---
_id: '8138'
abstract:
- lang: eng
text: Directional transport of the phytohormone auxin is a versatile, plant-specific
mechanism regulating many aspects of plant development. The recently identified
plant hormones, strigolactones (SLs), are implicated in many plant traits; among
others, they modify the phenotypic output of PIN-FORMED (PIN) auxin transporters
for fine-tuning of growth and developmental responses. Here, we show in pea and
Arabidopsis that SLs target processes dependent on the canalization of auxin flow,
which involves auxin feedback on PIN subcellular distribution. D14 receptor- and
MAX2 F-box-mediated SL signaling inhibits the formation of auxin-conducting channels
after wounding or from artificial auxin sources, during vasculature de novo formation
and regeneration. At the cellular level, SLs interfere with auxin effects on PIN
polar targeting, constitutive PIN trafficking as well as clathrin-mediated endocytosis.
Our results identify a non-transcriptional mechanism of SL action, uncoupling
auxin feedback on PIN polarity and trafficking, thereby regulating vascular tissue
formation and regeneration.
acknowledgement: We are grateful to David Nelson for providing published materials
and extremely helpful comments, and Elizabeth Dun and Christine Beveridge for helpful
discussions. The research leading to these results has received funding from the
European Research Council (ERC) under the European Union's Horizon 2020 research
and innovation programme (742985). This work was also supported by the Beijing Municipal
Natural Science Foundation (5192011), Beijing Outstanding University Discipline
Program, the National Natural Science Foundation of China (31370309), CEITEC 2020
(LQ1601) project with financial contribution made by the Ministry of Education,
Youth and Sports of the Czech Republic within special support paid from the National
Program of Sustainability II funds, Australian Research Council (FT180100081), and
China Postdoctoral Science Foundation (2019M660864).
article_processing_charge: No
article_type: original
author:
- first_name: J
full_name: Zhang, J
last_name: Zhang
- first_name: E
full_name: Mazur, E
last_name: Mazur
- first_name: J
full_name: Balla, J
last_name: Balla
- first_name: Michelle C
full_name: Gallei, Michelle C
id: 35A03822-F248-11E8-B48F-1D18A9856A87
last_name: Gallei
orcid: 0000-0003-1286-7368
- first_name: P
full_name: Kalousek, P
last_name: Kalousek
- first_name: Z
full_name: Medveďová, Z
last_name: Medveďová
- first_name: Y
full_name: Li, Y
last_name: Li
- first_name: Y
full_name: Wang, Y
last_name: Wang
- first_name: Tomas
full_name: Prat, Tomas
id: 3DA3BFEE-F248-11E8-B48F-1D18A9856A87
last_name: Prat
- first_name: Mina K
full_name: Vasileva, Mina K
id: 3407EB18-F248-11E8-B48F-1D18A9856A87
last_name: Vasileva
- first_name: V
full_name: Reinöhl, V
last_name: Reinöhl
- first_name: S
full_name: Procházka, S
last_name: Procházka
- first_name: R
full_name: Halouzka, R
last_name: Halouzka
- first_name: P
full_name: Tarkowski, P
last_name: Tarkowski
- first_name: C
full_name: Luschnig, C
last_name: Luschnig
- first_name: PB
full_name: Brewer, PB
last_name: Brewer
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Zhang J, Mazur E, Balla J, et al. Strigolactones inhibit auxin feedback on
PIN-dependent auxin transport canalization. Nature Communications. 2020;11(1):3508.
doi:10.1038/s41467-020-17252-y
apa: Zhang, J., Mazur, E., Balla, J., Gallei, M. C., Kalousek, P., Medveďová, Z.,
… Friml, J. (2020). Strigolactones inhibit auxin feedback on PIN-dependent auxin
transport canalization. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-020-17252-y
chicago: Zhang, J, E Mazur, J Balla, Michelle C Gallei, P Kalousek, Z Medveďová,
Y Li, et al. “Strigolactones Inhibit Auxin Feedback on PIN-Dependent Auxin Transport
Canalization.” Nature Communications. Springer Nature, 2020. https://doi.org/10.1038/s41467-020-17252-y.
ieee: J. Zhang et al., “Strigolactones inhibit auxin feedback on PIN-dependent
auxin transport canalization,” Nature Communications, vol. 11, no. 1. Springer
Nature, p. 3508, 2020.
ista: Zhang J, Mazur E, Balla J, Gallei MC, Kalousek P, Medveďová Z, Li Y, Wang
Y, Prat T, Vasileva MK, Reinöhl V, Procházka S, Halouzka R, Tarkowski P, Luschnig
C, Brewer P, Friml J. 2020. Strigolactones inhibit auxin feedback on PIN-dependent
auxin transport canalization. Nature Communications. 11(1), 3508.
mla: Zhang, J., et al. “Strigolactones Inhibit Auxin Feedback on PIN-Dependent Auxin
Transport Canalization.” Nature Communications, vol. 11, no. 1, Springer
Nature, 2020, p. 3508, doi:10.1038/s41467-020-17252-y.
short: J. Zhang, E. Mazur, J. Balla, M.C. Gallei, P. Kalousek, Z. Medveďová, Y.
Li, Y. Wang, T. Prat, M.K. Vasileva, V. Reinöhl, S. Procházka, R. Halouzka, P.
Tarkowski, C. Luschnig, P. Brewer, J. Friml, Nature Communications 11 (2020) 3508.
date_created: 2020-07-21T08:58:07Z
date_published: 2020-07-14T00:00:00Z
date_updated: 2023-08-22T08:13:44Z
day: '14'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.1038/s41467-020-17252-y
ec_funded: 1
external_id:
isi:
- '000550062200004'
pmid:
- '32665554'
file:
- access_level: open_access
content_type: application/pdf
creator: dernst
date_created: 2020-07-22T08:32:55Z
date_updated: 2020-07-22T08:32:55Z
file_id: '8148'
file_name: 2020_NatureComm_Zhang.pdf
file_size: 1759490
relation: main_file
success: 1
file_date_updated: 2020-07-22T08:32:55Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
issue: '1'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: '3508'
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
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
record:
- id: '11626'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Strigolactones inhibit auxin feedback on PIN-dependent auxin transport canalization
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: '7172'
abstract:
- lang: eng
text: "The development and growth of Arabidopsis thaliana is regulated by a combination
of genetic programing and also by the environmental influences. An important role
in these processes play the phytohormones and among them, auxin is crucial as
it controls many important functions. It is transported through the whole plant
body by creating local and temporal concentration maxima and minima, which have
an impact on the cell status, tissue and organ identity. Auxin has the property
to undergo a directional and finely regulated cell-to-cell transport, which is
enabled by the transport proteins, localized on the plasma membrane. An important
role in this process have the PIN auxin efflux proteins, which have an asymmetric/polar
subcellular localization and determine the directionality of the auxin transport.
During the last years, there were significant advances in understanding how the
trafficking molecular machineries function, including studies on molecular interactions,
function, subcellular localization and intracellular distribution. However, there
is still a lack of detailed characterization on the steps of endocytosis, exocytosis,
endocytic recycling and degradation. Due to this fact, I focused on the identification
of novel trafficking factors and better characterization of the intracellular
trafficking pathways. My PhD thesis consists of an introductory chapter, three
experimental chapters, a chapter containing general discussion, conclusions and
perspectives and also an appendix chapter with published collaborative papers.\r\nThe
first chapter is separated in two different parts: I start by a general introduction
to auxin biology and then I introduce the trafficking pathways in the model plant
Arabidopsis thaliana. Then, I explain also the phosphorylation-signals for polar
targeting and also the roles of the phytohormone strigolactone.\r\nThe second
chapter includes the characterization of bar1/sacsin mutant, which was identified
in a forward genetic screen for novel trafficking components in Arabidopsis thaliana,
where by the implementation of an EMS-treated pPIN1::PIN1-GFP marker line and
by using the established inhibitor of ARF-GEFs, Brefeldin A (BFA) as a tool to
study trafficking processes, we identified a novel factor, which is mediating
the adaptation of the plant cell to ARF-GEF inhibition. The mutation is in a previously
uncharacterized gene, encoding a very big protein that we, based on its homologies,
called SACSIN with domains suggesting roles as a molecular chaperon or as a component
of the ubiquitin-proteasome system. Our physiology and imaging studies revealed
that SACSIN is a crucial plant cell component of the adaptation to the ARF-GEF
inhibition.\r\nThe third chapter includes six subchapters, where I focus on the
role of the phytohormone strigolactone, which interferes with auxin feedback on
PIN internalization. Strigolactone moderates the polar auxin transport by increasing
the internalization of the PIN auxin efflux carriers, which reduces the canalization
related growth responses. In addition, I also studied the role of phosphorylation
in the strigolactone regulation of auxin feedback on PIN internalization. In this
chapter I also present my results on the MAX2-dependence of strigolactone-mediated
root growth inhibition and I also share my results on the auxin metabolomics profiling
after application of GR24.\r\nIn the fourth chapter I studied the effect of two
small molecules ES-9 and ES9-17, which were identified from a collection of small
molecules with the property to impair the clathrin-mediated endocytosis.\r\nIn
the fifth chapter, I discuss all my observations and experimental findings and
suggest alternative hypothesis to interpret my results.\r\nIn the appendix there
are three collaborative published projects. In the first, I participated in the
characterization of the role of ES9 as a small molecule, which is inhibitor of
clathrin- mediated endocytosis in different model organisms. In the second paper,
I contributed to the characterization of another small molecule ES9-17, which
is a non-protonophoric analog of ES9 and also impairs the clathrin-mediated endocytosis
not only in plant cells, but also in mammalian HeLa cells. Last but not least,
I also attach another paper, where I tried to establish the grafting method as
a technique in our lab to study canalization related processes."
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Mina K
full_name: Vasileva, Mina K
id: 3407EB18-F248-11E8-B48F-1D18A9856A87
last_name: Vasileva
citation:
ama: Vasileva MK. Molecular mechanisms of endomembrane trafficking in Arabidopsis
thaliana. 2019. doi:10.15479/AT:ISTA:7172
apa: Vasileva, M. K. (2019). Molecular mechanisms of endomembrane trafficking
in Arabidopsis thaliana. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:7172
chicago: Vasileva, Mina K. “Molecular Mechanisms of Endomembrane Trafficking in
Arabidopsis Thaliana.” Institute of Science and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:7172.
ieee: M. K. Vasileva, “Molecular mechanisms of endomembrane trafficking in Arabidopsis
thaliana,” Institute of Science and Technology Austria, 2019.
ista: Vasileva MK. 2019. Molecular mechanisms of endomembrane trafficking in Arabidopsis
thaliana. Institute of Science and Technology Austria.
mla: Vasileva, Mina K. Molecular Mechanisms of Endomembrane Trafficking in Arabidopsis
Thaliana. Institute of Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:7172.
short: M.K. Vasileva, Molecular Mechanisms of Endomembrane Trafficking in Arabidopsis
Thaliana, Institute of Science and Technology Austria, 2019.
date_created: 2019-12-11T21:24:39Z
date_published: 2019-12-12T00:00:00Z
date_updated: 2025-05-07T11:12:29Z
day: '12'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: JiFr
doi: 10.15479/AT:ISTA:7172
file:
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content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: mvasilev
date_created: 2019-12-12T09:32:36Z
date_updated: 2020-07-14T12:47:51Z
file_id: '7175'
file_name: Thesis_Mina_final_upload_7.docx
file_size: 20454014
relation: source_file
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checksum: 3882c4585e46c9cfb486e4225cad54ab
content_type: application/pdf
creator: mvasilev
date_created: 2019-12-12T09:33:10Z
date_updated: 2020-07-14T12:47:51Z
file_id: '7176'
file_name: Thesis_Mina_final_upload_7.pdf
file_size: 11565025
relation: main_file
file_date_updated: 2020-07-14T12:47:51Z
has_accepted_license: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: '192'
publication_identifier:
eissn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '6377'
relation: part_of_dissertation
status: public
- id: '449'
relation: part_of_dissertation
status: public
- id: '1346'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
title: Molecular mechanisms of endomembrane trafficking in Arabidopsis thaliana
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2019'
...
---
_id: '6377'
abstract:
- lang: eng
text: Clathrin-mediated endocytosis (CME) is a highly conserved and essential cellular
process in eukaryotic cells, but its dynamic and vital nature makes it challenging
to study using classical genetics tools. In contrast, although small molecules
can acutely and reversibly perturb CME, the few chemical CME inhibitors that have
been applied to plants are either ineffective or show undesirable side effects.
Here, we identify the previously described endosidin9 (ES9) as an inhibitor of
clathrin heavy chain (CHC) function in both Arabidopsis and human cells through
affinity-based target isolation, in vitro binding studies and X-ray crystallography.
Moreover, we present a chemically improved ES9 analog, ES9-17, which lacks the
undesirable side effects of ES9 while retaining the ability to target CHC. ES9
and ES9-17 have expanded the chemical toolbox used to probe CHC function, and
present chemical scaffolds for further design of more specific and potent CHC
inhibitors across different systems.
article_processing_charge: No
article_type: original
author:
- first_name: Wim
full_name: Dejonghe, Wim
last_name: Dejonghe
- first_name: Isha
full_name: Sharma, Isha
last_name: Sharma
- first_name: Bram
full_name: Denoo, Bram
last_name: Denoo
- first_name: Steven
full_name: De Munck, Steven
last_name: De Munck
- first_name: Qing
full_name: Lu, Qing
last_name: Lu
- first_name: Kiril
full_name: Mishev, Kiril
last_name: Mishev
- first_name: Haydar
full_name: Bulut, Haydar
last_name: Bulut
- first_name: Evelien
full_name: Mylle, Evelien
last_name: Mylle
- first_name: Riet
full_name: De Rycke, Riet
last_name: De Rycke
- first_name: Mina K
full_name: Vasileva, Mina K
id: 3407EB18-F248-11E8-B48F-1D18A9856A87
last_name: Vasileva
- first_name: Daniel V.
full_name: Savatin, Daniel V.
last_name: Savatin
- first_name: Wim
full_name: Nerinckx, Wim
last_name: Nerinckx
- first_name: An
full_name: Staes, An
last_name: Staes
- first_name: Andrzej
full_name: Drozdzecki, Andrzej
last_name: Drozdzecki
- first_name: Dominique
full_name: Audenaert, Dominique
last_name: Audenaert
- first_name: Klaas
full_name: Yperman, Klaas
last_name: Yperman
- first_name: Annemieke
full_name: Madder, Annemieke
last_name: Madder
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Daniël
full_name: Van Damme, Daniël
last_name: Van Damme
- first_name: Kris
full_name: Gevaert, Kris
last_name: Gevaert
- first_name: Volker
full_name: Haucke, Volker
last_name: Haucke
- first_name: Savvas N.
full_name: Savvides, Savvas N.
last_name: Savvides
- first_name: Johan
full_name: Winne, Johan
last_name: Winne
- first_name: Eugenia
full_name: Russinova, Eugenia
last_name: Russinova
citation:
ama: Dejonghe W, Sharma I, Denoo B, et al. Disruption of endocytosis through chemical
inhibition of clathrin heavy chain function. Nature Chemical Biology. 2019;15(6):641–649.
doi:10.1038/s41589-019-0262-1
apa: Dejonghe, W., Sharma, I., Denoo, B., De Munck, S., Lu, Q., Mishev, K., … Russinova,
E. (2019). Disruption of endocytosis through chemical inhibition of clathrin heavy
chain function. Nature Chemical Biology. Springer Nature. https://doi.org/10.1038/s41589-019-0262-1
chicago: Dejonghe, Wim, Isha Sharma, Bram Denoo, Steven De Munck, Qing Lu, Kiril
Mishev, Haydar Bulut, et al. “Disruption of Endocytosis through Chemical Inhibition
of Clathrin Heavy Chain Function.” Nature Chemical Biology. Springer Nature,
2019. https://doi.org/10.1038/s41589-019-0262-1.
ieee: W. Dejonghe et al., “Disruption of endocytosis through chemical inhibition
of clathrin heavy chain function,” Nature Chemical Biology, vol. 15, no.
6. Springer Nature, pp. 641–649, 2019.
ista: Dejonghe W, Sharma I, Denoo B, De Munck S, Lu Q, Mishev K, Bulut H, Mylle
E, De Rycke R, Vasileva MK, Savatin DV, Nerinckx W, Staes A, Drozdzecki A, Audenaert
D, Yperman K, Madder A, Friml J, Van Damme D, Gevaert K, Haucke V, Savvides SN,
Winne J, Russinova E. 2019. Disruption of endocytosis through chemical inhibition
of clathrin heavy chain function. Nature Chemical Biology. 15(6), 641–649.
mla: Dejonghe, Wim, et al. “Disruption of Endocytosis through Chemical Inhibition
of Clathrin Heavy Chain Function.” Nature Chemical Biology, vol. 15, no.
6, Springer Nature, 2019, pp. 641–649, doi:10.1038/s41589-019-0262-1.
short: W. Dejonghe, I. Sharma, B. Denoo, S. De Munck, Q. Lu, K. Mishev, H. Bulut,
E. Mylle, R. De Rycke, M.K. Vasileva, D.V. Savatin, W. Nerinckx, A. Staes, A.
Drozdzecki, D. Audenaert, K. Yperman, A. Madder, J. Friml, D. Van Damme, K. Gevaert,
V. Haucke, S.N. Savvides, J. Winne, E. Russinova, Nature Chemical Biology 15 (2019)
641–649.
date_created: 2019-05-05T21:59:11Z
date_published: 2019-06-01T00:00:00Z
date_updated: 2023-09-07T12:54:35Z
day: '01'
department:
- _id: JiFr
doi: 10.1038/s41589-019-0262-1
external_id:
isi:
- '000468195600018'
intvolume: ' 15'
isi: 1
issue: '6'
language:
- iso: eng
month: '06'
oa_version: None
page: 641–649
publication: Nature Chemical Biology
publication_identifier:
eissn:
- '15524469'
issn:
- '15524450'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
record:
- id: '7172'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Disruption of endocytosis through chemical inhibition of clathrin heavy chain
function
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 15
year: '2019'
...
---
_id: '449'
abstract:
- lang: eng
text: Auxin is unique among plant hormones due to its directional transport that
is mediated by the polarly distributed PIN auxin transporters at the plasma membrane.
The canalization hypothesis proposes that the auxin feedback on its polar flow
is a crucial, plant-specific mechanism mediating multiple self-organizing developmental
processes. Here, we used the auxin effect on the PIN polar localization in Arabidopsis
thaliana roots as a proxy for the auxin feedback on the PIN polarity during canalization.
We performed microarray experiments to find regulators of this process that act
downstream of auxin. We identified genes that were transcriptionally regulated
by auxin in an AXR3/IAA17- and ARF7/ARF19-dependent manner. Besides the known
components of the PIN polarity, such as PID and PIP5K kinases, a number of potential
new regulators were detected, among which the WRKY23 transcription factor, which
was characterized in more detail. Gain- and loss-of-function mutants confirmed
a role for WRKY23 in mediating the auxin effect on the PIN polarity. Accordingly,
processes requiring auxin-mediated PIN polarity rearrangements, such as vascular
tissue development during leaf venation, showed a higher WRKY23 expression and
required the WRKY23 activity. Our results provide initial insights into the auxin
transcriptional network acting upstream of PIN polarization and, potentially,
canalization-mediated plant development.
article_processing_charge: Yes
author:
- first_name: Tomas
full_name: Prat, Tomas
id: 3DA3BFEE-F248-11E8-B48F-1D18A9856A87
last_name: Prat
- first_name: Jakub
full_name: Hajny, Jakub
id: 4800CC20-F248-11E8-B48F-1D18A9856A87
last_name: Hajny
orcid: 0000-0003-2140-7195
- first_name: Wim
full_name: Grunewald, Wim
last_name: Grunewald
- first_name: Mina K
full_name: Vasileva, Mina K
id: 3407EB18-F248-11E8-B48F-1D18A9856A87
last_name: Vasileva
- first_name: Gergely
full_name: Molnar, Gergely
id: 34F1AF46-F248-11E8-B48F-1D18A9856A87
last_name: Molnar
- first_name: Ricardo
full_name: Tejos, Ricardo
last_name: Tejos
- first_name: Markus
full_name: Schmid, Markus
last_name: Schmid
- first_name: Michael
full_name: Sauer, Michael
last_name: Sauer
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Prat T, Hajny J, Grunewald W, et al. WRKY23 is a component of the transcriptional
network mediating auxin feedback on PIN polarity. PLoS Genetics. 2018;14(1).
doi:10.1371/journal.pgen.1007177
apa: Prat, T., Hajny, J., Grunewald, W., Vasileva, M. K., Molnar, G., Tejos, R.,
… Friml, J. (2018). WRKY23 is a component of the transcriptional network mediating
auxin feedback on PIN polarity. PLoS Genetics. Public Library of Science.
https://doi.org/10.1371/journal.pgen.1007177
chicago: Prat, Tomas, Jakub Hajny, Wim Grunewald, Mina K Vasileva, Gergely Molnar,
Ricardo Tejos, Markus Schmid, Michael Sauer, and Jiří Friml. “WRKY23 Is a Component
of the Transcriptional Network Mediating Auxin Feedback on PIN Polarity.” PLoS
Genetics. Public Library of Science, 2018. https://doi.org/10.1371/journal.pgen.1007177.
ieee: T. Prat et al., “WRKY23 is a component of the transcriptional network
mediating auxin feedback on PIN polarity,” PLoS Genetics, vol. 14, no.
1. Public Library of Science, 2018.
ista: Prat T, Hajny J, Grunewald W, Vasileva MK, Molnar G, Tejos R, Schmid M, Sauer
M, Friml J. 2018. WRKY23 is a component of the transcriptional network mediating
auxin feedback on PIN polarity. PLoS Genetics. 14(1).
mla: Prat, Tomas, et al. “WRKY23 Is a Component of the Transcriptional Network Mediating
Auxin Feedback on PIN Polarity.” PLoS Genetics, vol. 14, no. 1, Public
Library of Science, 2018, doi:10.1371/journal.pgen.1007177.
short: T. Prat, J. Hajny, W. Grunewald, M.K. Vasileva, G. Molnar, R. Tejos, M. Schmid,
M. Sauer, J. Friml, PLoS Genetics 14 (2018).
date_created: 2018-12-11T11:46:32Z
date_published: 2018-01-29T00:00:00Z
date_updated: 2025-05-07T11:12:28Z
day: '29'
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department:
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doi: 10.1371/journal.pgen.1007177
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isi:
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name: Polarity and subcellular dynamics in plants
publication: PLoS Genetics
publication_status: published
publisher: Public Library of Science
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status: public
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relation: dissertation_contains
status: public
- id: '8822'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: WRKY23 is a component of the transcriptional network mediating auxin feedback
on PIN polarity
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 14
year: '2018'
...
---
_id: '1346'
abstract:
- lang: eng
text: ATP production requires the establishment of an electrochemical proton gradient
across the inner mitochondrial membrane. Mitochondrial uncouplers dissipate this
proton gradient and disrupt numerous cellular processes, including vesicular trafficking,
mainly through energy depletion. Here we show that Endosidin9 (ES9), a novel mitochondrial
uncoupler, is a potent inhibitor of clathrin-mediated endocytosis (CME) in different
systems and that ES9 induces inhibition of CME not because of its effect on cellular
ATP, but rather due to its protonophore activity that leads to cytoplasm acidification.
We show that the known tyrosine kinase inhibitor tyrphostinA23, which is routinely
used to block CME, displays similar properties, thus questioning its use as a
specific inhibitor of cargo recognition by the AP-2 adaptor complex via tyrosine
motif-based endocytosis signals. Furthermore, we show that cytoplasm acidification
dramatically affects the dynamics and recruitment of clathrin and associated adaptors,
and leads to reduction of phosphatidylinositol 4,5-biphosphate from the plasma
membrane.
acknowledgement: "We thank Yvon Jaillais, Ikuko Hara-Nishimura, Akihiko Nakano, Takashi
Ueda and Jinxing Lin for providing materials, Natasha Raikhel, Glenn Hicks, Steffen
Vanneste, and Ricardo Tejos for useful suggestions, Patrick Callaerts for providing
S2 Drosophila cell cultures, Michael Sixt for providing HeLa cells, Annick Bleys
for literature searches, VIB Bio Imaging Core for help with imaging conditions and
Martine De Cock for help in preparing the article. This work was supported by the
Agency for Innovation by Science\r\nand Technology for a pre-doctoral fellowship
to W.D.; the Research fund KU Leuven\r\n(GOA), a Methusalem grant of the Flemish
government and VIB to S.K., J.K. and P.V.;\r\nby the Netherlands Organisation for
Scientific Research (NWO) for ALW grants\r\n846.11.002 (C.T.) and 867.15.020 (T.M.);
the European Research Council (project\r\nERC-2011-StG-20101109 PSDP) (to J.F.);
a European Research Council (ERC) Starting\r\nGrant (grant 260678) (to P.V.), the
Research Foundation-Flanders (grants G.0747.09,\r\nG094011 and G095511) (to P.V.),
the Hercules Foundation, an Interuniversity Attraction\r\nPoles Poles Program, initiated
by the Belgian State, Science Policy Office (to P.V.),\r\nthe Swedish VetenskapsRådet
grant to O.K., the Ghent University ‘Bijzonder\r\nOnderzoek Fonds’ (BOF) for a predoctoral
fellowship to F.A.O.-M., the Research\r\nFoundation-Flanders (FWO) to K.M. and E.R."
article_number: '11710'
author:
- first_name: Wim
full_name: Dejonghe, Wim
last_name: Dejonghe
- first_name: Sabine
full_name: Kuenen, Sabine
last_name: Kuenen
- first_name: Evelien
full_name: Mylle, Evelien
last_name: Mylle
- first_name: Mina K
full_name: Vasileva, Mina K
id: 3407EB18-F248-11E8-B48F-1D18A9856A87
last_name: Vasileva
- first_name: Olivier
full_name: Keech, Olivier
last_name: Keech
- first_name: Corrado
full_name: Viotti, Corrado
last_name: Viotti
- first_name: Jef
full_name: Swerts, Jef
last_name: Swerts
- first_name: Matyas
full_name: Fendrych, Matyas
id: 43905548-F248-11E8-B48F-1D18A9856A87
last_name: Fendrych
orcid: 0000-0002-9767-8699
- first_name: Fausto
full_name: Ortiz Morea, Fausto
last_name: Ortiz Morea
- first_name: Kiril
full_name: Mishev, Kiril
last_name: Mishev
- first_name: Simon
full_name: Delang, Simon
last_name: Delang
- first_name: Stefan
full_name: Scholl, Stefan
last_name: Scholl
- first_name: Xavier
full_name: Zarza, Xavier
last_name: Zarza
- first_name: Mareike
full_name: Heilmann, Mareike
last_name: Heilmann
- first_name: Jiorgos
full_name: Kourelis, Jiorgos
last_name: Kourelis
- first_name: Jaroslaw
full_name: Kasprowicz, Jaroslaw
last_name: Kasprowicz
- first_name: Le
full_name: Nguyen, Le
last_name: Nguyen
- first_name: Andrzej
full_name: Drozdzecki, Andrzej
last_name: Drozdzecki
- first_name: Isabelle
full_name: Van Houtte, Isabelle
last_name: Van Houtte
- first_name: Anna
full_name: Szatmári, Anna
last_name: Szatmári
- first_name: Mateusz
full_name: Majda, Mateusz
last_name: Majda
- first_name: Gary
full_name: Baisa, Gary
last_name: Baisa
- first_name: Sebastian
full_name: Bednarek, Sebastian
last_name: Bednarek
- first_name: Stéphanie
full_name: Robert, Stéphanie
last_name: Robert
- first_name: Dominique
full_name: Audenaert, Dominique
last_name: Audenaert
- first_name: Christa
full_name: Testerink, Christa
last_name: Testerink
- first_name: Teun
full_name: Munnik, Teun
last_name: Munnik
- first_name: Daniël
full_name: Van Damme, Daniël
last_name: Van Damme
- first_name: Ingo
full_name: Heilmann, Ingo
last_name: Heilmann
- first_name: Karin
full_name: Schumacher, Karin
last_name: Schumacher
- first_name: Johan
full_name: Winne, Johan
last_name: Winne
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Patrik
full_name: Verstreken, Patrik
last_name: Verstreken
- first_name: Eugenia
full_name: Russinova, Eugenia
last_name: Russinova
citation:
ama: Dejonghe W, Kuenen S, Mylle E, et al. Mitochondrial uncouplers inhibit clathrin-mediated
endocytosis largely through cytoplasmic acidification. Nature Communications.
2016;7. doi:10.1038/ncomms11710
apa: Dejonghe, W., Kuenen, S., Mylle, E., Vasileva, M. K., Keech, O., Viotti, C.,
… Russinova, E. (2016). Mitochondrial uncouplers inhibit clathrin-mediated endocytosis
largely through cytoplasmic acidification. Nature Communications. Nature
Publishing Group. https://doi.org/10.1038/ncomms11710
chicago: Dejonghe, Wim, Sabine Kuenen, Evelien Mylle, Mina K Vasileva, Olivier Keech,
Corrado Viotti, Jef Swerts, et al. “Mitochondrial Uncouplers Inhibit Clathrin-Mediated
Endocytosis Largely through Cytoplasmic Acidification.” Nature Communications.
Nature Publishing Group, 2016. https://doi.org/10.1038/ncomms11710.
ieee: W. Dejonghe et al., “Mitochondrial uncouplers inhibit clathrin-mediated
endocytosis largely through cytoplasmic acidification,” Nature Communications,
vol. 7. Nature Publishing Group, 2016.
ista: Dejonghe W, Kuenen S, Mylle E, Vasileva MK, Keech O, Viotti C, Swerts J, Fendrych
M, Ortiz Morea F, Mishev K, Delang S, Scholl S, Zarza X, Heilmann M, Kourelis
J, Kasprowicz J, Nguyen L, Drozdzecki A, Van Houtte I, Szatmári A, Majda M, Baisa
G, Bednarek S, Robert S, Audenaert D, Testerink C, Munnik T, Van Damme D, Heilmann
I, Schumacher K, Winne J, Friml J, Verstreken P, Russinova E. 2016. Mitochondrial
uncouplers inhibit clathrin-mediated endocytosis largely through cytoplasmic acidification.
Nature Communications. 7, 11710.
mla: Dejonghe, Wim, et al. “Mitochondrial Uncouplers Inhibit Clathrin-Mediated Endocytosis
Largely through Cytoplasmic Acidification.” Nature Communications, vol.
7, 11710, Nature Publishing Group, 2016, doi:10.1038/ncomms11710.
short: W. Dejonghe, S. Kuenen, E. Mylle, M.K. Vasileva, O. Keech, C. Viotti, J.
Swerts, M. Fendrych, F. Ortiz Morea, K. Mishev, S. Delang, S. Scholl, X. Zarza,
M. Heilmann, J. Kourelis, J. Kasprowicz, L. Nguyen, A. Drozdzecki, I. Van Houtte,
A. Szatmári, M. Majda, G. Baisa, S. Bednarek, S. Robert, D. Audenaert, C. Testerink,
T. Munnik, D. Van Damme, I. Heilmann, K. Schumacher, J. Winne, J. Friml, P. Verstreken,
E. Russinova, Nature Communications 7 (2016).
date_created: 2018-12-11T11:51:30Z
date_published: 2016-06-08T00:00:00Z
date_updated: 2023-09-07T12:54:35Z
day: '08'
ddc:
- '570'
department:
- _id: JiFr
doi: 10.1038/ncomms11710
ec_funded: 1
file:
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checksum: e8dc81b3e44db5a7718d7f1501ce1aa7
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creator: system
date_created: 2018-12-12T10:18:47Z
date_updated: 2020-07-14T12:44:45Z
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file_date_updated: 2020-07-14T12:44:45Z
has_accepted_license: '1'
intvolume: ' 7'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
project:
- _id: 25716A02-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '282300'
name: Polarity and subcellular dynamics in plants
publication: Nature Communications
publication_status: published
publisher: Nature Publishing Group
publist_id: '5906'
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quality_controlled: '1'
related_material:
record:
- id: '7172'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Mitochondrial uncouplers inhibit clathrin-mediated endocytosis largely through
cytoplasmic acidification
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 7
year: '2016'
...