---
_id: '10123'
abstract:
- lang: eng
text: Solution synthesis of particles emerged as an alternative to prepare thermoelectric
materials with less demanding processing conditions than conventional solid-state
synthetic methods. However, solution synthesis generally involves the presence
of additional molecules or ions belonging to the precursors or added to enable
solubility and/or regulate nucleation and growth. These molecules or ions can
end up in the particles as surface adsorbates and interfere in the material properties.
This work demonstrates that ionic adsorbates, in particular Na⁺ ions, are electrostatically
adsorbed in SnSe particles synthesized in water and play a crucial role not only
in directing the material nano/microstructure but also in determining the transport
properties of the consolidated material. In dense pellets prepared by sintering
SnSe particles, Na remains within the crystal lattice as dopant, in dislocations,
precipitates, and forming grain boundary complexions. These results highlight
the importance of considering all the possible unintentional impurities to establish
proper structure-property relationships and control material properties in solution-processed
thermoelectric materials.
acknowledged_ssus:
- _id: EM-Fac
- _id: NanoFab
acknowledgement: 'Y.L. and M.C. contributed equally to this work. This research was
supported by the Scientific Service Units (SSU) of IST Austria through resources
provided by Electron Microscopy Facility (EMF) and the Nanofabrication Facility
(NNF). This work was financially supported by IST Austria and the Werner Siemens
Foundation. Y.L. acknowledges funding from the European Union''s Horizon 2020 research
and innovation program under the Marie Sklodowska-Curie grant agreement No. 754411.
M.C. has received funding from the European Union''s Horizon 2020 research and innovation
program under the Marie Skłodowska-Curie Grant Agreement No. 665385. Y.Y. and O.C.-M.
acknowledge the financial support from DFG within the project SFB 917: Nanoswitches.
J.L. is a Serra Húnter Fellow and is grateful to ICREA Academia program. C.C. acknowledges
funding from the FWF “Lise Meitner Fellowship” grant agreement M 2889-N.'
article_number: '2106858'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Yu
full_name: Liu, Yu
id: 2A70014E-F248-11E8-B48F-1D18A9856A87
last_name: Liu
orcid: 0000-0001-7313-6740
- first_name: Mariano
full_name: Calcabrini, Mariano
id: 45D7531A-F248-11E8-B48F-1D18A9856A87
last_name: Calcabrini
orcid: 0000-0003-4566-5877
- first_name: Yuan
full_name: Yu, Yuan
last_name: Yu
- first_name: Aziz
full_name: Genç, Aziz
last_name: Genç
- first_name: Cheng
full_name: Chang, Cheng
id: 9E331C2E-9F27-11E9-AE48-5033E6697425
last_name: Chang
orcid: 0000-0002-9515-4277
- first_name: Tommaso
full_name: Costanzo, Tommaso
id: D93824F4-D9BA-11E9-BB12-F207E6697425
last_name: Costanzo
orcid: 0000-0001-9732-3815
- first_name: Tobias
full_name: Kleinhanns, Tobias
id: 8BD9DE16-AB3C-11E9-9C8C-2A03E6697425
last_name: Kleinhanns
- first_name: Seungho
full_name: Lee, Seungho
id: BB243B88-D767-11E9-B658-BC13E6697425
last_name: Lee
orcid: 0000-0002-6962-8598
- first_name: Jordi
full_name: Llorca, Jordi
last_name: Llorca
- first_name: Oana
full_name: Cojocaru‐Mirédin, Oana
last_name: Cojocaru‐Mirédin
- first_name: Maria
full_name: Ibáñez, Maria
id: 43C61214-F248-11E8-B48F-1D18A9856A87
last_name: Ibáñez
orcid: 0000-0001-5013-2843
citation:
ama: 'Liu Y, Calcabrini M, Yu Y, et al. The importance of surface adsorbates in
solution‐processed thermoelectric materials: The case of SnSe. Advanced Materials.
2021;33(52). doi:10.1002/adma.202106858'
apa: 'Liu, Y., Calcabrini, M., Yu, Y., Genç, A., Chang, C., Costanzo, T., … Ibáñez,
M. (2021). The importance of surface adsorbates in solution‐processed thermoelectric
materials: The case of SnSe. Advanced Materials. Wiley. https://doi.org/10.1002/adma.202106858'
chicago: 'Liu, Yu, Mariano Calcabrini, Yuan Yu, Aziz Genç, Cheng Chang, Tommaso
Costanzo, Tobias Kleinhanns, et al. “The Importance of Surface Adsorbates in Solution‐processed
Thermoelectric Materials: The Case of SnSe.” Advanced Materials. Wiley,
2021. https://doi.org/10.1002/adma.202106858.'
ieee: 'Y. Liu et al., “The importance of surface adsorbates in solution‐processed
thermoelectric materials: The case of SnSe,” Advanced Materials, vol. 33,
no. 52. Wiley, 2021.'
ista: 'Liu Y, Calcabrini M, Yu Y, Genç A, Chang C, Costanzo T, Kleinhanns T, Lee
S, Llorca J, Cojocaru‐Mirédin O, Ibáñez M. 2021. The importance of surface adsorbates
in solution‐processed thermoelectric materials: The case of SnSe. Advanced Materials.
33(52), 2106858.'
mla: 'Liu, Yu, et al. “The Importance of Surface Adsorbates in Solution‐processed
Thermoelectric Materials: The Case of SnSe.” Advanced Materials, vol. 33,
no. 52, 2106858, Wiley, 2021, doi:10.1002/adma.202106858.'
short: Y. Liu, M. Calcabrini, Y. Yu, A. Genç, C. Chang, T. Costanzo, T. Kleinhanns,
S. Lee, J. Llorca, O. Cojocaru‐Mirédin, M. Ibáñez, Advanced Materials 33 (2021).
date_created: 2021-10-11T20:07:24Z
date_published: 2021-12-29T00:00:00Z
date_updated: 2023-08-14T07:25:27Z
day: '29'
ddc:
- '620'
department:
- _id: EM-Fac
- _id: MaIb
doi: 10.1002/adma.202106858
ec_funded: 1
external_id:
isi:
- '000709899300001'
pmid:
- '34626034'
file:
- access_level: open_access
checksum: 990bccc527c64d85cf1c97885110b5f4
content_type: application/pdf
creator: cchlebak
date_created: 2022-02-03T13:16:14Z
date_updated: 2022-02-03T13:16:14Z
file_id: '10720'
file_name: 2021_AdvancedMaterials_Liu.pdf
file_size: 5595666
relation: main_file
success: 1
file_date_updated: 2022-02-03T13:16:14Z
has_accepted_license: '1'
intvolume: ' 33'
isi: 1
issue: '52'
keyword:
- mechanical engineering
- mechanics of materials
- general materials science
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 9B8804FC-BA93-11EA-9121-9846C619BF3A
grant_number: M02889
name: Bottom-up Engineering for Thermoelectric Applications
- _id: 9B8F7476-BA93-11EA-9121-9846C619BF3A
name: 'HighTE: The Werner Siemens Laboratory for the High Throughput Discovery of
Semiconductors for Waste Heat Recovery'
publication: Advanced Materials
publication_identifier:
eissn:
- 1521-4095
issn:
- 0935-9648
publication_status: published
publisher: Wiley
quality_controlled: '1'
related_material:
record:
- id: '12885'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: 'The importance of surface adsorbates in solution‐processed thermoelectric
materials: The case of SnSe'
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: 33
year: '2021'
...
---
_id: '10607'
abstract:
- lang: eng
text: The evidence linking innate immunity mechanisms and neurodegenerative diseases
is growing, but the specific mechanisms are incompletely understood. Experimental
data suggest that microglial TLR4 mediates the uptake and clearance of α-synuclein
also termed synucleinophagy. The accumulation of misfolded α-synuclein throughout
the brain is central to Parkinson's disease (PD). The distribution and progression
of the pathology is often attributed to the propagation of α-synuclein. Here,
we apply a classical α-synuclein propagation model of prodromal PD in wild type
and TLR4 deficient mice to study the role of TLR4 in the progression of the disease.
Our data suggest that TLR4 deficiency facilitates the α-synuclein seed spreading
associated with reduced lysosomal activity of microglia. Three months after seed
inoculation, more pronounced proteinase K-resistant α-synuclein inclusion pathology
is observed in mice with TLR4 deficiency. The facilitated propagation of α-synuclein
is associated with early loss of dopamine transporter (DAT) signal in the striatum
and loss of dopaminergic neurons in substantia nigra pars compacta of TLR4 deficient
mice. These new results support TLR4 signaling as a putative target for disease
modification to slow the progression of PD and related disorders.
acknowledgement: This study was supported by grants of the Austrian Science Fund (FWF)
F4414 and W1206-08. Electron microscopy was performed at the Scientific Service
Units (SSU) of IST-Austria through resources provided by the Electron Microscopy
Facility.
article_processing_charge: No
article_type: original
author:
- first_name: Serena
full_name: Venezia, Serena
last_name: Venezia
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Gregor K.
full_name: Wenning, Gregor K.
last_name: Wenning
- first_name: Nadia
full_name: Stefanova, Nadia
last_name: Stefanova
citation:
ama: Venezia S, Kaufmann W, Wenning GK, Stefanova N. Toll-like receptor 4 deficiency
facilitates α-synuclein propagation and neurodegeneration in a mouse model of
prodromal Parkinson’s disease. Parkinsonism & Related Disorders. 2021;91:59-65.
doi:10.1016/j.parkreldis.2021.09.007
apa: Venezia, S., Kaufmann, W., Wenning, G. K., & Stefanova, N. (2021). Toll-like
receptor 4 deficiency facilitates α-synuclein propagation and neurodegeneration
in a mouse model of prodromal Parkinson’s disease. Parkinsonism & Related
Disorders. Elsevier. https://doi.org/10.1016/j.parkreldis.2021.09.007
chicago: Venezia, Serena, Walter Kaufmann, Gregor K. Wenning, and Nadia Stefanova.
“Toll-like Receptor 4 Deficiency Facilitates α-Synuclein Propagation and Neurodegeneration
in a Mouse Model of Prodromal Parkinson’s Disease.” Parkinsonism & Related
Disorders. Elsevier, 2021. https://doi.org/10.1016/j.parkreldis.2021.09.007.
ieee: S. Venezia, W. Kaufmann, G. K. Wenning, and N. Stefanova, “Toll-like receptor
4 deficiency facilitates α-synuclein propagation and neurodegeneration in a mouse
model of prodromal Parkinson’s disease,” Parkinsonism & Related Disorders,
vol. 91. Elsevier, pp. 59–65, 2021.
ista: Venezia S, Kaufmann W, Wenning GK, Stefanova N. 2021. Toll-like receptor 4
deficiency facilitates α-synuclein propagation and neurodegeneration in a mouse
model of prodromal Parkinson’s disease. Parkinsonism & Related Disorders.
91, 59–65.
mla: Venezia, Serena, et al. “Toll-like Receptor 4 Deficiency Facilitates α-Synuclein
Propagation and Neurodegeneration in a Mouse Model of Prodromal Parkinson’s Disease.”
Parkinsonism & Related Disorders, vol. 91, Elsevier, 2021, pp. 59–65,
doi:10.1016/j.parkreldis.2021.09.007.
short: S. Venezia, W. Kaufmann, G.K. Wenning, N. Stefanova, Parkinsonism & Related
Disorders 91 (2021) 59–65.
date_created: 2022-01-09T23:01:26Z
date_published: 2021-10-01T00:00:00Z
date_updated: 2023-08-17T06:36:01Z
day: '01'
ddc:
- '610'
department:
- _id: EM-Fac
doi: 10.1016/j.parkreldis.2021.09.007
external_id:
isi:
- '000701142900012'
pmid:
- '34530328'
file:
- access_level: open_access
checksum: 360681585acb51e80d17c6b213c56b55
content_type: application/pdf
creator: alisjak
date_created: 2022-01-10T13:41:40Z
date_updated: 2022-01-10T13:41:40Z
file_id: '10612'
file_name: 2021_Parkinsonism_Venezia.pdf
file_size: 6848513
relation: main_file
success: 1
file_date_updated: 2022-01-10T13:41:40Z
has_accepted_license: '1'
intvolume: ' 91'
isi: 1
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: 59-65
pmid: 1
publication: Parkinsonism & Related Disorders
publication_identifier:
eissn:
- 1873-5126
issn:
- 1353-8020
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Toll-like receptor 4 deficiency facilitates α-synuclein propagation and neurodegeneration
in a mouse model of prodromal Parkinson's disease
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: 91
year: '2021'
...
---
_id: '9756'
abstract:
- lang: eng
text: High-resolution visualization and quantification of membrane proteins contribute
to the understanding of their functions and the roles they play in physiological
and pathological conditions. Sodium dodecyl sulfate-digested freeze-fracture replica
labeling (SDS-FRL) is a powerful electron microscopy method to study quantitatively
the two-dimensional distribution of transmembrane proteins and their tightly associated
proteins. During treatment with SDS, intracellular organelles and proteins not
anchored to the replica are dissolved, whereas integral membrane proteins captured
and stabilized by carbon/platinum deposition remain on the replica. Their intra-
and extracellular domains become exposed on the surface of the replica, facilitating
the accessibility of antibodies and, therefore, providing higher labeling efficiency
than those obtained with other immunoelectron microscopy techniques. In this chapter,
we describe the protocols of SDS-FRL adapted for mammalian brain samples, and
optimization of the SDS treatment to increase the labeling efficiency for quantification
of Cav2.1, the alpha subunit of P/Q-type voltage-dependent calcium channels utilizing
deep learning algorithms.
acknowledgement: This work was supported by the European Union (European Research
Council Advanced grant no. 694539 and Human Brain Project Ref. 720270 to R. S.)
and the Austrian Academy of Sciences (DOC fellowship to D.K.).
alternative_title:
- Neuromethods
article_processing_charge: No
author:
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: David
full_name: Kleindienst, David
id: 42E121A4-F248-11E8-B48F-1D18A9856A87
last_name: Kleindienst
- first_name: Harumi
full_name: Harada, Harumi
id: 2E55CDF2-F248-11E8-B48F-1D18A9856A87
last_name: Harada
orcid: 0000-0001-7429-7896
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: 'Kaufmann W, Kleindienst D, Harada H, Shigemoto R. High-Resolution localization
and quantitation of membrane proteins by SDS-digested freeze-fracture replica
labeling (SDS-FRL). In: Receptor and Ion Channel Detection in the Brain.
Vol 169. Neuromethods. New York: Humana; 2021:267-283. doi:10.1007/978-1-0716-1522-5_19'
apa: 'Kaufmann, W., Kleindienst, D., Harada, H., & Shigemoto, R. (2021). High-Resolution
localization and quantitation of membrane proteins by SDS-digested freeze-fracture
replica labeling (SDS-FRL). In Receptor and Ion Channel Detection in the Brain
(Vol. 169, pp. 267–283). New York: Humana. https://doi.org/10.1007/978-1-0716-1522-5_19'
chicago: 'Kaufmann, Walter, David Kleindienst, Harumi Harada, and Ryuichi Shigemoto.
“High-Resolution Localization and Quantitation of Membrane Proteins by SDS-Digested
Freeze-Fracture Replica Labeling (SDS-FRL).” In Receptor and Ion Channel Detection
in the Brain, 169:267–83. Neuromethods. New York: Humana, 2021. https://doi.org/10.1007/978-1-0716-1522-5_19.'
ieee: 'W. Kaufmann, D. Kleindienst, H. Harada, and R. Shigemoto, “High-Resolution
localization and quantitation of membrane proteins by SDS-digested freeze-fracture
replica labeling (SDS-FRL),” in Receptor and Ion Channel Detection in the
Brain, vol. 169, New York: Humana, 2021, pp. 267–283.'
ista: 'Kaufmann W, Kleindienst D, Harada H, Shigemoto R. 2021.High-Resolution localization
and quantitation of membrane proteins by SDS-digested freeze-fracture replica
labeling (SDS-FRL). In: Receptor and Ion Channel Detection in the Brain. Neuromethods,
vol. 169, 267–283.'
mla: Kaufmann, Walter, et al. “High-Resolution Localization and Quantitation of
Membrane Proteins by SDS-Digested Freeze-Fracture Replica Labeling (SDS-FRL).”
Receptor and Ion Channel Detection in the Brain, vol. 169, Humana, 2021,
pp. 267–83, doi:10.1007/978-1-0716-1522-5_19.
short: W. Kaufmann, D. Kleindienst, H. Harada, R. Shigemoto, in:, Receptor and
Ion Channel Detection in the Brain, Humana, New York, 2021, pp. 267–283.
date_created: 2021-07-30T09:34:56Z
date_published: 2021-07-27T00:00:00Z
date_updated: 2024-03-25T23:30:16Z
day: '27'
ddc:
- '573'
department:
- _id: RySh
- _id: EM-Fac
doi: 10.1007/978-1-0716-1522-5_19
ec_funded: 1
has_accepted_license: '1'
intvolume: ' 169'
keyword:
- 'Freeze-fracture replica: Deep learning'
- Immunogold labeling
- Integral membrane protein
- Electron microscopy
language:
- iso: eng
month: '07'
oa_version: None
page: 267-283
place: New York
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: 25CBA828-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '720270'
name: Human Brain Project Specific Grant Agreement 1 (HBP SGA 1)
publication: ' Receptor and Ion Channel Detection in the Brain'
publication_identifier:
eisbn:
- '9781071615225'
isbn:
- '9781071615218'
publication_status: published
publisher: Humana
quality_controlled: '1'
related_material:
record:
- id: '9562'
relation: dissertation_contains
status: public
series_title: Neuromethods
status: public
title: High-Resolution localization and quantitation of membrane proteins by SDS-digested
freeze-fracture replica labeling (SDS-FRL)
type: book_chapter
user_id: D865714E-FA4E-11E9-B85B-F5C5E5697425
volume: 169
year: '2021'
...
---
_id: '9887'
abstract:
- lang: eng
text: Clathrin-mediated endocytosis is the major route of entry of cargos into cells
and thus underpins many physiological processes. During endocytosis, an area of
flat membrane is remodeled by proteins to create a spherical vesicle against intracellular
forces. The protein machinery which mediates this membrane bending in plants is
unknown. However, it is known that plant endocytosis is actin independent, thus
indicating that plants utilize a unique mechanism to mediate membrane bending
against high-turgor pressure compared to other model systems. Here, we investigate
the TPLATE complex, a plant-specific endocytosis protein complex. It has been
thought to function as a classical adaptor functioning underneath the clathrin
coat. However, by using biochemical and advanced live microscopy approaches, we
found that TPLATE is peripherally associated with clathrin-coated vesicles and
localizes at the rim of endocytosis events. As this localization is more fitting
to the protein machinery involved in membrane bending during endocytosis, we examined
cells in which the TPLATE complex was disrupted and found that the clathrin structures
present as flat patches. This suggests a requirement of the TPLATE complex for
membrane bending during plant clathrin–mediated endocytosis. Next, we used in
vitro biophysical assays to confirm that the TPLATE complex possesses protein
domains with intrinsic membrane remodeling activity. These results redefine the
role of the TPLATE complex and implicate it as a key component of the evolutionarily
distinct plant endocytosis mechanism, which mediates endocytic membrane bending
against the high-turgor pressure in plant cells.
acknowledged_ssus:
- _id: EM-Fac
- _id: LifeSc
- _id: Bio
acknowledgement: 'We gratefully thank Julie Neveu and Dr. Amanda Barranco of the Grégory
Vert laboratory for help preparing plants in France, Dr. Zuzana Gelova for help
and advice with protoplast generation, Dr. Stéphane Vassilopoulos and Dr. Florian
Schur for advice regarding EM tomography, Alejandro Marquiegui Alvaro for help with
material generation, and Dr. Lukasz Kowalski for generously gifting us the mWasabi
protein. This research was supported by the Scientific Service Units of Institute
of Science and Technology Austria (IST Austria) through resources provided by the
Electron Microscopy Facility, Lab Support Facility (particularly Dorota Jaworska),
and the Bioimaging Facility. We acknowledge the Advanced Microscopy Facility of
the Vienna BioCenter Core Facilities for use of the 3D SIM. For the mass spectrometry
analysis of proteins, we acknowledge the University of Natural Resources and Life
Sciences (BOKU) Core Facility Mass Spectrometry. This work was supported by the
following funds: A.J. is supported by funding from the Austrian Science Fund I3630B25
to J.F. P.M. and E.B. are supported by Agence Nationale de la Recherche ANR-11-EQPX-0029
Morphoscope2 and ANR-10-INBS-04 France BioImaging. S.Y.B. is supported by the NSF
No. 1121998 and 1614915. J.W. and D.V.D. are supported by the European Research
Council Grant 682436 (to D.V.D.), a China Scholarship Council Grant 201508440249
(to J.W.), and by a Ghent University Special Research Co-funding Grant ST01511051
(to J.W.).'
article_number: e2113046118
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: Dana A
full_name: Dahhan, Dana A
last_name: Dahhan
- 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: Vanessa
full_name: Zheden, Vanessa
id: 39C5A68A-F248-11E8-B48F-1D18A9856A87
last_name: Zheden
orcid: 0000-0002-9438-4783
- first_name: Tommaso
full_name: Costanzo, Tommaso
id: D93824F4-D9BA-11E9-BB12-F207E6697425
last_name: Costanzo
orcid: 0000-0001-9732-3815
- first_name: Pierre
full_name: Mahou, Pierre
last_name: Mahou
- first_name: Mónika
full_name: Hrtyan, Mónika
id: 45A71A74-F248-11E8-B48F-1D18A9856A87
last_name: Hrtyan
- first_name: Jie
full_name: Wang, Jie
last_name: Wang
- first_name: Juan L
full_name: Aguilera Servin, Juan L
id: 2A67C376-F248-11E8-B48F-1D18A9856A87
last_name: Aguilera Servin
orcid: 0000-0002-2862-8372
- first_name: Daniël
full_name: van Damme, Daniël
last_name: van Damme
- first_name: Emmanuel
full_name: Beaurepaire, Emmanuel
last_name: Beaurepaire
- first_name: Martin
full_name: Loose, Martin
id: 462D4284-F248-11E8-B48F-1D18A9856A87
last_name: Loose
orcid: 0000-0001-7309-9724
- first_name: Sebastian Y
full_name: Bednarek, Sebastian Y
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, Dahhan DA, Gnyliukh N, et al. The TPLATE complex mediates membrane
bending during plant clathrin-mediated endocytosis. Proceedings of the National
Academy of Sciences. 2021;118(51). doi:10.1073/pnas.2113046118
apa: Johnson, A. J., Dahhan, D. A., Gnyliukh, N., Kaufmann, W., Zheden, V., Costanzo,
T., … Friml, J. (2021). The TPLATE complex mediates membrane bending during plant
clathrin-mediated endocytosis. Proceedings of the National Academy of Sciences.
National Academy of Sciences. https://doi.org/10.1073/pnas.2113046118
chicago: Johnson, Alexander J, Dana A Dahhan, Nataliia Gnyliukh, Walter Kaufmann,
Vanessa Zheden, Tommaso Costanzo, Pierre Mahou, et al. “The TPLATE Complex Mediates
Membrane Bending during Plant Clathrin-Mediated Endocytosis.” Proceedings of
the National Academy of Sciences. National Academy of Sciences, 2021. https://doi.org/10.1073/pnas.2113046118.
ieee: A. J. Johnson et al., “The TPLATE complex mediates membrane bending
during plant clathrin-mediated endocytosis,” Proceedings of the National Academy
of Sciences, vol. 118, no. 51. National Academy of Sciences, 2021.
ista: Johnson AJ, Dahhan DA, Gnyliukh N, Kaufmann W, Zheden V, Costanzo T, Mahou
P, Hrtyan M, Wang J, Aguilera Servin JL, van Damme D, Beaurepaire E, Loose M,
Bednarek SY, Friml J. 2021. The TPLATE complex mediates membrane bending during
plant clathrin-mediated endocytosis. Proceedings of the National Academy of Sciences.
118(51), e2113046118.
mla: Johnson, Alexander J., et al. “The TPLATE Complex Mediates Membrane Bending
during Plant Clathrin-Mediated Endocytosis.” Proceedings of the National Academy
of Sciences, vol. 118, no. 51, e2113046118, National Academy of Sciences,
2021, doi:10.1073/pnas.2113046118.
short: A.J. Johnson, D.A. Dahhan, N. Gnyliukh, W. Kaufmann, V. Zheden, T. Costanzo,
P. Mahou, M. Hrtyan, J. Wang, J.L. Aguilera Servin, D. van Damme, E. Beaurepaire,
M. Loose, S.Y. Bednarek, J. Friml, Proceedings of the National Academy of Sciences
118 (2021).
date_created: 2021-08-11T14:11:43Z
date_published: 2021-12-14T00:00:00Z
date_updated: 2024-02-19T11:06:09Z
day: '14'
ddc:
- '580'
department:
- _id: JiFr
- _id: MaLo
- _id: EvBe
- _id: EM-Fac
- _id: NanoFab
doi: 10.1073/pnas.2113046118
external_id:
isi:
- '000736417600043'
pmid:
- '34907016'
file:
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checksum: 8d01e72e22c4fb1584e72d8601947069
content_type: application/pdf
creator: cchlebak
date_created: 2021-12-15T08:59:40Z
date_updated: 2021-12-15T08:59:40Z
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file_name: 2021_PNAS_Johnson.pdf
file_size: 2757340
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file_date_updated: 2021-12-15T08:59:40Z
has_accepted_license: '1'
intvolume: ' 118'
isi: 1
issue: '51'
language:
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month: '12'
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
publication: Proceedings of the National Academy of Sciences
publication_identifier:
eissn:
- 1091-6490
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
related_material:
link:
- relation: earlier_version
url: https://doi.org/10.1101/2021.04.26.441441
record:
- id: '14510'
relation: dissertation_contains
status: public
- id: '14988'
relation: research_data
status: public
status: public
title: The TPLATE complex mediates membrane bending during plant clathrin-mediated
endocytosis
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: 118
year: '2021'
...
---
_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: 2023-12-01T13:51:07Z
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:
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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'
...
---
_id: '8744'
abstract:
- lang: eng
text: Understanding the conformational sampling of translation-arrested ribosome
nascent chain complexes is key to understand co-translational folding. Up to now,
coupling of cysteine oxidation, disulfide bond formation and structure formation
in nascent chains has remained elusive. Here, we investigate the eye-lens protein
γB-crystallin in the ribosomal exit tunnel. Using mass spectrometry, theoretical
simulations, dynamic nuclear polarization-enhanced solid-state nuclear magnetic
resonance and cryo-electron microscopy, we show that thiol groups of cysteine
residues undergo S-glutathionylation and S-nitrosylation and form non-native disulfide
bonds. Thus, covalent modification chemistry occurs already prior to nascent chain
release as the ribosome exit tunnel provides sufficient space even for disulfide
bond formation which can guide protein folding.
acknowledgement: 'We acknowledge help from Anja Seybert, Margot Frangakis, Diana Grewe,
Mikhail Eltsov, Utz Ermel, and Shintaro Aibara. The work was supported by Deutsche
Forschungsgemeinschaft in the CLiC graduate school. Work at the Center for Biomolecular
Magnetic Resonance (BMRZ) is supported by the German state of Hesse. The work at
BMRZ has been supported by the state of Hesse. L.S. has been supported by the DFG
graduate college: CLiC.'
article_number: '5569'
article_processing_charge: No
article_type: original
author:
- first_name: Linda
full_name: Schulte, Linda
last_name: Schulte
- first_name: Jiafei
full_name: Mao, Jiafei
last_name: Mao
- first_name: Julian
full_name: Reitz, Julian
last_name: Reitz
- first_name: Sridhar
full_name: Sreeramulu, Sridhar
last_name: Sreeramulu
- first_name: Denis
full_name: Kudlinzki, Denis
last_name: Kudlinzki
- first_name: Victor-Valentin
full_name: Hodirnau, Victor-Valentin
id: 3661B498-F248-11E8-B48F-1D18A9856A87
last_name: Hodirnau
- first_name: Jakob
full_name: Meier-Credo, Jakob
last_name: Meier-Credo
- first_name: Krishna
full_name: Saxena, Krishna
last_name: Saxena
- first_name: Florian
full_name: Buhr, Florian
last_name: Buhr
- first_name: Julian D.
full_name: Langer, Julian D.
last_name: Langer
- first_name: Martin
full_name: Blackledge, Martin
last_name: Blackledge
- first_name: Achilleas S.
full_name: Frangakis, Achilleas S.
last_name: Frangakis
- first_name: Clemens
full_name: Glaubitz, Clemens
last_name: Glaubitz
- first_name: Harald
full_name: Schwalbe, Harald
last_name: Schwalbe
citation:
ama: Schulte L, Mao J, Reitz J, et al. Cysteine oxidation and disulfide formation
in the ribosomal exit tunnel. Nature Communications. 2020;11. doi:10.1038/s41467-020-19372-x
apa: Schulte, L., Mao, J., Reitz, J., Sreeramulu, S., Kudlinzki, D., Hodirnau, V.-V.,
… Schwalbe, H. (2020). Cysteine oxidation and disulfide formation in the ribosomal
exit tunnel. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-020-19372-x
chicago: Schulte, Linda, Jiafei Mao, Julian Reitz, Sridhar Sreeramulu, Denis Kudlinzki,
Victor-Valentin Hodirnau, Jakob Meier-Credo, et al. “Cysteine Oxidation and Disulfide
Formation in the Ribosomal Exit Tunnel.” Nature Communications. Springer
Nature, 2020. https://doi.org/10.1038/s41467-020-19372-x.
ieee: L. Schulte et al., “Cysteine oxidation and disulfide formation in the
ribosomal exit tunnel,” Nature Communications, vol. 11. Springer Nature,
2020.
ista: Schulte L, Mao J, Reitz J, Sreeramulu S, Kudlinzki D, Hodirnau V-V, Meier-Credo
J, Saxena K, Buhr F, Langer JD, Blackledge M, Frangakis AS, Glaubitz C, Schwalbe
H. 2020. Cysteine oxidation and disulfide formation in the ribosomal exit tunnel.
Nature Communications. 11, 5569.
mla: Schulte, Linda, et al. “Cysteine Oxidation and Disulfide Formation in the Ribosomal
Exit Tunnel.” Nature Communications, vol. 11, 5569, Springer Nature, 2020,
doi:10.1038/s41467-020-19372-x.
short: L. Schulte, J. Mao, J. Reitz, S. Sreeramulu, D. Kudlinzki, V.-V. Hodirnau,
J. Meier-Credo, K. Saxena, F. Buhr, J.D. Langer, M. Blackledge, A.S. Frangakis,
C. Glaubitz, H. Schwalbe, Nature Communications 11 (2020).
date_created: 2020-11-09T07:49:36Z
date_published: 2020-11-04T00:00:00Z
date_updated: 2023-08-22T12:36:07Z
day: '04'
ddc:
- '570'
department:
- _id: EM-Fac
doi: 10.1038/s41467-020-19372-x
external_id:
isi:
- '000592028600001'
file:
- access_level: open_access
checksum: b2688f0347e69e6629bba582077278c5
content_type: application/pdf
creator: dernst
date_created: 2020-11-09T07:56:24Z
date_updated: 2020-11-09T07:56:24Z
file_id: '8745'
file_name: 2020_NatureComm_Schulte.pdf
file_size: 1670898
relation: main_file
success: 1
file_date_updated: 2020-11-09T07:56:24Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- General Physics and Astronomy
- General Chemistry
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Cysteine oxidation and disulfide formation in the ribosomal exit tunnel
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: 11
year: '2020'
...
---
_id: '8787'
abstract:
- lang: eng
text: Breakdown of vascular barriers is a major complication of inflammatory diseases.
Anucleate platelets form blood-clots during thrombosis, but also play a crucial
role in inflammation. While spatio-temporal dynamics of clot formation are well
characterized, the cell-biological mechanisms of platelet recruitment to inflammatory
micro-environments remain incompletely understood. Here we identify Arp2/3-dependent
lamellipodia formation as a prominent morphological feature of immune-responsive
platelets. Platelets use lamellipodia to scan for fibrin(ogen) deposited on the
inflamed vasculature and to directionally spread, to polarize and to govern haptotactic
migration along gradients of the adhesive ligand. Platelet-specific abrogation
of Arp2/3 interferes with haptotactic repositioning of platelets to microlesions,
thus impairing vascular sealing and provoking inflammatory microbleeding. During
infection, haptotaxis promotes capture of bacteria and prevents hematogenic dissemination,
rendering platelets gate-keepers of the inflamed microvasculature. Consequently,
these findings identify haptotaxis as a key effector function of immune-responsive
platelets.
acknowledgement: "We thank Sebastian Helmer, Nicole Blount, Christine Mann, and Beate
Jantz for technical assistance; Hellen Ishikawa-Ankerhold for help and advice; Michael
Sixt for critical\r\ndiscussions. This study was supported by the DFG SFB 914 (S.M.
[B02 and Z01], K.Sch.\r\n[B02], B.W. [A02 and Z03], C.A.R. [B03], C.S. [A10], J.P.
[Gerok position]), the DFG\r\nSFB 1123 (S.M. [B06]), the DFG FOR 2033 (S.M. and
F.G.), the German Center for\r\nCardiovascular Research (DZHK) (Clinician Scientist
Program [L.N.], MHA 1.4VD\r\n[S.M.], Postdoc Start-up Grant, 81×3600213 [F.G.]),
FP7 program (project 260309,\r\nPRESTIGE [S.M.]), FöFoLe project 1015/1009 (L.N.),
FöFoLe project 947 (F.G.), the\r\nFriedrich-Baur-Stiftung project 41/16 (F.G.),
and LMUexcellence NFF (F.G.). This project has received funding from the European
Research Council (ERC) under the European Union’s Horizon 2020 research and innovation
program (grant agreement no.\r\n833440) (S.M.). F.G. received funding from the European
Union’s Horizon 2020 research\r\nand innovation program under the Marie Skłodowska-Curie
grant agreement no.\r\n747687."
article_number: '5778'
article_processing_charge: No
article_type: original
author:
- first_name: Leo
full_name: Nicolai, Leo
last_name: Nicolai
- first_name: Karin
full_name: Schiefelbein, Karin
last_name: Schiefelbein
- first_name: Silvia
full_name: Lipsky, Silvia
last_name: Lipsky
- first_name: Alexander
full_name: Leunig, Alexander
last_name: Leunig
- first_name: Marie
full_name: Hoffknecht, Marie
last_name: Hoffknecht
- first_name: Kami
full_name: Pekayvaz, Kami
last_name: Pekayvaz
- first_name: Ben
full_name: Raude, Ben
last_name: Raude
- first_name: Charlotte
full_name: Marx, Charlotte
last_name: Marx
- first_name: Andreas
full_name: Ehrlich, Andreas
last_name: Ehrlich
- first_name: Joachim
full_name: Pircher, Joachim
last_name: Pircher
- first_name: Zhe
full_name: Zhang, Zhe
last_name: Zhang
- first_name: Inas
full_name: Saleh, Inas
last_name: Saleh
- first_name: Anna-Kristina
full_name: Marel, Anna-Kristina
last_name: Marel
- first_name: Achim
full_name: Löf, Achim
last_name: Löf
- first_name: Tobias
full_name: Petzold, Tobias
last_name: Petzold
- first_name: Michael
full_name: Lorenz, Michael
last_name: Lorenz
- first_name: Konstantin
full_name: Stark, Konstantin
last_name: Stark
- first_name: Robert
full_name: Pick, Robert
last_name: Pick
- first_name: Gerhild
full_name: Rosenberger, Gerhild
last_name: Rosenberger
- first_name: Ludwig
full_name: Weckbach, Ludwig
last_name: Weckbach
- first_name: Bernd
full_name: Uhl, Bernd
last_name: Uhl
- first_name: Sheng
full_name: Xia, Sheng
last_name: Xia
- first_name: Christoph Andreas
full_name: Reichel, Christoph Andreas
last_name: Reichel
- first_name: Barbara
full_name: Walzog, Barbara
last_name: Walzog
- first_name: Christian
full_name: Schulz, Christian
last_name: Schulz
- first_name: Vanessa
full_name: Zheden, Vanessa
id: 39C5A68A-F248-11E8-B48F-1D18A9856A87
last_name: Zheden
orcid: 0000-0002-9438-4783
- first_name: Markus
full_name: Bender, Markus
last_name: Bender
- first_name: Rong
full_name: Li, Rong
last_name: Li
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
citation:
ama: Nicolai L, Schiefelbein K, Lipsky S, et al. Vascular surveillance by haptotactic
blood platelets in inflammation and infection. Nature Communications. 2020;11.
doi:10.1038/s41467-020-19515-0
apa: Nicolai, L., Schiefelbein, K., Lipsky, S., Leunig, A., Hoffknecht, M., Pekayvaz,
K., … Gärtner, F. R. (2020). Vascular surveillance by haptotactic blood platelets
in inflammation and infection. Nature Communications. Springer Nature.
https://doi.org/10.1038/s41467-020-19515-0
chicago: Nicolai, Leo, Karin Schiefelbein, Silvia Lipsky, Alexander Leunig, Marie
Hoffknecht, Kami Pekayvaz, Ben Raude, et al. “Vascular Surveillance by Haptotactic
Blood Platelets in Inflammation and Infection.” Nature Communications.
Springer Nature, 2020. https://doi.org/10.1038/s41467-020-19515-0.
ieee: L. Nicolai et al., “Vascular surveillance by haptotactic blood platelets
in inflammation and infection,” Nature Communications, vol. 11. Springer
Nature, 2020.
ista: Nicolai L, Schiefelbein K, Lipsky S, Leunig A, Hoffknecht M, Pekayvaz K, Raude
B, Marx C, Ehrlich A, Pircher J, Zhang Z, Saleh I, Marel A-K, Löf A, Petzold T,
Lorenz M, Stark K, Pick R, Rosenberger G, Weckbach L, Uhl B, Xia S, Reichel CA,
Walzog B, Schulz C, Zheden V, Bender M, Li R, Massberg S, Gärtner FR. 2020. Vascular
surveillance by haptotactic blood platelets in inflammation and infection. Nature
Communications. 11, 5778.
mla: Nicolai, Leo, et al. “Vascular Surveillance by Haptotactic Blood Platelets
in Inflammation and Infection.” Nature Communications, vol. 11, 5778, Springer
Nature, 2020, doi:10.1038/s41467-020-19515-0.
short: L. Nicolai, K. Schiefelbein, S. Lipsky, A. Leunig, M. Hoffknecht, K. Pekayvaz,
B. Raude, C. Marx, A. Ehrlich, J. Pircher, Z. Zhang, I. Saleh, A.-K. Marel, A.
Löf, T. Petzold, M. Lorenz, K. Stark, R. Pick, G. Rosenberger, L. Weckbach, B.
Uhl, S. Xia, C.A. Reichel, B. Walzog, C. Schulz, V. Zheden, M. Bender, R. Li,
S. Massberg, F.R. Gärtner, Nature Communications 11 (2020).
date_created: 2020-11-22T23:01:23Z
date_published: 2020-11-13T00:00:00Z
date_updated: 2023-08-22T13:26:26Z
day: '13'
ddc:
- '570'
department:
- _id: MiSi
- _id: EM-Fac
doi: 10.1038/s41467-020-19515-0
ec_funded: 1
external_id:
isi:
- '000594648000014'
pmid:
- '33188196'
file:
- access_level: open_access
checksum: 485b7b6cf30198ba0ce126491a28f125
content_type: application/pdf
creator: dernst
date_created: 2020-11-23T13:29:49Z
date_updated: 2020-11-23T13:29:49Z
file_id: '8798'
file_name: 2020_NatureComm_Nicolai.pdf
file_size: 7035340
relation: main_file
success: 1
file_date_updated: 2020-11-23T13:29:49Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Nature Communications
publication_identifier:
eissn:
- '20411723'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1038/s41467-022-31310-7
scopus_import: '1'
status: public
title: Vascular surveillance by haptotactic blood platelets in inflammation and infection
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: 11
year: '2020'
...
---
_id: '8971'
abstract:
- lang: eng
text: The actin-related protein (Arp)2/3 complex nucleates branched actin filament
networks pivotal for cell migration, endocytosis and pathogen infection. Its activation
is tightly regulated and involves complex structural rearrangements and actin
filament binding, which are yet to be understood. Here, we report a 9.0 Å resolution
structure of the actin filament Arp2/3 complex branch junction in cells using
cryo-electron tomography and subtomogram averaging. This allows us to generate
an accurate model of the active Arp2/3 complex in the branch junction and its
interaction with actin filaments. Notably, our model reveals a previously undescribed
set of interactions of the Arp2/3 complex with the mother filament, significantly
different to the previous branch junction model. Our structure also indicates
a central role for the ArpC3 subunit in stabilizing the active conformation.
acknowledged_ssus:
- _id: ScienComp
- _id: LifeSc
- _id: Bio
- _id: EM-Fac
acknowledgement: "This research was supported by the Scientific Service Units (SSUs)
of IST Austria through resources provided by Scientific Computing (SciComp), the
Life Science Facility (LSF), the BioImaging Facility (BIF), and the Electron Microscopy
Facility (EMF). We also thank Dimitry Tegunov (MPI for Biophysical Chemistry) for
helpful discussions\r\nabout the M software, and Michael Sixt (IST Austria) and
Klemens Rottner (Technical University Braunschweig, HZI Braunschweig) for critical
reading of the manuscript. We also thank Gregory Voth (University of Chicago) for
providing us the MD-derived branch junction model for comparison. The authors acknowledge
support from IST Austria and from the Austrian Science Fund (FWF): M02495 to G.D.
and Austrian Science Fund (FWF): P33367 to F.K.M.S. "
article_number: '6437'
article_processing_charge: No
article_type: original
author:
- first_name: Florian
full_name: Fäßler, Florian
id: 404F5528-F248-11E8-B48F-1D18A9856A87
last_name: Fäßler
orcid: 0000-0001-7149-769X
- first_name: Georgi A
full_name: Dimchev, Georgi A
id: 38C393BE-F248-11E8-B48F-1D18A9856A87
last_name: Dimchev
orcid: 0000-0001-8370-6161
- first_name: Victor-Valentin
full_name: Hodirnau, Victor-Valentin
id: 3661B498-F248-11E8-B48F-1D18A9856A87
last_name: Hodirnau
- first_name: William
full_name: Wan, William
last_name: Wan
- first_name: Florian KM
full_name: Schur, Florian KM
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
citation:
ama: Fäßler F, Dimchev GA, Hodirnau V-V, Wan W, Schur FK. Cryo-electron tomography
structure of Arp2/3 complex in cells reveals new insights into the branch junction.
Nature Communications. 2020;11. doi:10.1038/s41467-020-20286-x
apa: Fäßler, F., Dimchev, G. A., Hodirnau, V.-V., Wan, W., & Schur, F. K. (2020).
Cryo-electron tomography structure of Arp2/3 complex in cells reveals new insights
into the branch junction. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-020-20286-x
chicago: Fäßler, Florian, Georgi A Dimchev, Victor-Valentin Hodirnau, William Wan,
and Florian KM Schur. “Cryo-Electron Tomography Structure of Arp2/3 Complex in
Cells Reveals New Insights into the Branch Junction.” Nature Communications.
Springer Nature, 2020. https://doi.org/10.1038/s41467-020-20286-x.
ieee: F. Fäßler, G. A. Dimchev, V.-V. Hodirnau, W. Wan, and F. K. Schur, “Cryo-electron
tomography structure of Arp2/3 complex in cells reveals new insights into the
branch junction,” Nature Communications, vol. 11. Springer Nature, 2020.
ista: Fäßler F, Dimchev GA, Hodirnau V-V, Wan W, Schur FK. 2020. Cryo-electron tomography
structure of Arp2/3 complex in cells reveals new insights into the branch junction.
Nature Communications. 11, 6437.
mla: Fäßler, Florian, et al. “Cryo-Electron Tomography Structure of Arp2/3 Complex
in Cells Reveals New Insights into the Branch Junction.” Nature Communications,
vol. 11, 6437, Springer Nature, 2020, doi:10.1038/s41467-020-20286-x.
short: F. Fäßler, G.A. Dimchev, V.-V. Hodirnau, W. Wan, F.K. Schur, Nature Communications
11 (2020).
date_created: 2020-12-23T08:25:45Z
date_published: 2020-12-22T00:00:00Z
date_updated: 2023-08-24T11:01:50Z
day: '22'
ddc:
- '570'
department:
- _id: FlSc
- _id: EM-Fac
doi: 10.1038/s41467-020-20286-x
external_id:
isi:
- '000603078000003'
file:
- access_level: open_access
checksum: 55d43ea0061cc4027ba45e966e1db8cc
content_type: application/pdf
creator: dernst
date_created: 2020-12-28T08:16:10Z
date_updated: 2020-12-28T08:16:10Z
file_id: '8975'
file_name: 2020_NatureComm_Faessler.pdf
file_size: 3958727
relation: main_file
success: 1
file_date_updated: 2020-12-28T08:16:10Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- General Physics and Astronomy
- General Chemistry
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 9B954C5C-BA93-11EA-9121-9846C619BF3A
grant_number: P33367
name: Structure and isoform diversity of the Arp2/3 complex
- _id: 2674F658-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02495
name: Protein structure and function in filopodia across scales
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
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/cutting-edge-technology-reveals-structures-within-cells/
scopus_import: '1'
status: public
title: Cryo-electron tomography structure of Arp2/3 complex in cells reveals new insights
into the branch junction
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: 11
year: '2020'
...
---
_id: '7490'
abstract:
- lang: eng
text: In plants, clathrin mediated endocytosis (CME) represents the major route
for cargo internalisation from the cell surface. It has been assumed to operate
in an evolutionary conserved manner as in yeast and animals. Here we report characterisation
of ultrastructure, dynamics and mechanisms of plant CME as allowed by our advancement
in electron microscopy and quantitative live imaging techniques. Arabidopsis CME
appears to follow the constant curvature model and the bona fide CME population
generates vesicles of a predominantly hexagonal-basket type; larger and with faster
kinetics than in other models. Contrary to the existing paradigm, actin is dispensable
for CME events at the plasma membrane but plays a unique role in collecting endocytic
vesicles, sorting of internalised cargos and directional endosome movement that
itself actively promote CME events. Internalized vesicles display a strongly delayed
and sequential uncoating. These unique features highlight the independent evolution
of the plant CME mechanism during the autonomous rise of multicellularity in eukaryotes.
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
- _id: EM-Fac
article_number: e52067
article_processing_charge: No
article_type: original
author:
- first_name: Madhumitha
full_name: Narasimhan, Madhumitha
id: 44BF24D0-F248-11E8-B48F-1D18A9856A87
last_name: Narasimhan
orcid: 0000-0002-8600-0671
- 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: Roshan
full_name: Prizak, Roshan
id: 4456104E-F248-11E8-B48F-1D18A9856A87
last_name: Prizak
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Shutang
full_name: Tan, Shutang
id: 2DE75584-F248-11E8-B48F-1D18A9856A87
last_name: Tan
orcid: 0000-0002-0471-8285
- first_name: Barbara E
full_name: Casillas Perez, Barbara E
id: 351ED2AA-F248-11E8-B48F-1D18A9856A87
last_name: Casillas Perez
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Narasimhan M, Johnson AJ, Prizak R, et al. Evolutionarily unique mechanistic
framework of clathrin-mediated endocytosis in plants. eLife. 2020;9. doi:10.7554/eLife.52067
apa: Narasimhan, M., Johnson, A. J., Prizak, R., Kaufmann, W., Tan, S., Casillas
Perez, B. E., & Friml, J. (2020). Evolutionarily unique mechanistic framework
of clathrin-mediated endocytosis in plants. ELife. eLife Sciences Publications.
https://doi.org/10.7554/eLife.52067
chicago: Narasimhan, Madhumitha, Alexander J Johnson, Roshan Prizak, Walter Kaufmann,
Shutang Tan, Barbara E Casillas Perez, and Jiří Friml. “Evolutionarily Unique
Mechanistic Framework of Clathrin-Mediated Endocytosis in Plants.” ELife.
eLife Sciences Publications, 2020. https://doi.org/10.7554/eLife.52067.
ieee: M. Narasimhan et al., “Evolutionarily unique mechanistic framework
of clathrin-mediated endocytosis in plants,” eLife, vol. 9. eLife Sciences
Publications, 2020.
ista: Narasimhan M, Johnson AJ, Prizak R, Kaufmann W, Tan S, Casillas Perez BE,
Friml J. 2020. Evolutionarily unique mechanistic framework of clathrin-mediated
endocytosis in plants. eLife. 9, e52067.
mla: Narasimhan, Madhumitha, et al. “Evolutionarily Unique Mechanistic Framework
of Clathrin-Mediated Endocytosis in Plants.” ELife, vol. 9, e52067, eLife
Sciences Publications, 2020, doi:10.7554/eLife.52067.
short: M. Narasimhan, A.J. Johnson, R. Prizak, W. Kaufmann, S. Tan, B.E. Casillas
Perez, J. Friml, ELife 9 (2020).
date_created: 2020-02-16T23:00:50Z
date_published: 2020-01-23T00:00:00Z
date_updated: 2023-08-18T06:33:07Z
day: '23'
ddc:
- '570'
- '580'
department:
- _id: JiFr
- _id: GaTk
- _id: EM-Fac
- _id: SyCr
doi: 10.7554/eLife.52067
ec_funded: 1
external_id:
isi:
- '000514104100001'
pmid:
- '31971511'
file:
- access_level: open_access
checksum: 2052daa4be5019534f3a42f200a09f32
content_type: application/pdf
creator: dernst
date_created: 2020-02-18T07:21:16Z
date_updated: 2020-07-14T12:47:59Z
file_id: '7494'
file_name: 2020_eLife_Narasimhan.pdf
file_size: 7247468
relation: main_file
file_date_updated: 2020-07-14T12:47:59Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
month: '01'
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: 26538374-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I03630
name: Molecular mechanisms of endocytic cargo recognition in plants
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Evolutionarily unique mechanistic framework of clathrin-mediated endocytosis
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: 9
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: 2024-03-25T23:30:10Z
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: '6087'
abstract:
- lang: eng
text: Cell fate specification by lateral inhibition typically involves contact signaling
through the Delta-Notch signaling pathway. However, whether this is the only signaling
mode mediating lateral inhibition remains unclear. Here we show that in zebrafish
oogenesis, a group of cells within the granulosa cell layer at the oocyte animal
pole acquire elevated levels of the transcriptional coactivator TAZ in their nuclei.
One of these cells, the future micropyle precursor cell (MPC), accumulates increasingly
high levels of nuclear TAZ and grows faster than its surrounding cells, mechanically
compressing those cells, which ultimately lose TAZ from their nuclei. Strikingly,
relieving neighbor-cell compression by MPC ablation or aspiration restores nuclear
TAZ accumulation in neighboring cells, eventually leading to MPC re-specification
from these cells. Conversely, MPC specification is defective in taz−/− follicles.
These findings uncover a novel mode of lateral inhibition in cell fate specification
based on mechanical signals controlling TAZ activity.
acknowledged_ssus:
- _id: Bio
- _id: EM-Fac
- _id: LifeSc
acknowledgement: We thank Roland Dosch, Makoto Furutani-Seiki, Brian Link, Mary Mullins,
and Masazumi Tada for providing transgenic and/or mutant zebrafish lines; Alexandra
Schauer, Shayan Shami-Pour, and the rest of the Heisenberg lab for technical assistance
and feedback on the manuscript; and the Bioimaging, Electron Microscopy, and Zebrafish
facilities of IST Austria for continuous support. This work was supported by an
ERC advanced grant ( MECSPEC to C.-P.H.).
article_processing_charge: No
article_type: original
author:
- first_name: Peng
full_name: Xia, Peng
id: 4AB6C7D0-F248-11E8-B48F-1D18A9856A87
last_name: Xia
orcid: 0000-0002-5419-7756
- first_name: Daniel J
full_name: Gütl, Daniel J
id: 381929CE-F248-11E8-B48F-1D18A9856A87
last_name: Gütl
- first_name: Vanessa
full_name: Zheden, Vanessa
id: 39C5A68A-F248-11E8-B48F-1D18A9856A87
last_name: Zheden
orcid: 0000-0002-9438-4783
- 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: Xia P, Gütl DJ, Zheden V, Heisenberg C-PJ. Lateral inhibition in cell specification
mediated by mechanical signals modulating TAZ activity. Cell. 2019;176(6):1379-1392.e14.
doi:10.1016/j.cell.2019.01.019
apa: Xia, P., Gütl, D. J., Zheden, V., & Heisenberg, C.-P. J. (2019). Lateral
inhibition in cell specification mediated by mechanical signals modulating TAZ
activity. Cell. Elsevier. https://doi.org/10.1016/j.cell.2019.01.019
chicago: Xia, Peng, Daniel J Gütl, Vanessa Zheden, and Carl-Philipp J Heisenberg.
“Lateral Inhibition in Cell Specification Mediated by Mechanical Signals Modulating
TAZ Activity.” Cell. Elsevier, 2019. https://doi.org/10.1016/j.cell.2019.01.019.
ieee: P. Xia, D. J. Gütl, V. Zheden, and C.-P. J. Heisenberg, “Lateral inhibition
in cell specification mediated by mechanical signals modulating TAZ activity,”
Cell, vol. 176, no. 6. Elsevier, p. 1379–1392.e14, 2019.
ista: Xia P, Gütl DJ, Zheden V, Heisenberg C-PJ. 2019. Lateral inhibition in cell
specification mediated by mechanical signals modulating TAZ activity. Cell. 176(6),
1379–1392.e14.
mla: Xia, Peng, et al. “Lateral Inhibition in Cell Specification Mediated by Mechanical
Signals Modulating TAZ Activity.” Cell, vol. 176, no. 6, Elsevier, 2019,
p. 1379–1392.e14, doi:10.1016/j.cell.2019.01.019.
short: P. Xia, D.J. Gütl, V. Zheden, C.-P.J. Heisenberg, Cell 176 (2019) 1379–1392.e14.
date_created: 2019-03-10T22:59:19Z
date_published: 2019-03-07T00:00:00Z
date_updated: 2023-08-25T08:02:23Z
day: '07'
department:
- _id: CaHe
- _id: EM-Fac
doi: 10.1016/j.cell.2019.01.019
ec_funded: 1
external_id:
isi:
- '000460509600013'
pmid:
- '30773315'
intvolume: ' 176'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cell.2019.01.019
month: '03'
oa: 1
oa_version: Published Version
page: 1379-1392.e14
pmid: 1
project:
- _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
publication: Cell
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/in-zebrafish-eggs-most-rapidly-growing-cell-inhibits-its-neighbours-through-mechanical-signals/
scopus_import: '1'
status: public
title: Lateral inhibition in cell specification mediated by mechanical signals modulating
TAZ activity
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 176
year: '2019'
...
---
_id: '308'
abstract:
- lang: eng
text: Migrating cells penetrate tissue barriers during development, inflammatory
responses, and tumor metastasis. We study if migration in vivo in such three-dimensionally
confined environments requires changes in the mechanical properties of the surrounding
cells using embryonic Drosophila melanogaster hemocytes, also called macrophages,
as a model. We find that macrophage invasion into the germband through transient
separation of the apposing ectoderm and mesoderm requires cell deformations and
reductions in apical tension in the ectoderm. Interestingly, the genetic pathway
governing these mechanical shifts acts downstream of the only known tumor necrosis
factor superfamily member in Drosophila, Eiger, and its receptor, Grindelwald.
Eiger-Grindelwald signaling reduces levels of active Myosin in the germband ectodermal
cortex through the localization of a Crumbs complex component, Patj (Pals-1-associated
tight junction protein). We therefore elucidate a distinct molecular pathway that
controls tissue tension and demonstrate the importance of such regulation for
invasive migration in vivo.
acknowledged_ssus:
- _id: SSU
article_processing_charge: No
article_type: original
author:
- first_name: Aparna
full_name: Ratheesh, Aparna
id: 2F064CFE-F248-11E8-B48F-1D18A9856A87
last_name: Ratheesh
orcid: 0000-0001-7190-0776
- first_name: Julia
full_name: Biebl, Julia
id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87
last_name: Biebl
- first_name: Michael
full_name: Smutny, Michael
last_name: Smutny
- first_name: Jana
full_name: Veselá, Jana
id: 433253EE-F248-11E8-B48F-1D18A9856A87
last_name: Veselá
- first_name: Ekaterina
full_name: Papusheva, Ekaterina
id: 41DB591E-F248-11E8-B48F-1D18A9856A87
last_name: Papusheva
- 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: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Alessandra M
full_name: Casano, Alessandra M
id: 3DBA3F4E-F248-11E8-B48F-1D18A9856A87
last_name: Casano
orcid: 0000-0002-6009-6804
- 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: Ratheesh A, Bicher J, Smutny M, et al. Drosophila TNF modulates tissue tension
in the embryo to facilitate macrophage invasive migration. Developmental Cell.
2018;45(3):331-346. doi:10.1016/j.devcel.2018.04.002
apa: Ratheesh, A., Bicher, J., Smutny, M., Veselá, J., Papusheva, E., Krens, G.,
… Siekhaus, D. E. (2018). Drosophila TNF modulates tissue tension in the embryo
to facilitate macrophage invasive migration. Developmental Cell. Elsevier.
https://doi.org/10.1016/j.devcel.2018.04.002
chicago: Ratheesh, Aparna, Julia Bicher, Michael Smutny, Jana Veselá, Ekaterina
Papusheva, Gabriel Krens, Walter Kaufmann, Attila György, Alessandra M Casano,
and Daria E Siekhaus. “Drosophila TNF Modulates Tissue Tension in the Embryo to
Facilitate Macrophage Invasive Migration.” Developmental Cell. Elsevier,
2018. https://doi.org/10.1016/j.devcel.2018.04.002.
ieee: A. Ratheesh et al., “Drosophila TNF modulates tissue tension in the
embryo to facilitate macrophage invasive migration,” Developmental Cell,
vol. 45, no. 3. Elsevier, pp. 331–346, 2018.
ista: Ratheesh A, Bicher J, Smutny M, Veselá J, Papusheva E, Krens G, Kaufmann W,
György A, Casano AM, Siekhaus DE. 2018. Drosophila TNF modulates tissue tension
in the embryo to facilitate macrophage invasive migration. Developmental Cell.
45(3), 331–346.
mla: Ratheesh, Aparna, et al. “Drosophila TNF Modulates Tissue Tension in the Embryo
to Facilitate Macrophage Invasive Migration.” Developmental Cell, vol.
45, no. 3, Elsevier, 2018, pp. 331–46, doi:10.1016/j.devcel.2018.04.002.
short: A. Ratheesh, J. Bicher, M. Smutny, J. Veselá, E. Papusheva, G. Krens, W.
Kaufmann, A. György, A.M. Casano, D.E. Siekhaus, Developmental Cell 45 (2018)
331–346.
date_created: 2018-12-11T11:45:44Z
date_published: 2018-05-07T00:00:00Z
date_updated: 2023-09-11T13:22:13Z
day: '07'
department:
- _id: DaSi
- _id: CaHe
- _id: Bio
- _id: EM-Fac
- _id: MiSi
doi: 10.1016/j.devcel.2018.04.002
ec_funded: 1
external_id:
isi:
- '000432461400009'
pmid:
- '29738712'
intvolume: ' 45'
isi: 1
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.devcel.2018.04.002
month: '05'
oa: 1
oa_version: Published Version
page: 331 - 346
pmid: 1
project:
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: Drosophila TNFa´s Funktion in Immunzellen
- _id: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
publication: Developmental Cell
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/cells-change-tension-to-make-tissue-barriers-easier-to-get-through/
scopus_import: '1'
status: public
title: Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage
invasive migration
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 45
year: '2018'
...
---
_id: '163'
abstract:
- lang: eng
text: For ultrafast fixation of biological samples to avoid artifacts, high-pressure
freezing (HPF) followed by freeze substitution (FS) is preferred over chemical
fixation at room temperature. After HPF, samples are maintained at low temperature
during dehydration and fixation, while avoiding damaging recrystallization. This
is a notoriously slow process. McDonald and Webb demonstrated, in 2011, that sample
agitation during FS dramatically reduces the necessary time. Then, in 2015, we
(H.G. and S.R.) introduced an agitation module into the cryochamber of an automated
FS unit and demonstrated that the preparation of algae could be shortened from
days to a couple of hours. We argued that variability in the processing, reproducibility,
and safety issues are better addressed using automated FS units. For dissemination,
we started low-cost manufacturing of agitation modules for two of the most widely
used FS units, the Automatic Freeze Substitution Systems, AFS(1) and AFS2, from
Leica Microsystems, using three dimensional (3D)-printing of the major components.
To test them, several labs independently used the modules on a wide variety of
specimens that had previously been processed by manual agitation, or without agitation.
We demonstrate that automated processing with sample agitation saves time, increases
flexibility with respect to sample requirements and protocols, and produces data
of at least as good quality as other approaches.
article_processing_charge: No
article_type: original
author:
- first_name: Siegfried
full_name: Reipert, Siegfried
last_name: Reipert
- first_name: Helmuth
full_name: Goldammer, Helmuth
last_name: Goldammer
- first_name: Christine
full_name: Richardson, Christine
last_name: Richardson
- first_name: Martin
full_name: Goldberg, Martin
last_name: Goldberg
- first_name: Timothy
full_name: Hawkins, Timothy
last_name: Hawkins
- first_name: Elena
full_name: Hollergschwandtner, Elena
id: 3C054040-F248-11E8-B48F-1D18A9856A87
last_name: Hollergschwandtner
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Sebastian
full_name: Antreich, Sebastian
last_name: Antreich
- first_name: York
full_name: Stierhof, York
last_name: Stierhof
citation:
ama: 'Reipert S, Goldammer H, Richardson C, et al. Agitation modules: Flexible means
to accelerate automated freeze substitution. Journal of Histochemistry and
Cytochemistry. 2018;66(12):903-921. doi:10.1369/0022155418786698'
apa: 'Reipert, S., Goldammer, H., Richardson, C., Goldberg, M., Hawkins, T., Saeckl,
E., … Stierhof, Y. (2018). Agitation modules: Flexible means to accelerate automated
freeze substitution. Journal of Histochemistry and Cytochemistry. SAGE
Publications. https://doi.org/10.1369/0022155418786698'
chicago: 'Reipert, Siegfried, Helmuth Goldammer, Christine Richardson, Martin Goldberg,
Timothy Hawkins, Elena Saeckl, Walter Kaufmann, Sebastian Antreich, and York Stierhof.
“Agitation Modules: Flexible Means to Accelerate Automated Freeze Substitution.”
Journal of Histochemistry and Cytochemistry. SAGE Publications, 2018. https://doi.org/10.1369/0022155418786698.'
ieee: 'S. Reipert et al., “Agitation modules: Flexible means to accelerate
automated freeze substitution,” Journal of Histochemistry and Cytochemistry,
vol. 66, no. 12. SAGE Publications, pp. 903–921, 2018.'
ista: 'Reipert S, Goldammer H, Richardson C, Goldberg M, Hawkins T, Saeckl E, Kaufmann
W, Antreich S, Stierhof Y. 2018. Agitation modules: Flexible means to accelerate
automated freeze substitution. Journal of Histochemistry and Cytochemistry. 66(12),
903–921.'
mla: 'Reipert, Siegfried, et al. “Agitation Modules: Flexible Means to Accelerate
Automated Freeze Substitution.” Journal of Histochemistry and Cytochemistry,
vol. 66, no. 12, SAGE Publications, 2018, pp. 903–21, doi:10.1369/0022155418786698.'
short: S. Reipert, H. Goldammer, C. Richardson, M. Goldberg, T. Hawkins, E. Saeckl,
W. Kaufmann, S. Antreich, Y. Stierhof, Journal of Histochemistry and Cytochemistry
66 (2018) 903–921.
date_created: 2018-12-11T11:44:57Z
date_published: 2018-12-01T00:00:00Z
date_updated: 2023-10-17T08:42:24Z
day: '01'
department:
- _id: RySh
- _id: EM-Fac
doi: 10.1369/0022155418786698
external_id:
isi:
- '000452277700005'
pmid:
- '29969056'
intvolume: ' 66'
isi: 1
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1369/0022155418786698
month: '12'
oa: 1
oa_version: Published Version
page: 903-921
pmid: 1
publication: Journal of Histochemistry and Cytochemistry
publication_identifier:
issn:
- 0022-1554
publication_status: published
publisher: SAGE Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Agitation modules: Flexible means to accelerate automated freeze substitution'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 66
year: '2018'
...
---
_id: '672'
abstract:
- lang: eng
text: Trafficking cells frequently transmigrate through epithelial and endothelial
monolayers. How monolayers cooperate with the penetrating cells to support their
transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic
capillaries as a model system for transendothelial migration. We find that the
chemokine CCL21, which is the decisive guidance cue for intravasation, mainly
localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial
cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes
extracellularly enriched at the sites of endothelial cell-cell junctions. When
we reconstitute the transmigration process in vitro, we find that secretion of
CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and
selective calcium chelation in lymphatic endothelium attenuates transmigration.
Altogether, our data demonstrate a chemokine-mediated feedback between DCs and
lymphatic endothelium, which facilitates transendothelial migration.
article_processing_charge: Yes
author:
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
- first_name: Matthias
full_name: Mehling, Matthias
id: 3C23B994-F248-11E8-B48F-1D18A9856A87
last_name: Mehling
orcid: 0000-0001-8599-1226
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the
chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia.
Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027
apa: Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling,
M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes
dendritic cell transmigration across lymphatic endothelia. Cell Reports.
Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027
chicago: Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander
F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered
Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic
Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027.
ieee: K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21
promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports,
vol. 19, no. 5. Cell Press, pp. 902–909, 2017.
ista: Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann
W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic
cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909.
mla: Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21
Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports,
vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027.
short: K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling,
W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.
date_created: 2018-12-11T11:47:50Z
date_published: 2017-05-02T00:00:00Z
date_updated: 2023-02-23T12:50:09Z
day: '02'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
- _id: EM-Fac
doi: 10.1016/j.celrep.2017.04.027
ec_funded: 1
file:
- access_level: open_access
checksum: 8fdddaab1f1d76a6ec9ca94dcb6b07a2
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:54Z
date_updated: 2020-07-14T12:47:38Z
file_id: '5109'
file_name: IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf
file_size: 2248814
relation: main_file
file_date_updated: 2020-07-14T12:47:38Z
has_accepted_license: '1'
intvolume: ' 19'
issue: '5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 902 - 909
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Cell Reports
publication_identifier:
issn:
- '22111247'
publication_status: published
publisher: Cell Press
publist_id: '7052'
pubrep_id: '900'
quality_controlled: '1'
scopus_import: 1
status: public
title: Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration
across lymphatic endothelia
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2017'
...
---
_id: '693'
abstract:
- lang: eng
text: 'Many central synapses contain a single presynaptic active zone and a single
postsynaptic density. Vesicular release statistics at such “simple synapses” indicate
that they contain a small complement of docking sites where vesicles repetitively
dock and fuse. In this work, we investigate functional and morphological aspects
of docking sites at simple synapses made between cerebellar parallel fibers and
molecular layer interneurons. Using immunogold labeling of SDS-treated freeze-fracture
replicas, we find that Cav2.1 channels form several clusters per active zone with
about nine channels per cluster. The mean value and range of intersynaptic variation
are similar for Cav2.1 cluster numbers and for functional estimates of docking-site
numbers obtained from the maximum numbers of released vesicles per action potential.
Both numbers grow in relation with synaptic size and decrease by a similar extent
with age between 2 wk and 4 wk postnatal. Thus, the mean docking-site numbers
were 3.15 at 2 wk (range: 1–10) and 2.03 at 4 wk (range: 1–4), whereas the mean
numbers of Cav2.1 clusters were 2.84 at 2 wk (range: 1–8) and 2.37 at 4 wk (range:
1–5). These changes were accompanied by decreases of miniature current amplitude
(from 93 pA to 56 pA), active-zone surface area (from 0.0427 μm2 to 0.0234 μm2),
and initial success rate (from 0.609 to 0.353), indicating a tightening of synaptic
transmission with development. Altogether, these results suggest a close correspondence
between the number of functionally defined vesicular docking sites and that of
clusters of voltage-gated calcium channels. '
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Takafumi
full_name: Miki, Takafumi
last_name: Miki
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Gerardo
full_name: Malagon, Gerardo
last_name: Malagon
- first_name: Laura
full_name: Gomez, Laura
last_name: Gomez
- first_name: Katsuhiko
full_name: Tabuchi, Katsuhiko
last_name: Tabuchi
- first_name: Masahiko
full_name: Watanabe, Masahiko
last_name: Watanabe
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Alain
full_name: Marty, Alain
last_name: Marty
citation:
ama: Miki T, Kaufmann W, Malagon G, et al. Numbers of presynaptic Ca2+ channel clusters
match those of functionally defined vesicular docking sites in single central
synapses. PNAS. 2017;114(26):E5246-E5255. doi:10.1073/pnas.1704470114
apa: Miki, T., Kaufmann, W., Malagon, G., Gomez, L., Tabuchi, K., Watanabe, M.,
… Marty, A. (2017). Numbers of presynaptic Ca2+ channel clusters match those of
functionally defined vesicular docking sites in single central synapses. PNAS.
National Academy of Sciences. https://doi.org/10.1073/pnas.1704470114
chicago: Miki, Takafumi, Walter Kaufmann, Gerardo Malagon, Laura Gomez, Katsuhiko
Tabuchi, Masahiko Watanabe, Ryuichi Shigemoto, and Alain Marty. “Numbers of Presynaptic
Ca2+ Channel Clusters Match Those of Functionally Defined Vesicular Docking Sites
in Single Central Synapses.” PNAS. National Academy of Sciences, 2017.
https://doi.org/10.1073/pnas.1704470114.
ieee: T. Miki et al., “Numbers of presynaptic Ca2+ channel clusters match
those of functionally defined vesicular docking sites in single central synapses,”
PNAS, vol. 114, no. 26. National Academy of Sciences, pp. E5246–E5255,
2017.
ista: Miki T, Kaufmann W, Malagon G, Gomez L, Tabuchi K, Watanabe M, Shigemoto R,
Marty A. 2017. Numbers of presynaptic Ca2+ channel clusters match those of functionally
defined vesicular docking sites in single central synapses. PNAS. 114(26), E5246–E5255.
mla: Miki, Takafumi, et al. “Numbers of Presynaptic Ca2+ Channel Clusters Match
Those of Functionally Defined Vesicular Docking Sites in Single Central Synapses.”
PNAS, vol. 114, no. 26, National Academy of Sciences, 2017, pp. E5246–55,
doi:10.1073/pnas.1704470114.
short: T. Miki, W. Kaufmann, G. Malagon, L. Gomez, K. Tabuchi, M. Watanabe, R. Shigemoto,
A. Marty, PNAS 114 (2017) E5246–E5255.
date_created: 2018-12-11T11:47:57Z
date_published: 2017-06-27T00:00:00Z
date_updated: 2023-02-23T12:54:57Z
day: '27'
ddc:
- '570'
department:
- _id: EM-Fac
- _id: RySh
doi: 10.1073/pnas.1704470114
external_id:
pmid:
- '28607047'
file:
- access_level: open_access
checksum: 2ab75d554f3df4a34d20fa8040589b7e
content_type: application/pdf
creator: kschuh
date_created: 2020-01-03T13:27:29Z
date_updated: 2020-07-14T12:47:44Z
file_id: '7223'
file_name: 2017_PNAS_Miki.pdf
file_size: 2721544
relation: main_file
file_date_updated: 2020-07-14T12:47:44Z
has_accepted_license: '1'
intvolume: ' 114'
issue: '26'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: E5246 - E5255
pmid: 1
publication: PNAS
publication_identifier:
issn:
- '00278424'
publication_status: published
publisher: National Academy of Sciences
publist_id: '7013'
quality_controlled: '1'
scopus_import: 1
status: public
title: Numbers of presynaptic Ca2+ channel clusters match those of functionally defined
vesicular docking sites in single central synapses
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 114
year: '2017'
...
---
_id: '1562'
abstract:
- lang: eng
text: The plant hormone auxin is a key regulator of plant growth and development.
Auxin levels are sensed and interpreted by distinct receptor systems that activate
a broad range of cellular responses. The Auxin-Binding Protein1 (ABP1) that has
been identified based on its ability to bind auxin with high affinity is a prime
candidate for the extracellular receptor responsible for mediating a range of
auxin effects, in particular, the fast non-transcriptional ones. Contradictory
genetic studies suggested prominent or no importance of ABP1 in many developmental
processes. However, how crucial the role of auxin binding to ABP1 is for its functions
has not been addressed. Here, we show that the auxin-binding pocket of ABP1 is
essential for its gain-of-function cellular and developmental roles. In total,
16 different abp1 mutants were prepared that possessed substitutions in the metal
core or in the hydrophobic amino acids of the auxin-binding pocket as well as
neutral mutations. Their analysis revealed that an intact auxin-binding pocket
is a prerequisite for ABP1 to activate downstream components of the ABP1 signalling
pathway, such as Rho of Plants (ROPs) and to mediate the clathrin association
with membranes for endocytosis regulation. In planta analyses demonstrated the
importance of the auxin binding pocket for all known ABP1-mediated postembryonic
developmental processes, including morphology of leaf epidermal cells, root growth
and root meristem activity, and vascular tissue differentiation. Taken together,
these findings suggest that auxin binding to ABP1 is central to its function,
supporting the role of ABP1 as auxin receptor.
acknowledgement: This work was supported by ERC Independent Research grant (ERC-2011-StG-
20101109-PSDP to JF); the European Social Fund and the state budget of the Czech
Republic [the project ‘Employment of Newly Graduated Doctors of Science for Scientific
Excellence’ (CZ.1.07/2.3.00/30.0009) to TN]; the Czech Science Foundation (GACR)
[project 13-40637S to JF].
article_type: original
author:
- first_name: Peter
full_name: Grones, Peter
id: 399876EC-F248-11E8-B48F-1D18A9856A87
last_name: Grones
- first_name: Xu
full_name: Chen, Xu
id: 4E5ADCAA-F248-11E8-B48F-1D18A9856A87
last_name: Chen
- first_name: Sibu
full_name: Simon, Sibu
id: 4542EF9A-F248-11E8-B48F-1D18A9856A87
last_name: Simon
orcid: 0000-0002-1998-6741
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Riet
full_name: De Rycke, Riet
last_name: De Rycke
- first_name: Tomasz
full_name: Nodzyński, Tomasz
last_name: Nodzyński
- first_name: Eva
full_name: Zažímalová, Eva
last_name: Zažímalová
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Grones P, Chen X, Simon S, et al. Auxin-binding pocket of ABP1 is crucial for
its gain-of-function cellular and developmental roles. Journal of Experimental
Botany. 2015;66(16):5055-5065. doi:10.1093/jxb/erv177
apa: Grones, P., Chen, X., Simon, S., Kaufmann, W., De Rycke, R., Nodzyński, T.,
… Friml, J. (2015). Auxin-binding pocket of ABP1 is crucial for its gain-of-function
cellular and developmental roles. Journal of Experimental Botany. Oxford
University Press. https://doi.org/10.1093/jxb/erv177
chicago: Grones, Peter, Xu Chen, Sibu Simon, Walter Kaufmann, Riet De Rycke, Tomasz
Nodzyński, Eva Zažímalová, and Jiří Friml. “Auxin-Binding Pocket of ABP1 Is Crucial
for Its Gain-of-Function Cellular and Developmental Roles.” Journal of Experimental
Botany. Oxford University Press, 2015. https://doi.org/10.1093/jxb/erv177.
ieee: P. Grones et al., “Auxin-binding pocket of ABP1 is crucial for its
gain-of-function cellular and developmental roles,” Journal of Experimental
Botany, vol. 66, no. 16. Oxford University Press, pp. 5055–5065, 2015.
ista: Grones P, Chen X, Simon S, Kaufmann W, De Rycke R, Nodzyński T, Zažímalová
E, Friml J. 2015. Auxin-binding pocket of ABP1 is crucial for its gain-of-function
cellular and developmental roles. Journal of Experimental Botany. 66(16), 5055–5065.
mla: Grones, Peter, et al. “Auxin-Binding Pocket of ABP1 Is Crucial for Its Gain-of-Function
Cellular and Developmental Roles.” Journal of Experimental Botany, vol.
66, no. 16, Oxford University Press, 2015, pp. 5055–65, doi:10.1093/jxb/erv177.
short: P. Grones, X. Chen, S. Simon, W. Kaufmann, R. De Rycke, T. Nodzyński, E.
Zažímalová, J. Friml, Journal of Experimental Botany 66 (2015) 5055–5065.
date_created: 2018-12-11T11:52:44Z
date_published: 2015-08-01T00:00:00Z
date_updated: 2023-02-23T10:04:26Z
day: '01'
department:
- _id: JiFr
- _id: EM-Fac
doi: 10.1093/jxb/erv177
ec_funded: 1
intvolume: ' 66'
issue: '16'
language:
- iso: eng
month: '08'
oa_version: None
page: 5055 - 5065
project:
- _id: 25716A02-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '282300'
name: Polarity and subcellular dynamics in plants
publication: Journal of Experimental Botany
publication_status: published
publisher: Oxford University Press
publist_id: '5609'
quality_controlled: '1'
scopus_import: 1
status: public
title: Auxin-binding pocket of ABP1 is crucial for its gain-of-function cellular and
developmental roles
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 66
year: '2015'
...