT
acknowledgement: Also, I would like to express my appreciation and thanks to the Bioimaging
facility, LSF, GSO, library, and IT people at IST Austria.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Shamsi
full_name: Emtenani, Shamsi
id: 49D32318-F248-11E8-B48F-1D18A9856A87
last_name: Emtenani
orcid: 0000-0001-6981-6938
citation:
ama: Emtenani S. Metabolic regulation of Drosophila macrophage tissue invasion.
2020. doi:10.15479/AT:ISTA:8983
apa: Emtenani, S. (2020). Metabolic regulation of Drosophila macrophage tissue
invasion. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8983
chicago: Emtenani, Shamsi. “Metabolic Regulation of Drosophila Macrophage Tissue
Invasion.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8983.
ieee: S. Emtenani, “Metabolic regulation of Drosophila macrophage tissue invasion,”
Institute of Science and Technology Austria, 2020.
ista: Emtenani S. 2020. Metabolic regulation of Drosophila macrophage tissue invasion.
Institute of Science and Technology Austria.
mla: Emtenani, Shamsi. Metabolic Regulation of Drosophila Macrophage Tissue Invasion.
Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8983.
short: S. Emtenani, Metabolic Regulation of Drosophila Macrophage Tissue Invasion,
Institute of Science and Technology Austria, 2020.
corr_author: '1'
date_created: 2020-12-30T15:41:26Z
date_published: 2020-12-30T00:00:00Z
date_updated: 2026-04-08T07:28:54Z
day: '30'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: DaSi
doi: 10.15479/AT:ISTA:8983
file:
- access_level: open_access
checksum: ec2797ab7a6f253b35df0572b36d1b43
content_type: application/pdf
creator: semtenan
date_created: 2020-12-30T15:34:01Z
date_updated: 2021-12-31T23:30:04Z
embargo: 2021-12-30
file_id: '8984'
file_name: Thesis_Shamsi_Emtenani_pdfA.pdf
file_size: 10848175
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publisher: Institute of Science and Technology Austria
related_material:
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relation: part_of_dissertation
status: public
status: public
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: Metabolic regulation of Drosophila macrophage tissue invasion
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2020'
...
---
_id: '8557'
abstract:
- lang: eng
text: The infiltration of immune cells into tissues underlies the establishment
of tissue resident macrophages, and responses to infections and tumors. Yet the
mechanisms immune cells utilize to negotiate tissue barriers in living organisms
are not well understood, and a role for cortical actin has not been examined.
Here we find that the tissue invasion of Drosophila macrophages, also known as
plasmatocytes or hemocytes, utilizes enhanced cortical F-actin levels stimulated
by the Drosophila member of the fos proto oncogene transcription factor family
(Dfos, Kayak). RNA sequencing analysis and live imaging show that Dfos enhances
F-actin levels around the entire macrophage surface by increasing mRNA levels
of the membrane spanning molecular scaffold tetraspanin TM4SF, and the actin cross-linking
filamin Cheerio which are themselves required for invasion. Cortical F-actin levels
are critical as expressing a dominant active form of Diaphanous, a actin polymerizing
Formin, can rescue the Dfos Dominant Negative macrophage invasion defect. In vivo
imaging shows that Dfos is required to enhance the efficiency of the initial phases
of macrophage tissue entry. Genetic evidence argues that this Dfos-induced program
in macrophages counteracts the constraint produced by the tension of surrounding
tissues and buffers the mechanical properties of the macrophage nucleus from affecting
tissue entry. We thus identify tuning the cortical actin cytoskeleton through
Dfos as a key process allowing efficient forward movement of an immune cell into
surrounding tissues.
acknowledged_ssus:
- _id: LifeSc
acknowledgement: 'We thank the following for their contributions: The Drosophila Genomics
Resource Center supported by NIH grant 2P40OD010949-10A1 for plasmids, K. Brueckner.
B. Stramer, M. Uhlirova, O. Schuldiner, the Bloomington Drosophila Stock Center
supported by NIH grant P40OD018537 and the Vienna Drosophila Resource Center for
fly stocks, FlyBase (Thurmond et al., 2019) for essential genomic information, and
the BDGP in situ database for data (Tomancak et al., 2002, 2007). For antibodies,
we thank the Developmental Studies Hybridoma Bank, which was created by the Eunice
Kennedy Shriver National Institute of Child Health and Human Development of the
NIH, and is maintained at the University of Iowa, as well as J. Zeitlinger for her
generous gift of Dfos antibody. We thank the Vienna BioCenter Core Facilities for
RNA sequencing and analysis and the Life Scientific Service Units at IST Austria
for technical support and assistance with microscopy and FACS analysis. We thank
C.P. Heisenberg, P. Martin, M. Sixt and Siekhaus group members for discussions and
T.Hurd, A. Ratheesh and P. Rangan for comments on the manuscript. A.G. was supported
by the Austrian Science Fund (FWF) grant DASI_FWF01_P29638S, D.E.S. by Marie Curie
CIG 334077/IRTIM. M.S. is supported by the FWF, PhD program W1212 915 and the European
Research Council (ERC) Advanced grant (ERC-2015-AdG TNT-Tumors 694883). S.W. is
supported by an OEAW, DOC fellowship.'
article_processing_charge: No
author:
- 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: Igor
full_name: Gridchyn, Igor
id: 4B60654C-F248-11E8-B48F-1D18A9856A87
last_name: Gridchyn
orcid: 0000-0002-1807-1929
- first_name: Markus
full_name: Linder, Markus
last_name: Linder
- first_name: Shamsi
full_name: Emtenani, Shamsi
id: 49D32318-F248-11E8-B48F-1D18A9856A87
last_name: Emtenani
orcid: 0000-0001-6981-6938
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Maria
full_name: Sibilia, Maria
last_name: Sibilia
- 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: Belyaeva V, Wachner S, Gridchyn I, et al. Cortical actin properties controlled
by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance.
bioRxiv. doi:10.1101/2020.09.18.301481
apa: Belyaeva, V., Wachner, S., Gridchyn, I., Linder, M., Emtenani, S., György,
A., … Siekhaus, D. E. (n.d.). Cortical actin properties controlled by Drosophila
Fos aid macrophage infiltration against surrounding tissue resistance. bioRxiv.
https://doi.org/10.1101/2020.09.18.301481
chicago: Belyaeva, Vera, Stephanie Wachner, Igor Gridchyn, Markus Linder, Shamsi
Emtenani, Attila György, Maria Sibilia, and Daria E Siekhaus. “Cortical Actin
Properties Controlled by Drosophila Fos Aid Macrophage Infiltration against Surrounding
Tissue Resistance.” BioRxiv, n.d. https://doi.org/10.1101/2020.09.18.301481.
ieee: V. Belyaeva et al., “Cortical actin properties controlled by Drosophila
Fos aid macrophage infiltration against surrounding tissue resistance,” bioRxiv.
.
ista: Belyaeva V, Wachner S, Gridchyn I, Linder M, Emtenani S, György A, Sibilia
M, Siekhaus DE. Cortical actin properties controlled by Drosophila Fos aid macrophage
infiltration against surrounding tissue resistance. bioRxiv, 10.1101/2020.09.18.301481.
mla: Belyaeva, Vera, et al. “Cortical Actin Properties Controlled by Drosophila
Fos Aid Macrophage Infiltration against Surrounding Tissue Resistance.” BioRxiv,
doi:10.1101/2020.09.18.301481.
short: V. Belyaeva, S. Wachner, I. Gridchyn, M. Linder, S. Emtenani, A. György,
M. Sibilia, D.E. Siekhaus, BioRxiv (n.d.).
corr_author: '1'
date_created: 2020-09-23T09:36:47Z
date_published: 2020-09-18T00:00:00Z
date_updated: 2026-05-15T22:30:56Z
day: '18'
department:
- _id: DaSi
- _id: JoCs
doi: 10.1101/2020.09.18.301481
ec_funded: 1
language:
- iso: eng
main_file_link:
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url: https://doi.org/10.1101/2020.09.18.301481
month: '09'
oa: 1
oa_version: Preprint
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: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
- _id: 26199CA4-B435-11E9-9278-68D0E5697425
grant_number: '24800'
name: Implications of a TGFβ/Dpp-activated subpopulation for Drosophila macrophage
migration
publication: bioRxiv
publication_status: draft
related_material:
record:
- id: '10614'
relation: later_version
status: public
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relation: dissertation_contains
status: public
status: public
title: Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration
against surrounding tissue resistance
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
OA_place: publisher
_id: '8340'
abstract:
- lang: eng
text: Mitochondria are sites of oxidative phosphorylation in eukaryotic cells. Oxidative
phosphorylation operates by a chemiosmotic mechanism made possible by redox-driven
proton pumping machines which establish a proton motive force across the inner
mitochondrial membrane. This electrochemical proton gradient is used to drive
ATP synthesis, which powers the majority of cellular processes such as protein
synthesis, locomotion and signalling. In this thesis I investigate the structures
and molecular mechanisms of two inner mitochondrial proton pumping enzymes, respiratory
complex I and transhydrogenase. I present the first high-resolution structure
of the full transhydrogenase from any species, and a significantly improved structure
of complex I. Improving the resolution from 3.3 Å available previously to up to
2.3 Å in this thesis allowed us to model bound water molecules, crucial in the
proton pumping mechanism. For both enzymes, up to five cryo-EM datasets with different
substrates and inhibitors bound were solved to delineate the catalytic cycle and
understand the proton pumping mechanism. In transhydrogenase, the proton channel
is gated by reversible detachment of the NADP(H)-binding domain which opens the
proton channel to the opposite sites of the membrane. In complex I, the proton
channels are gated by reversible protonation of key glutamate and lysine residues
and breaking of the water wire connecting the proton pumps with the quinone reduction
site. The tight coupling between the redox and the proton pumping reactions in
transhydrogenase is achieved by controlling the NADP(H) exchange which can only
happen when the NADP(H)-binding domain interacts with the membrane domain. In
complex I, coupling is achieved by cycling of the whole complex between the closed
state, in which quinone can get reduced, and the open state, in which NADH can
induce quinol ejection from the binding pocket. On the basis of these results
I propose detailed mechanisms for catalytic cycles of transhydrogenase and complex
I that are consistent with a large amount of previous work. In both enzymes, conformational
and electrostatic mechanisms contribute to the overall catalytic process. Results
presented here could be used for better understanding of the human pathologies
arising from deficiencies of complex I or transhydrogenase and could be used to
develop novel therapies.
acknowledged_ssus:
- _id: EM-Fac
acknowledgement: 'I acknowledge the support of IST facilities, especially the Electron
Miscroscopy facility for providing training and resources. Special thanks also go
to cryo-EM specialists who helped me to collect the data present here: Dr Valentin
Hodirnau (IST Austria), Dr Tom Heuser (IMBA, Vienna), Dr Rebecca Thompson (Uni.
of Leeds) and Dr Jirka Nováček (CEITEC). This work has been supported by iNEXT,
project number 653706, funded by the Horizon 2020 programme of the European Union.
This project has received funding from the European Union’s Horizon 2020 research
and innovation programme under the Marie Skłodowska-Curie Grant Agreement No. 665385.'
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Domen
full_name: Kampjut, Domen
id: 37233050-F248-11E8-B48F-1D18A9856A87
last_name: Kampjut
orcid: 0000-0002-6018-3422
citation:
ama: Kampjut D. Molecular mechanisms of mitochondrial redox-coupled proton pumping
enzymes. 2020. doi:10.15479/AT:ISTA:8340
apa: Kampjut, D. (2020). Molecular mechanisms of mitochondrial redox-coupled
proton pumping enzymes. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8340
chicago: Kampjut, Domen. “Molecular Mechanisms of Mitochondrial Redox-Coupled Proton
Pumping Enzymes.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8340.
ieee: D. Kampjut, “Molecular mechanisms of mitochondrial redox-coupled proton pumping
enzymes,” Institute of Science and Technology Austria, 2020.
ista: Kampjut D. 2020. Molecular mechanisms of mitochondrial redox-coupled proton
pumping enzymes. Institute of Science and Technology Austria.
mla: Kampjut, Domen. Molecular Mechanisms of Mitochondrial Redox-Coupled Proton
Pumping Enzymes. Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8340.
short: D. Kampjut, Molecular Mechanisms of Mitochondrial Redox-Coupled Proton Pumping
Enzymes, Institute of Science and Technology Austria, 2020.
corr_author: '1'
date_created: 2020-09-07T18:42:23Z
date_published: 2020-09-09T00:00:00Z
date_updated: 2026-04-08T07:43:58Z
day: '09'
ddc:
- '572'
degree_awarded: PhD
department:
- _id: LeSa
doi: 10.15479/AT:ISTA:8340
ec_funded: 1
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date_created: 2020-09-14T15:02:20Z
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language:
- iso: eng
month: '09'
oa: 1
oa_version: None
page: '242'
project:
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
publication_identifier:
isbn:
- 978-3-99078-008-4
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '6848'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Leonid A
full_name: Sazanov, Leonid A
id: 338D39FE-F248-11E8-B48F-1D18A9856A87
last_name: Sazanov
orcid: 0000-0002-0977-7989
title: Molecular mechanisms of mitochondrial redox-coupled proton pumping enzymes
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2020'
...
---
_id: '7652'
abstract:
- lang: eng
text: Organisms cope with change by taking advantage of transcriptional regulators.
However, when faced with rare environments, the evolution of transcriptional regulators
and their promoters may be too slow. Here, we investigate whether the intrinsic
instability of gene duplication and amplification provides a generic alternative
to canonical gene regulation. Using real-time monitoring of gene-copy-number mutations
in Escherichia coli, we show that gene duplications and amplifications enable
adaptation to fluctuating environments by rapidly generating copy-number and,
therefore, expression-level polymorphisms. This amplification-mediated gene expression
tuning (AMGET) occurs on timescales that are similar to canonical gene regulation
and can respond to rapid environmental changes. Mathematical modelling shows that
amplifications also tune gene expression in stochastic environments in which transcription-factor-based
schemes are hard to evolve or maintain. The fleeting nature of gene amplifications
gives rise to a generic population-level mechanism that relies on genetic heterogeneity
to rapidly tune the expression of any gene, without leaving any genomic signature.
acknowledgement: We thank L. Hurst, N. Barton, M. Pleska, M. Steinrück, B. Kavcic
and A. Staron for input on the manuscript, and To. Bergmiller and R. Chait for help
with microfluidics experiments. I.T. is a recipient the OMV fellowship. R.G. is
a recipient of a DOC (Doctoral Fellowship Programme of the Austrian Academy of Sciences)
Fellowship of the Austrian Academy of Sciences.
article_processing_charge: No
article_type: original
author:
- first_name: Isabella
full_name: Tomanek, Isabella
id: 3981F020-F248-11E8-B48F-1D18A9856A87
last_name: Tomanek
orcid: 0000-0001-6197-363X
- first_name: Rok
full_name: Grah, Rok
id: 483E70DE-F248-11E8-B48F-1D18A9856A87
last_name: Grah
orcid: 0000-0003-2539-3560
- first_name: M.
full_name: Lagator, M.
last_name: Lagator
- first_name: A. M. C.
full_name: Andersson, A. M. C.
last_name: Andersson
- 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: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
citation:
ama: Tomanek I, Grah R, Lagator M, et al. Gene amplification as a form of population-level
gene expression regulation. Nature Ecology & Evolution. 2020;4(4):612-625.
doi:10.1038/s41559-020-1132-7
apa: Tomanek, I., Grah, R., Lagator, M., Andersson, A. M. C., Bollback, J. P., Tkačik,
G., & Guet, C. C. (2020). Gene amplification as a form of population-level
gene expression regulation. Nature Ecology & Evolution. Springer Nature.
https://doi.org/10.1038/s41559-020-1132-7
chicago: Tomanek, Isabella, Rok Grah, M. Lagator, A. M. C. Andersson, Jonathan P
Bollback, Gašper Tkačik, and Calin C Guet. “Gene Amplification as a Form of Population-Level
Gene Expression Regulation.” Nature Ecology & Evolution. Springer Nature,
2020. https://doi.org/10.1038/s41559-020-1132-7.
ieee: I. Tomanek et al., “Gene amplification as a form of population-level
gene expression regulation,” Nature Ecology & Evolution, vol. 4, no.
4. Springer Nature, pp. 612–625, 2020.
ista: Tomanek I, Grah R, Lagator M, Andersson AMC, Bollback JP, Tkačik G, Guet CC.
2020. Gene amplification as a form of population-level gene expression regulation.
Nature Ecology & Evolution. 4(4), 612–625.
mla: Tomanek, Isabella, et al. “Gene Amplification as a Form of Population-Level
Gene Expression Regulation.” Nature Ecology & Evolution, vol. 4, no.
4, Springer Nature, 2020, pp. 612–25, doi:10.1038/s41559-020-1132-7.
short: I. Tomanek, R. Grah, M. Lagator, A.M.C. Andersson, J.P. Bollback, G. Tkačik,
C.C. Guet, Nature Ecology & Evolution 4 (2020) 612–625.
date_created: 2020-04-08T15:20:53Z
date_published: 2020-04-01T00:00:00Z
date_updated: 2026-05-15T22:30:58Z
day: '01'
ddc:
- '570'
department:
- _id: GaTk
- _id: CaGu
doi: 10.1038/s41559-020-1132-7
external_id:
isi:
- '000519008300005'
pmid:
- '32152532'
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project:
- _id: 267C84F4-B435-11E9-9278-68D0E5697425
name: Biophysically realistic genotype-phenotype maps for regulatory networks
publication: Nature Ecology & Evolution
publication_identifier:
issn:
- 2397-334X
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/how-to-thrive-without-gene-regulation/
record:
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relation: research_data
status: public
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relation: research_data
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- id: '8653'
relation: used_in_publication
status: public
scopus_import: '1'
status: public
title: Gene amplification as a form of population-level gene expression regulation
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 4
year: '2020'
...
---
OA_place: publisher
_id: '8653'
abstract:
- lang: eng
text: "Mutations are the raw material of evolution and come in many different flavors.
Point mutations change a single letter in the DNA sequence, while copy number
mutations like duplications or deletions add or remove many letters of the DNA
sequence simultaneously. Each type of mutation exhibits specific properties like
its rate of formation and reversal. \r\nGene expression is a fundamental phenotype
that can be altered by both, point and copy number mutations. The following thesis
is concerned with the dynamics of gene expression evolution and how it is affected
by the properties exhibited by point and copy number mutations. Specifically,
we are considering i) copy number mutations during adaptation to fluctuating environments
and ii) the interaction of copy number and point mutations during adaptation to
constant environments. "
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Isabella
full_name: Tomanek, Isabella
id: 3981F020-F248-11E8-B48F-1D18A9856A87
last_name: Tomanek
orcid: 0000-0001-6197-363X
citation:
ama: Tomanek I. The evolution of gene expression by copy number and point mutations.
2020. doi:10.15479/AT:ISTA:8653
apa: Tomanek, I. (2020). The evolution of gene expression by copy number and
point mutations. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8653
chicago: Tomanek, Isabella. “The Evolution of Gene Expression by Copy Number and
Point Mutations.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8653.
ieee: I. Tomanek, “The evolution of gene expression by copy number and point mutations,”
Institute of Science and Technology Austria, 2020.
ista: Tomanek I. 2020. The evolution of gene expression by copy number and point
mutations. Institute of Science and Technology Austria.
mla: Tomanek, Isabella. The Evolution of Gene Expression by Copy Number and Point
Mutations. Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8653.
short: I. Tomanek, The Evolution of Gene Expression by Copy Number and Point Mutations,
Institute of Science and Technology Austria, 2020.
corr_author: '1'
date_created: 2020-10-13T13:02:33Z
date_published: 2020-10-13T00:00:00Z
date_updated: 2026-04-08T07:29:19Z
day: '13'
ddc:
- '576'
degree_awarded: PhD
department:
- _id: CaGu
doi: 10.15479/AT:ISTA:8653
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has_accepted_license: '1'
keyword:
- duplication
- amplification
- promoter
- CNV
- AMGET
- experimental evolution
- Escherichia coli
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: '117'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
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relation: research_data
status: public
status: public
supervisor:
- first_name: Calin C
full_name: Guet, Calin C
id: 47F8433E-F248-11E8-B48F-1D18A9856A87
last_name: Guet
orcid: 0000-0001-6220-2052
title: The evolution of gene expression by copy number and point mutations
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2020'
...