---
_id: '14316'
abstract:
- lang: eng
text: Clathrin-mediated vesicle trafficking plays central roles in post-Golgi transport.
In yeast (Saccharomyces cerevisiae), the AP-1 complex and GGA adaptors are predicted
to generate distinct transport vesicles at the trans-Golgi network (TGN), and
the epsin-related proteins Ent3p and Ent5p (collectively Ent3p/5p) act as accessories
for these adaptors. Recently, we showed that vesicle transport from the TGN is
crucial for yeast Rab5 (Vps21p)-mediated endosome formation, and that Ent3p/5p
are crucial for this process, whereas AP-1 and GGA adaptors are dispensable. However,
these observations were incompatible with previous studies showing that these
adaptors are required for Ent3p/5p recruitment to the TGN, and thus the overall
mechanism responsible for regulation of Vps21p activity remains ambiguous. Here,
we investigated the functional relationships between clathrin adaptors in post-Golgi-mediated
Vps21p activation. We show that AP-1 disruption in the ent3Δ5Δ mutant impaired
transport of the Vps21p guanine nucleotide exchange factor Vps9p transport to
the Vps21p compartment and severely reduced Vps21p activity. Additionally, GGA
adaptors, the phosphatidylinositol-4-kinase Pik1p and Rab11 GTPases Ypt31p and
Ypt32p were found to have partially overlapping functions for recruitment of AP-1
and Ent3p/5p to the TGN. These findings suggest a distinct role of clathrin adaptors
for Vps21p activation in the TGN–endosome trafficking pathway.
article_number: jcs261448
article_processing_charge: No
article_type: original
author:
- first_name: Makoto
full_name: Nagano, Makoto
last_name: Nagano
- first_name: Kaito
full_name: Aoshima, Kaito
last_name: Aoshima
- first_name: Hiroki
full_name: Shimamura, Hiroki
last_name: Shimamura
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
- first_name: Junko Y.
full_name: Toshima, Junko Y.
last_name: Toshima
- first_name: Jiro
full_name: Toshima, Jiro
last_name: Toshima
citation:
ama: Nagano M, Aoshima K, Shimamura H, Siekhaus DE, Toshima JY, Toshima J. Distinct
role of TGN-resident clathrin adaptors for Vps21p activation in the TGN-endosome
trafficking pathway. Journal of Cell Science. 2023;136(17). doi:10.1242/jcs.261448
apa: Nagano, M., Aoshima, K., Shimamura, H., Siekhaus, D. E., Toshima, J. Y., &
Toshima, J. (2023). Distinct role of TGN-resident clathrin adaptors for Vps21p
activation in the TGN-endosome trafficking pathway. Journal of Cell Science.
The Company of Biologists. https://doi.org/10.1242/jcs.261448
chicago: Nagano, Makoto, Kaito Aoshima, Hiroki Shimamura, Daria E Siekhaus, Junko
Y. Toshima, and Jiro Toshima. “Distinct Role of TGN-Resident Clathrin Adaptors
for Vps21p Activation in the TGN-Endosome Trafficking Pathway.” Journal of
Cell Science. The Company of Biologists, 2023. https://doi.org/10.1242/jcs.261448.
ieee: M. Nagano, K. Aoshima, H. Shimamura, D. E. Siekhaus, J. Y. Toshima, and J.
Toshima, “Distinct role of TGN-resident clathrin adaptors for Vps21p activation
in the TGN-endosome trafficking pathway,” Journal of Cell Science, vol.
136, no. 17. The Company of Biologists, 2023.
ista: Nagano M, Aoshima K, Shimamura H, Siekhaus DE, Toshima JY, Toshima J. 2023.
Distinct role of TGN-resident clathrin adaptors for Vps21p activation in the TGN-endosome
trafficking pathway. Journal of Cell Science. 136(17), jcs261448.
mla: Nagano, Makoto, et al. “Distinct Role of TGN-Resident Clathrin Adaptors for
Vps21p Activation in the TGN-Endosome Trafficking Pathway.” Journal of Cell
Science, vol. 136, no. 17, jcs261448, The Company of Biologists, 2023, doi:10.1242/jcs.261448.
short: M. Nagano, K. Aoshima, H. Shimamura, D.E. Siekhaus, J.Y. Toshima, J. Toshima,
Journal of Cell Science 136 (2023).
date_created: 2023-09-10T22:01:12Z
date_published: 2023-09-01T00:00:00Z
date_updated: 2023-09-20T09:14:15Z
day: '01'
department:
- _id: DaSi
doi: 10.1242/jcs.261448
external_id:
pmid:
- '37539494'
intvolume: ' 136'
issue: '17'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2023.03.27.534325
month: '09'
oa: 1
oa_version: Preprint
pmid: 1
publication: Journal of Cell Science
publication_identifier:
eissn:
- 1477-9137
issn:
- 0021-9533
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Distinct role of TGN-resident clathrin adaptors for Vps21p activation in the
TGN-endosome trafficking pathway
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 136
year: '2023'
...
---
_id: '13316'
abstract:
- lang: eng
text: Although budding yeast has been extensively used as a model organism for studying
organelle functions and intracellular vesicle trafficking, whether it possesses
an independent endocytic early/sorting compartment that sorts endocytic cargos
to the endo-lysosomal pathway or the recycling pathway has long been unclear.
The structure and properties of the endocytic early/sorting compartment differ
significantly between organisms; in plant cells, the trans-Golgi network (TGN)
serves this role, whereas in mammalian cells a separate intracellular structure
performs this function. The yeast syntaxin homolog Tlg2p, widely localizing to
the TGN and endosomal compartments, is presumed to act as a Q-SNARE for endocytic
vesicles, but which compartment is the direct target for endocytic vesicles remained
unanswered. Here we demonstrate by high-speed and high-resolution 4D imaging of
fluorescently labeled endocytic cargos that the Tlg2p-residing compartment within
the TGN functions as the early/sorting compartment. After arriving here, endocytic
cargos are recycled to the plasma membrane or transported to the yeast Rab5-residing
endosomal compartment through the pathway requiring the clathrin adaptors GGAs.
Interestingly, Gga2p predominantly localizes at the Tlg2p-residing compartment,
and the deletion of GGAs has little effect on another TGN region where Sec7p is
present but suppresses dynamics of the Tlg2-residing early/sorting compartment,
indicating that the Tlg2p- and Sec7p-residing regions are discrete entities in
the mutant. Thus, the Tlg2p-residing region seems to serve as an early/sorting
compartment and function independently of the Sec7p-residing region within the
TGN.
acknowledgement: 'This work was supported by JSPS KAKENHI grant #18K062291, and the
Takeda Science Foundation to JYT., as well as JSPS KAKENHI grant #19K065710, the
Takeda Science Foundation, and Life Science Foundation of Japan to JT.'
article_number: e84850
article_processing_charge: Yes
article_type: original
author:
- first_name: Junko Y.
full_name: Toshima, Junko Y.
last_name: Toshima
- first_name: Ayana
full_name: Tsukahara, Ayana
last_name: Tsukahara
- first_name: Makoto
full_name: Nagano, Makoto
last_name: Nagano
- first_name: Takuro
full_name: Tojima, Takuro
last_name: Tojima
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
- first_name: Akihiko
full_name: Nakano, Akihiko
last_name: Nakano
- first_name: Jiro
full_name: Toshima, Jiro
last_name: Toshima
citation:
ama: Toshima JY, Tsukahara A, Nagano M, et al. The yeast endocytic early/sorting
compartment exists as an independent sub-compartment within the trans-Golgi network.
eLife. 2023;12. doi:10.7554/eLife.84850
apa: Toshima, J. Y., Tsukahara, A., Nagano, M., Tojima, T., Siekhaus, D. E., Nakano,
A., & Toshima, J. (2023). The yeast endocytic early/sorting compartment exists
as an independent sub-compartment within the trans-Golgi network. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.84850
chicago: Toshima, Junko Y., Ayana Tsukahara, Makoto Nagano, Takuro Tojima, Daria
E Siekhaus, Akihiko Nakano, and Jiro Toshima. “The Yeast Endocytic Early/Sorting
Compartment Exists as an Independent Sub-Compartment within the Trans-Golgi Network.”
ELife. eLife Sciences Publications, 2023. https://doi.org/10.7554/eLife.84850.
ieee: J. Y. Toshima et al., “The yeast endocytic early/sorting compartment
exists as an independent sub-compartment within the trans-Golgi network,” eLife,
vol. 12. eLife Sciences Publications, 2023.
ista: Toshima JY, Tsukahara A, Nagano M, Tojima T, Siekhaus DE, Nakano A, Toshima
J. 2023. The yeast endocytic early/sorting compartment exists as an independent
sub-compartment within the trans-Golgi network. eLife. 12, e84850.
mla: Toshima, Junko Y., et al. “The Yeast Endocytic Early/Sorting Compartment Exists
as an Independent Sub-Compartment within the Trans-Golgi Network.” ELife,
vol. 12, e84850, eLife Sciences Publications, 2023, doi:10.7554/eLife.84850.
short: J.Y. Toshima, A. Tsukahara, M. Nagano, T. Tojima, D.E. Siekhaus, A. Nakano,
J. Toshima, ELife 12 (2023).
date_created: 2023-07-30T22:01:02Z
date_published: 2023-07-21T00:00:00Z
date_updated: 2023-12-13T11:37:36Z
day: '21'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.7554/eLife.84850
external_id:
isi:
- '001035372800001'
pmid:
- '37477116'
file:
- access_level: open_access
checksum: 2af111a00cf5e3a956f7f0fd13199b15
content_type: application/pdf
creator: dernst
date_created: 2023-07-31T07:43:00Z
date_updated: 2023-07-31T07:43:00Z
file_id: '13324'
file_name: 2023_eLife_Toshima.pdf
file_size: 11980913
relation: main_file
success: 1
file_date_updated: 2023-07-31T07:43:00Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: The yeast endocytic early/sorting compartment exists as an independent sub-compartment
within the trans-Golgi network
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2023'
...
---
_id: '10712'
abstract:
- lang: eng
text: Solute carriers are increasingly recognized as participating in a plethora
of pathologies, including cancer. We describe here the involvement of the orphan
solute carrier MFSD1 in the regulation of tumor cell migration. Loss of MFSD1
enabled higher levels of metastasis in a mouse model. We identified an increased
migratory potential in MFSD1-/- tumor cells which was mediated by increased focal
adhesion turn-over, reduced stability of mature inactive β1 integrin, and the
resulting increased integrin activation index. We show that MFSD1 promoted recycling
to the cell surface of endocytosed inactive β1 integrin and thereby protected
β1 integrin from proteolytic degradation; this led to dampening of the integrin
activation index. Furthermore, down-regulation of MFSD1 expression was observed
during early steps of tumorigenesis and higher MFSD1 expression levels correlate
with a better cancer patient prognosis. In sum, we describe a requirement for
endolysosomal MFSD1 in efficient β1 integrin recycling to suppress tumor spread.
acknowledged_ssus:
- _id: Bio
acknowledgement: We thank M. Sixt, A. Leithner, and J. Alanko for helpful advice and
the BioImaging Facility at IST Austria for technical support and assistance. We
thank the Siekhaus Lab for the careful review of the manuscript and their input.
MR and DS were funded by the NO Forschungs- und Bildungsges.m.b.H. (LS16-021) and
IST core funding. MD was funded by Deutsche Forschungsgemeinschaft (DA 1785-1).
article_number: '777634'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: Julia
full_name: Bicher, Julia
id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87
last_name: Bicher
- first_name: Merel
full_name: van Gogh, Merel
last_name: van Gogh
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Rita
full_name: Seeböck, Rita
last_name: Seeböck
- first_name: Bozena
full_name: Szulc, Bozena
last_name: Szulc
- first_name: Markus
full_name: Damme, Markus
last_name: Damme
- first_name: Mariusz
full_name: Olczak, Mariusz
last_name: Olczak
- first_name: Lubor
full_name: Borsig, Lubor
last_name: Borsig
- 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: Roblek M, Bicher J, van Gogh M, et al. The solute carrier MFSD1 decreases β1
integrin’s activation status and thus tumor metastasis. Frontiers in Oncology.
2022;12. doi:10.3389/fonc.2022.777634
apa: Roblek, M., Bicher, J., van Gogh, M., György, A., Seeböck, R., Szulc, B., …
Siekhaus, D. E. (2022). The solute carrier MFSD1 decreases β1 integrin’s activation
status and thus tumor metastasis. Frontiers in Oncology. Frontiers. https://doi.org/10.3389/fonc.2022.777634
chicago: Roblek, Marko, Julia Bicher, Merel van Gogh, Attila György, Rita Seeböck,
Bozena Szulc, Markus Damme, Mariusz Olczak, Lubor Borsig, and Daria E Siekhaus.
“The Solute Carrier MFSD1 Decreases Β1 Integrin’s Activation Status and Thus Tumor
Metastasis.” Frontiers in Oncology. Frontiers, 2022. https://doi.org/10.3389/fonc.2022.777634.
ieee: M. Roblek et al., “The solute carrier MFSD1 decreases β1 integrin’s
activation status and thus tumor metastasis,” Frontiers in Oncology, vol.
12. Frontiers, 2022.
ista: Roblek M, Bicher J, van Gogh M, György A, Seeböck R, Szulc B, Damme M, Olczak
M, Borsig L, Siekhaus DE. 2022. The solute carrier MFSD1 decreases β1 integrin’s
activation status and thus tumor metastasis. Frontiers in Oncology. 12, 777634.
mla: Roblek, Marko, et al. “The Solute Carrier MFSD1 Decreases Β1 Integrin’s Activation
Status and Thus Tumor Metastasis.” Frontiers in Oncology, vol. 12, 777634,
Frontiers, 2022, doi:10.3389/fonc.2022.777634.
short: M. Roblek, J. Bicher, M. van Gogh, A. György, R. Seeböck, B. Szulc, M. Damme,
M. Olczak, L. Borsig, D.E. Siekhaus, Frontiers in Oncology 12 (2022).
date_created: 2022-02-01T10:33:50Z
date_published: 2022-02-08T00:00:00Z
date_updated: 2023-08-02T14:05:44Z
day: '08'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.3389/fonc.2022.777634
external_id:
isi:
- '000760618800001'
file:
- access_level: open_access
checksum: 63dfecf30c5bbf9408b3512bd603f78c
content_type: application/pdf
creator: cchlebak
date_created: 2022-02-08T13:26:40Z
date_updated: 2022-02-08T13:26:40Z
file_id: '10751'
file_name: 2022_FrontiersOncol_Roblek.pdf
file_size: 6303227
relation: main_file
success: 1
file_date_updated: 2022-02-08T13:26:40Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
project:
- _id: 2637E9C0-B435-11E9-9278-68D0E5697425
grant_number: 'LSC16-021 '
name: Investigating the role of the novel major superfamily facilitator transporter
family member MFSD1 in metastasis
publication: Frontiers in Oncology
publication_identifier:
issn:
- 2234-943X
publication_status: published
publisher: Frontiers
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: confirmation
url: https://ist.ac.at/en/news/suppressing-the-spread-of-tumors/
scopus_import: '1'
status: public
title: The solute carrier MFSD1 decreases β1 integrin’s activation status and thus
tumor metastasis
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: 12
year: '2022'
...
---
_id: '10713'
abstract:
- lang: eng
text: Cells migrate through crowded microenvironments within tissues during normal
development, immune response, and cancer metastasis. Although migration through
pores and tracks in the extracellular matrix (ECM) has been well studied, little
is known about cellular traversal into confining cell-dense tissues. We find that
embryonic tissue invasion by Drosophila macrophages requires division of an epithelial
ectodermal cell at the site of entry. Dividing ectodermal cells disassemble ECM
attachment formed by integrin-mediated focal adhesions next to mesodermal cells,
allowing macrophages to move their nuclei ahead and invade between two immediately
adjacent tissues. Invasion efficiency depends on division frequency, but reduction
of adhesion strength allows macrophage entry independently of division. This work
demonstrates that tissue dynamics can regulate cellular infiltration.
acknowledged_ssus:
- _id: Bio
acknowledgement: 'We thank J. Friml, C. Guet, T. Hurd, M. Fendrych and members of
the laboratory for comments on the manuscript; the Bioimaging Facility of IST Austria
for excellent support and T. Lecuit, E. Hafen, R. Levayer and A. Martin for fly
strains. This work was supported by a grant from the Austrian Science Fund FWF:
Lise Meitner Fellowship M2379-B28 to M.A and D.S., and internal funding from IST
Austria to D.S. and EMBL to S.D.R.'
article_processing_charge: No
article_type: original
author:
- first_name: Maria
full_name: Akhmanova, Maria
id: 3425EC26-F248-11E8-B48F-1D18A9856A87
last_name: Akhmanova
orcid: 0000-0003-1522-3162
- first_name: Shamsi
full_name: Emtenani, Shamsi
id: 49D32318-F248-11E8-B48F-1D18A9856A87
last_name: Emtenani
orcid: 0000-0001-6981-6938
- first_name: Daniel
full_name: Krueger, Daniel
last_name: Krueger
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Mariana
full_name: Pereira Guarda, Mariana
id: 6de81d9d-e2f2-11eb-945a-af8bc2a60b26
last_name: Pereira Guarda
- first_name: Mikhail
full_name: Vlasov, Mikhail
last_name: Vlasov
- first_name: Fedor
full_name: Vlasov, Fedor
last_name: Vlasov
- first_name: Andrei
full_name: Akopian, Andrei
last_name: Akopian
- first_name: Aparna
full_name: Ratheesh, Aparna
id: 2F064CFE-F248-11E8-B48F-1D18A9856A87
last_name: Ratheesh
- first_name: Stefano
full_name: De Renzis, Stefano
last_name: De Renzis
- 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: Akhmanova M, Emtenani S, Krueger D, et al. Cell division in tissues enables
macrophage infiltration. Science. 2022;376(6591):394-396. doi:10.1126/science.abj0425
apa: Akhmanova, M., Emtenani, S., Krueger, D., György, A., Pereira Guarda, M., Vlasov,
M., … Siekhaus, D. E. (2022). Cell division in tissues enables macrophage infiltration.
Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.abj0425
chicago: Akhmanova, Maria, Shamsi Emtenani, Daniel Krueger, Attila György, Mariana
Pereira Guarda, Mikhail Vlasov, Fedor Vlasov, et al. “Cell Division in Tissues
Enables Macrophage Infiltration.” Science. American Association for the
Advancement of Science, 2022. https://doi.org/10.1126/science.abj0425.
ieee: M. Akhmanova et al., “Cell division in tissues enables macrophage infiltration,”
Science, vol. 376, no. 6591. American Association for the Advancement of
Science, pp. 394–396, 2022.
ista: Akhmanova M, Emtenani S, Krueger D, György A, Pereira Guarda M, Vlasov M,
Vlasov F, Akopian A, Ratheesh A, De Renzis S, Siekhaus DE. 2022. Cell division
in tissues enables macrophage infiltration. Science. 376(6591), 394–396.
mla: Akhmanova, Maria, et al. “Cell Division in Tissues Enables Macrophage Infiltration.”
Science, vol. 376, no. 6591, American Association for the Advancement of
Science, 2022, pp. 394–96, doi:10.1126/science.abj0425.
short: M. Akhmanova, S. Emtenani, D. Krueger, A. György, M. Pereira Guarda, M. Vlasov,
F. Vlasov, A. Akopian, A. Ratheesh, S. De Renzis, D.E. Siekhaus, Science 376 (2022)
394–396.
date_created: 2022-02-01T11:23:18Z
date_published: 2022-04-22T00:00:00Z
date_updated: 2023-08-02T14:06:15Z
day: '22'
department:
- _id: DaSi
doi: 10.1126/science.abj0425
external_id:
isi:
- '000788553700039'
pmid:
- '35446632'
intvolume: ' 376'
isi: 1
issue: '6591'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2021.04.19.438995
month: '04'
oa: 1
oa_version: Preprint
page: 394-396
pmid: 1
project:
- _id: 264CBBAC-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02379
name: Modeling epithelial tissue mechanics during cell invasion
publication: Science
publication_identifier:
issn:
- 0036-8075
publication_status: published
publisher: American Association for the Advancement of Science
quality_controlled: '1'
status: public
title: Cell division in tissues enables macrophage infiltration
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 376
year: '2022'
...
---
_id: '10714'
abstract:
- lang: eng
text: Ribosomal defects perturb stem cell differentiation, causing diseases called
ribosomopathies. How ribosome levels control stem cell differentiation is not
fully known. Here, we discovered three RNA helicases are required for ribosome
biogenesis and for Drosophila oogenesis. Loss of these helicases, which we named
Aramis, Athos and Porthos, lead to aberrant stabilization of p53, cell cycle arrest
and stalled GSC differentiation. Unexpectedly, Aramis is required for efficient
translation of a cohort of mRNAs containing a 5’-Terminal-Oligo-Pyrimidine (TOP)-motif,
including mRNAs that encode ribosomal proteins and a conserved p53 inhibitor,
Novel Nucleolar protein 1 (Non1). The TOP-motif co-regulates the translation of
growth-related mRNAs in mammals. As in mammals, the La-related protein co-regulates
the translation of TOP-motif containing RNAs during Drosophila oogenesis. Thus,
a previously unappreciated TOP-motif in Drosophila responds to reduced ribosome
biogenesis to co-regulate the translation of ribosomal proteins and a p53 repressor,
thus coupling ribosome biogenesis to GSC differentiation.
acknowledgement: We are grateful to all members of the Rangan and Fuchs labs for their
discussion and comments on the manuscript. We also thanks Dr. Sammons, Dr. Marlow,
Life Science Editors, for their thoughts and comments the manuscript Additionally,
we thank the Bloomington Stock Center, the Vienna Drosophila Resource Center, the
BDGP Gene Disruption Project, and Flybase for fly stocks, reagents, and other resources.
P.R. is funded by the NIH/NIGMS (R01GM111779-06 and RO1GM135628-01), G.F. is funded
by NSF MCB-2047629 and NIH RO3 AI144839, D.E.S. was funded by Marie Curie CIG 334077/IRTIM
and the Austrian Science Fund (FWF) grant ASI_FWF01_P29638S, and A.B is funded by
NIH R01GM116889 and American Cancer Society RSG-17-197-01-RMC.
article_processing_charge: No
article_type: original
author:
- first_name: Elliot T.
full_name: Martin, Elliot T.
last_name: Martin
- first_name: Patrick
full_name: Blatt, Patrick
last_name: Blatt
- first_name: Elaine
full_name: Ngyuen, Elaine
last_name: Ngyuen
- first_name: Roni
full_name: Lahr, Roni
last_name: Lahr
- first_name: Sangeetha
full_name: Selvam, Sangeetha
last_name: Selvam
- first_name: Hyun Ah M.
full_name: Yoon, Hyun Ah M.
last_name: Yoon
- first_name: Tyler
full_name: Pocchiari, Tyler
last_name: Pocchiari
- first_name: Shamsi
full_name: Emtenani, Shamsi
id: 49D32318-F248-11E8-B48F-1D18A9856A87
last_name: Emtenani
orcid: 0000-0001-6981-6938
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
- first_name: Andrea
full_name: Berman, Andrea
last_name: Berman
- first_name: Gabriele
full_name: Fuchs, Gabriele
last_name: Fuchs
- first_name: Prashanth
full_name: Rangan, Prashanth
last_name: Rangan
citation:
ama: Martin ET, Blatt P, Ngyuen E, et al. A translation control module coordinates
germline stem cell differentiation with ribosome biogenesis during Drosophila
oogenesis. Developmental Cell. 2022;57(7):883-900.e10. doi:10.1016/j.devcel.2022.03.005
apa: Martin, E. T., Blatt, P., Ngyuen, E., Lahr, R., Selvam, S., Yoon, H. A. M.,
… Rangan, P. (2022). A translation control module coordinates germline stem cell
differentiation with ribosome biogenesis during Drosophila oogenesis. Developmental
Cell. Elsevier. https://doi.org/10.1016/j.devcel.2022.03.005
chicago: Martin, Elliot T., Patrick Blatt, Elaine Ngyuen, Roni Lahr, Sangeetha Selvam,
Hyun Ah M. Yoon, Tyler Pocchiari, et al. “A Translation Control Module Coordinates
Germline Stem Cell Differentiation with Ribosome Biogenesis during Drosophila
Oogenesis.” Developmental Cell. Elsevier, 2022. https://doi.org/10.1016/j.devcel.2022.03.005.
ieee: E. T. Martin et al., “A translation control module coordinates germline
stem cell differentiation with ribosome biogenesis during Drosophila oogenesis,”
Developmental Cell, vol. 57, no. 7. Elsevier, p. 883–900.e10, 2022.
ista: Martin ET, Blatt P, Ngyuen E, Lahr R, Selvam S, Yoon HAM, Pocchiari T, Emtenani
S, Siekhaus DE, Berman A, Fuchs G, Rangan P. 2022. A translation control module
coordinates germline stem cell differentiation with ribosome biogenesis during
Drosophila oogenesis. Developmental Cell. 57(7), 883–900.e10.
mla: Martin, Elliot T., et al. “A Translation Control Module Coordinates Germline
Stem Cell Differentiation with Ribosome Biogenesis during Drosophila Oogenesis.”
Developmental Cell, vol. 57, no. 7, Elsevier, 2022, p. 883–900.e10, doi:10.1016/j.devcel.2022.03.005.
short: E.T. Martin, P. Blatt, E. Ngyuen, R. Lahr, S. Selvam, H.A.M. Yoon, T. Pocchiari,
S. Emtenani, D.E. Siekhaus, A. Berman, G. Fuchs, P. Rangan, Developmental Cell
57 (2022) 883–900.e10.
date_created: 2022-02-01T13:15:05Z
date_published: 2022-04-11T00:00:00Z
date_updated: 2023-08-02T14:07:13Z
day: '11'
department:
- _id: DaSi
doi: 10.1016/j.devcel.2022.03.005
ec_funded: 1
external_id:
isi:
- '000789021800005'
intvolume: ' 57'
isi: 1
issue: '7'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2021.04.04.438367
month: '04'
oa: 1
oa_version: Preprint
page: 883-900.e10
project:
- _id: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: Drosophila TNFa´s Funktion in Immunzellen
publication: Developmental Cell
publication_identifier:
eissn:
- 1878-1551
issn:
- 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: A translation control module coordinates germline stem cell differentiation
with ribosome biogenesis during Drosophila oogenesis
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 57
year: '2022'
...
---
_id: '10918'
abstract:
- lang: eng
text: Cellular metabolism must adapt to changing demands to enable homeostasis.
During immune responses or cancer metastasis, cells leading migration into challenging
environments require an energy boost, but what controls this capacity is unclear.
Here, we study a previously uncharacterized nuclear protein, Atossa (encoded by
CG9005), which supports macrophage invasion into the germband of Drosophila by
controlling cellular metabolism. First, nuclear Atossa increases mRNA levels of
Porthos, a DEAD-box protein, and of two metabolic enzymes, lysine-α-ketoglutarate
reductase (LKR/SDH) and NADPH glyoxylate reductase (GR/HPR), thus enhancing mitochondrial
bioenergetics. Then Porthos supports ribosome assembly and thereby raises the
translational efficiency of a subset of mRNAs, including those affecting mitochondrial
functions, the electron transport chain, and metabolism. Mitochondrial respiration
measurements, metabolomics, and live imaging indicate that Atossa and Porthos
power up OxPhos and energy production to promote the forging of a path into tissues
by leading macrophages. Since many crucial physiological responses require increases
in mitochondrial energy output, this previously undescribed genetic program may
modulate a wide range of cellular behaviors.
acknowledged_ssus:
- _id: Bio
acknowledgement: "We thank the DGRC (NIH grant 2P40OD010949-10A1) for plasmids, the
BDSC (NIH grant P40OD018537) and the VDRC for fly stocks, FlyBase for essential
genomic information, the BDGP in situ database for data (Tomancak et al, 2007),
the IST Austria Bioimaging facility for support, the VBC Core Facilities for RNA
sequencing and analysis, and C. Guet, C. Navarro, C. Desplan, T. Lecuit, I. Miguel-Aliaga,
and Siekhaus group members for comments on the manuscript. The VBCF Metabolomics
Facility is funded by the City of Vienna through the Vienna Business Agency. This
work was supported by the Marie Curie CIG 334077/IRTIM (DES), Austrian Science Fund
(FWF) Lise Meitner Fellowship M2379-B28 (MA and DES), Austrian Science Fund (FWF)
grant ASI_FWF01_P29638S (DES), NIH/NIGMS (R01GM111779-06 (PR), RO1GM135628-01 (PR),
European Research Council (ERC) grant no. 677006 “CMIL” (AB), and Natural Sciences
and Engineering Research Council of Canada\r\n(RGPIN-2019-06766) (TRH). "
article_number: e109049
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Shamsi
full_name: Emtenani, Shamsi
id: 49D32318-F248-11E8-B48F-1D18A9856A87
last_name: Emtenani
orcid: 0000-0001-6981-6938
- first_name: Elliot T
full_name: Martin, Elliot T
last_name: Martin
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Julia
full_name: Bicher, Julia
id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87
last_name: Bicher
- first_name: Jakob-Wendelin
full_name: Genger, Jakob-Wendelin
last_name: Genger
- first_name: Thomas
full_name: Köcher, Thomas
last_name: Köcher
- first_name: Maria
full_name: Akhmanova, Maria
id: 3425EC26-F248-11E8-B48F-1D18A9856A87
last_name: Akhmanova
orcid: 0000-0003-1522-3162
- first_name: Mariana
full_name: Pereira Guarda, Mariana
id: 6de81d9d-e2f2-11eb-945a-af8bc2a60b26
last_name: Pereira Guarda
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: Andreas
full_name: Bergthaler, Andreas
last_name: Bergthaler
- first_name: Thomas R
full_name: Hurd, Thomas R
last_name: Hurd
- first_name: Prashanth
full_name: Rangan, Prashanth
last_name: Rangan
- 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: Emtenani S, Martin ET, György A, et al. Macrophage mitochondrial bioenergetics
and tissue invasion are boosted by an Atossa-Porthos axis in Drosophila. The
Embo Journal. 2022;41. doi:10.15252/embj.2021109049
apa: Emtenani, S., Martin, E. T., György, A., Bicher, J., Genger, J.-W., Köcher,
T., … Siekhaus, D. E. (2022). Macrophage mitochondrial bioenergetics and tissue
invasion are boosted by an Atossa-Porthos axis in Drosophila. The Embo Journal.
Embo Press. https://doi.org/10.15252/embj.2021109049
chicago: Emtenani, Shamsi, Elliot T Martin, Attila György, Julia Bicher, Jakob-Wendelin
Genger, Thomas Köcher, Maria Akhmanova, et al. “Macrophage Mitochondrial Bioenergetics
and Tissue Invasion Are Boosted by an Atossa-Porthos Axis in Drosophila.” The
Embo Journal. Embo Press, 2022. https://doi.org/10.15252/embj.2021109049.
ieee: S. Emtenani et al., “Macrophage mitochondrial bioenergetics and tissue
invasion are boosted by an Atossa-Porthos axis in Drosophila,” The Embo Journal,
vol. 41. Embo Press, 2022.
ista: Emtenani S, Martin ET, György A, Bicher J, Genger J-W, Köcher T, Akhmanova
M, Pereira Guarda M, Roblek M, Bergthaler A, Hurd TR, Rangan P, Siekhaus DE. 2022.
Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos
axis in Drosophila. The Embo Journal. 41, e109049.
mla: Emtenani, Shamsi, et al. “Macrophage Mitochondrial Bioenergetics and Tissue
Invasion Are Boosted by an Atossa-Porthos Axis in Drosophila.” The Embo Journal,
vol. 41, e109049, Embo Press, 2022, doi:10.15252/embj.2021109049.
short: S. Emtenani, E.T. Martin, A. György, J. Bicher, J.-W. Genger, T. Köcher,
M. Akhmanova, M. Pereira Guarda, M. Roblek, A. Bergthaler, T.R. Hurd, P. Rangan,
D.E. Siekhaus, The Embo Journal 41 (2022).
date_created: 2022-03-24T13:23:09Z
date_published: 2022-03-23T00:00:00Z
date_updated: 2023-08-03T06:13:14Z
day: '23'
ddc:
- '570'
department:
- _id: DaSi
- _id: LoSw
doi: 10.15252/embj.2021109049
ec_funded: 1
external_id:
isi:
- '000771957000001'
file:
- access_level: open_access
checksum: dba48580fe0fefaa4c63078d1d2a35df
content_type: application/pdf
creator: siekhaus
date_created: 2022-03-24T13:22:41Z
date_updated: 2022-03-24T13:22:41Z
file_id: '10919'
file_name: Macrophage mitochondrial bioenergetics and tissue invasion are boosted
by an Atossa-Porthos axis in Drosopila.pdf
file_size: 4344585
relation: main_file
file_date_updated: 2022-03-24T13:22:41Z
has_accepted_license: '1'
intvolume: ' 41'
isi: 1
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
project:
- _id: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
- _id: 264CBBAC-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02379
name: Modeling epithelial tissue mechanics during cell invasion
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: Drosophila TNFa´s Funktion in Immunzellen
publication: The Embo Journal
publication_identifier:
eissn:
- 1460-2075
publication_status: published
publisher: Embo Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an
Atossa-Porthos axis in Drosophila
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: 41
year: '2022'
...
---
_id: '11193'
abstract:
- lang: eng
text: "The infiltration of immune cells into tissues underlies the establishment
of tissue-resident\r\nmacrophages and responses to infections and tumors. However,
the mechanisms immune\r\ncells utilize to collectively migrate through tissue
barriers in vivo are not yet well understood.\r\nIn this thesis, I describe two
mechanisms that Drosophila immune cells (hemocytes) use to\r\novercome the tissue
barrier of the germband in the embryo. One strategy is the strengthening\r\nof
the actin cortex through developmentally controlled transcriptional regulation
induced by\r\nthe Drosophila proto-oncogene family member Dfos, which I show in
Chapter 2. Dfos induces\r\nexpression of the tetraspanin TM4SF and the filamin
Cher leading to higher levels of the\r\nactivated formin Dia at the cortex and
increased cortical F-actin. This enhanced cortical\r\nstrength allows hemocytes
to overcome the physical resistance of the surrounding tissue and\r\ntranslocate
their nucleus to move forward. This mechanism affects the speed of migration\r\nwhen
hemocytes face a confined environment in vivo.\r\nAnother aspect of the invasion
process is the initial step of the leading hemocytes entering\r\nthe tissue, which
potentially guides the follower cells. In Chapter 3, I describe a novel\r\nsubpopulation
of hemocytes activated by BMP signaling prior to tissue invasion that leads\r\npenetration
into the germband. Hemocytes that are deficient in BMP signaling activation\r\nshow
impaired persistence at the tissue entry, while their migration speed remains\r\nunaffected.\r\nThis
suggests that there might be different mechanisms controlling immune cell migration\r\nwithin
the confined environment in vivo, one of these being the general ability to overcome\r\nthe
resistance of the surrounding tissue and another affecting the order of hemocytes
that\r\ncollectively invade the tissue in a stream of individual cells.\r\nTogether,
my findings provide deeper insights into transcriptional changes in immune\r\ncells
that enable efficient tissue invasion and pave the way for future studies investigating
the\r\nearly colonization of tissues by macrophages in higher organisms. Moreover,
they extend the\r\ncurrent view of Drosophila immune cell heterogeneity and point
toward a potentially\r\nconserved role for canonical BMP signaling in specifying
immune cells that lead the migration\r\nof tissue resident macrophages during
embryogenesis."
acknowledged_ssus:
- _id: LifeSc
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Stephanie
full_name: Wachner, Stephanie
id: 2A95E7B0-F248-11E8-B48F-1D18A9856A87
last_name: Wachner
citation:
ama: Wachner S. Transcriptional regulation by Dfos and BMP-signaling support tissue
invasion of Drosophila immune cells. 2022. doi:10.15479/at:ista:11193
apa: Wachner, S. (2022). Transcriptional regulation by Dfos and BMP-signaling
support tissue invasion of Drosophila immune cells. Institute of Science and
Technology Austria. https://doi.org/10.15479/at:ista:11193
chicago: Wachner, Stephanie. “Transcriptional Regulation by Dfos and BMP-Signaling
Support Tissue Invasion of Drosophila Immune Cells.” Institute of Science and
Technology Austria, 2022. https://doi.org/10.15479/at:ista:11193.
ieee: S. Wachner, “Transcriptional regulation by Dfos and BMP-signaling support
tissue invasion of Drosophila immune cells,” Institute of Science and Technology
Austria, 2022.
ista: Wachner S. 2022. Transcriptional regulation by Dfos and BMP-signaling support
tissue invasion of Drosophila immune cells. Institute of Science and Technology
Austria.
mla: Wachner, Stephanie. Transcriptional Regulation by Dfos and BMP-Signaling
Support Tissue Invasion of Drosophila Immune Cells. Institute of Science and
Technology Austria, 2022, doi:10.15479/at:ista:11193.
short: S. Wachner, Transcriptional Regulation by Dfos and BMP-Signaling Support
Tissue Invasion of Drosophila Immune Cells, Institute of Science and Technology
Austria, 2022.
date_created: 2022-04-20T08:59:07Z
date_published: 2022-04-20T00:00:00Z
date_updated: 2023-09-19T10:15:54Z
day: '20'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
- _id: DaSi
doi: 10.15479/at:ista:11193
file:
- access_level: open_access
checksum: 999ab16884c4522486136ebc5ae8dbff
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creator: cchlebak
date_created: 2022-04-20T09:03:57Z
date_updated: 2023-04-21T22:30:03Z
embargo: 2023-04-20
file_id: '11195'
file_name: Thesis_Stephanie_Wachner_20200414_formatted.pdf
file_size: 8820951
relation: main_file
- access_level: closed
checksum: fd92b1e38d53bdf8b458213882d41383
content_type: application/x-zip-compressed
creator: cchlebak
date_created: 2022-04-22T12:41:00Z
date_updated: 2023-04-21T22:30:03Z
embargo_to: open_access
file_id: '11329'
file_name: Thesis_Stephanie_Wachner_20200414.zip
file_size: 65864612
relation: source_file
file_date_updated: 2023-04-21T22:30:03Z
has_accepted_license: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: '170'
project:
- _id: 26199CA4-B435-11E9-9278-68D0E5697425
grant_number: '24800'
name: Tissue barrier penetration is crucial for immunity and metastasis
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '10614'
relation: part_of_dissertation
status: public
- id: '544'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
title: Transcriptional regulation by Dfos and BMP-signaling support tissue invasion
of Drosophila immune cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: dissertation
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2022'
...
---
_id: '10614'
abstract:
- lang: eng
text: 'The infiltration of immune cells into tissues underlies the establishment
of tissue-resident macrophages and responses to infections and tumors. Yet the
mechanisms immune cells utilize to negotiate tissue barriers in living organisms
are not well understood, and a role for cortical actin has not been examined.
Here, we find that the tissue invasion of Drosophila macrophages, also known as
plasmatocytes or hemocytes, utilizes enhanced cortical F-actin levels stimulated
by the Drosophila member of the fos proto oncogene transcription factor family
(Dfos, Kayak). RNA sequencing analysis and live imaging show that Dfos enhances
F-actin levels around the entire macrophage surface by increasing mRNA levels
of the membrane spanning molecular scaffold tetraspanin TM4SF, and the actin cross-linking
filamin Cheerio, which are themselves required for invasion. Both the filamin
and the tetraspanin enhance the cortical activity of Rho1 and the formin Diaphanous
and thus the assembly of cortical actin, which is a critical function since expressing
a dominant active form of Diaphanous can rescue the Dfos macrophage invasion defect.
In vivo imaging shows that Dfos enhances the efficiency of the initial phases
of macrophage tissue entry. Genetic evidence argues that this Dfos-induced program
in macrophages counteracts the constraint produced by the tension of surrounding
tissues and buffers the properties of the macrophage nucleus from affecting tissue
entry. We thus identify strengthening the cortical actin cytoskeleton through
Dfos as a key process allowing efficient forward movement of an immune cell into
surrounding tissues. '
acknowledged_ssus:
- _id: LifeSc
acknowledgement: 'We thank the following for their contributions: Plasmids were supplied
by the Drosophila Genomics Resource Center (NIH 2P40OD010949-10A1); fly stocks were
provided by K. Brueckner, B. Stramer, M. Uhlirova, O. Schuldiner, the Bloomington
Drosophila Stock Center (NIH P40OD018537) and the Vienna Drosophila Resource Center,
FlyBase for essential genomic information, and the BDGP in situ database for data.
For antibodies, we thank the Developmental Studies Hybridoma Bank, which was created
by the Eunice Kennedy Shriver National Institute of Child Health and Human Development
of the NIH and is maintained at the University of Iowa, as well as J. Zeitlinger
for her generous gift of Dfos antibody. We thank the Vienna BioCenter Core Facilities
for RNA sequencing and analysis and the Life Scientific Service Units at IST Austria
for technical support and assistance with microscopy and FACS analysis. We thank
C. P. Heisenberg, P. Martin, M. Sixt, and Siekhaus group members for discussions
and T. Hurd, A. Ratheesh, and P. Rangan for comments on the manuscript.'
article_processing_charge: No
article_type: original
author:
- first_name: Vera
full_name: Belyaeva, Vera
id: 47F080FE-F248-11E8-B48F-1D18A9856A87
last_name: Belyaeva
- first_name: Stephanie
full_name: Wachner, Stephanie
id: 2A95E7B0-F248-11E8-B48F-1D18A9856A87
last_name: Wachner
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Shamsi
full_name: Emtenani, Shamsi
id: 49D32318-F248-11E8-B48F-1D18A9856A87
last_name: Emtenani
orcid: 0000-0001-6981-6938
- first_name: Igor
full_name: Gridchyn, Igor
id: 4B60654C-F248-11E8-B48F-1D18A9856A87
last_name: Gridchyn
orcid: 0000-0002-1807-1929
- first_name: Maria
full_name: Akhmanova, Maria
id: 3425EC26-F248-11E8-B48F-1D18A9856A87
last_name: Akhmanova
orcid: 0000-0003-1522-3162
- first_name: M
full_name: Linder, M
last_name: Linder
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: M
full_name: Sibilia, M
last_name: Sibilia
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
citation:
ama: Belyaeva V, Wachner S, György A, et al. Fos regulates macrophage infiltration
against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila.
PLoS Biology. 2022;20(1):e3001494. doi:10.1371/journal.pbio.3001494
apa: Belyaeva, V., Wachner, S., György, A., Emtenani, S., Gridchyn, I., Akhmanova,
M., … Siekhaus, D. E. (2022). Fos regulates macrophage infiltration against surrounding
tissue resistance by a cortical actin-based mechanism in Drosophila. PLoS Biology.
Public Library of Science. https://doi.org/10.1371/journal.pbio.3001494
chicago: Belyaeva, Vera, Stephanie Wachner, Attila György, Shamsi Emtenani, Igor
Gridchyn, Maria Akhmanova, M Linder, Marko Roblek, M Sibilia, and Daria E Siekhaus.
“Fos Regulates Macrophage Infiltration against Surrounding Tissue Resistance by
a Cortical Actin-Based Mechanism in Drosophila.” PLoS Biology. Public Library
of Science, 2022. https://doi.org/10.1371/journal.pbio.3001494.
ieee: V. Belyaeva et al., “Fos regulates macrophage infiltration against
surrounding tissue resistance by a cortical actin-based mechanism in Drosophila,”
PLoS Biology, vol. 20, no. 1. Public Library of Science, p. e3001494, 2022.
ista: Belyaeva V, Wachner S, György A, Emtenani S, Gridchyn I, Akhmanova M, Linder
M, Roblek M, Sibilia M, Siekhaus DE. 2022. Fos regulates macrophage infiltration
against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila.
PLoS Biology. 20(1), e3001494.
mla: Belyaeva, Vera, et al. “Fos Regulates Macrophage Infiltration against Surrounding
Tissue Resistance by a Cortical Actin-Based Mechanism in Drosophila.” PLoS
Biology, vol. 20, no. 1, Public Library of Science, 2022, p. e3001494, doi:10.1371/journal.pbio.3001494.
short: V. Belyaeva, S. Wachner, A. György, S. Emtenani, I. Gridchyn, M. Akhmanova,
M. Linder, M. Roblek, M. Sibilia, D.E. Siekhaus, PLoS Biology 20 (2022) e3001494.
date_created: 2022-01-12T10:18:17Z
date_published: 2022-01-06T00:00:00Z
date_updated: 2024-03-25T23:30:15Z
day: '06'
ddc:
- '570'
department:
- _id: DaSi
- _id: JoCs
doi: 10.1371/journal.pbio.3001494
ec_funded: 1
external_id:
isi:
- '000971223700001'
pmid:
- '34990456'
file:
- access_level: open_access
checksum: f454212a5522a7818ba4b2892315c478
content_type: application/pdf
creator: cchlebak
date_created: 2022-01-12T13:50:04Z
date_updated: 2022-01-12T13:50:04Z
file_id: '10615'
file_name: 2022_PLOSBio_Belyaeva.pdf
file_size: 5426932
relation: main_file
success: 1
file_date_updated: 2022-01-12T13:50:04Z
has_accepted_license: '1'
intvolume: ' 20'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: e3001494
pmid: 1
project:
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: Drosophila TNFa´s Funktion in Immunzellen
- _id: 26199CA4-B435-11E9-9278-68D0E5697425
grant_number: '24800'
name: Tissue barrier penetration is crucial for immunity and metastasis
- _id: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
publication: PLoS Biology
publication_identifier:
eissn:
- 1545-7885
issn:
- 1544-9173
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
related_material:
link:
- relation: earlier_version
url: https://www.biorxiv.org/content/10.1101/2020.09.18.301481
- description: News on the ISTA Website
relation: press_release
url: https://ista.ac.at/en/news/resisting-the-pressure/
record:
- id: '8557'
relation: earlier_version
status: public
- id: '11193'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Fos regulates macrophage infiltration against surrounding tissue resistance
by a cortical actin-based mechanism in Drosophila
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: 20
year: '2022'
...
---
_id: '12080'
abstract:
- lang: eng
text: 'Endocytosis is a multistep process involving the sequential recruitment and
action of numerous proteins. This process can be divided into two phases: an early
phase, in which sites of endocytosis are formed, and a late phase in which clathrin-coated
vesicles are formed and internalized into the cytosol, but how these phases link
to each other remains unclear. In this study, we demonstrate that anchoring the
yeast Eps15-like protein Pan1p to the peroxisome triggers most of the events occurring
during the late phase at the peroxisome. At this ectopic location, Pan1p recruits
most proteins that function in the late phases—including actin nucleation promoting
factors—and then initiates actin polymerization. Pan1p also recruited Prk1 kinase
and actin depolymerizing factors, thereby triggering disassembly immediately after
actin assembly and inducing dissociation of endocytic proteins from the peroxisome.
These observations suggest that Pan1p is a key regulator for initiating, processing,
and completing the late phase of endocytosis.'
acknowledgement: 'This work was supported by JSPS KAKENHI GRANT #18K062291, and the
Takeda Science Foundation to J.Y. Toshima, as well as JSPS KAKENHI GRANT #19K065710,
the Uehara Memorial Foundation, and Life Science Foundation of JAPAN to J. Toshima.'
article_number: e202112138
article_processing_charge: No
article_type: original
author:
- first_name: Mariko
full_name: Enshoji, Mariko
last_name: Enshoji
- first_name: Yoshiko
full_name: Miyano, Yoshiko
last_name: Miyano
- first_name: Nao
full_name: Yoshida, Nao
last_name: Yoshida
- first_name: Makoto
full_name: Nagano, Makoto
last_name: Nagano
- first_name: Minami
full_name: Watanabe, Minami
last_name: Watanabe
- first_name: Mayumi
full_name: Kunihiro, Mayumi
last_name: Kunihiro
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
- first_name: Junko Y.
full_name: Toshima, Junko Y.
last_name: Toshima
- first_name: Jiro
full_name: Toshima, Jiro
last_name: Toshima
citation:
ama: Enshoji M, Miyano Y, Yoshida N, et al. Eps15/Pan1p is a master regulator of
the late stages of the endocytic pathway. Journal of Cell Biology. 2022;221(10).
doi:10.1083/jcb.202112138
apa: Enshoji, M., Miyano, Y., Yoshida, N., Nagano, M., Watanabe, M., Kunihiro, M.,
… Toshima, J. (2022). Eps15/Pan1p is a master regulator of the late stages of
the endocytic pathway. Journal of Cell Biology. Rockefeller University
Press. https://doi.org/10.1083/jcb.202112138
chicago: Enshoji, Mariko, Yoshiko Miyano, Nao Yoshida, Makoto Nagano, Minami Watanabe,
Mayumi Kunihiro, Daria E Siekhaus, Junko Y. Toshima, and Jiro Toshima. “Eps15/Pan1p
Is a Master Regulator of the Late Stages of the Endocytic Pathway.” Journal
of Cell Biology. Rockefeller University Press, 2022. https://doi.org/10.1083/jcb.202112138.
ieee: M. Enshoji et al., “Eps15/Pan1p is a master regulator of the late stages
of the endocytic pathway,” Journal of Cell Biology, vol. 221, no. 10. Rockefeller
University Press, 2022.
ista: Enshoji M, Miyano Y, Yoshida N, Nagano M, Watanabe M, Kunihiro M, Siekhaus
DE, Toshima JY, Toshima J. 2022. Eps15/Pan1p is a master regulator of the late
stages of the endocytic pathway. Journal of Cell Biology. 221(10), e202112138.
mla: Enshoji, Mariko, et al. “Eps15/Pan1p Is a Master Regulator of the Late Stages
of the Endocytic Pathway.” Journal of Cell Biology, vol. 221, no. 10, e202112138,
Rockefeller University Press, 2022, doi:10.1083/jcb.202112138.
short: M. Enshoji, Y. Miyano, N. Yoshida, M. Nagano, M. Watanabe, M. Kunihiro, D.E.
Siekhaus, J.Y. Toshima, J. Toshima, Journal of Cell Biology 221 (2022).
date_created: 2022-09-11T22:01:54Z
date_published: 2022-08-19T00:00:00Z
date_updated: 2023-08-03T13:49:07Z
day: '19'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.1083/jcb.202112138
external_id:
isi:
- '000932770500001'
pmid:
- '35984332'
file:
- access_level: open_access
checksum: f2e581e66b5cdab9df81b56e850b3eaa
content_type: application/pdf
creator: dernst
date_created: 2023-01-20T09:32:53Z
date_updated: 2023-02-21T23:30:39Z
embargo: 2023-02-20
file_id: '12321'
file_name: 2022_JCB_Enshoji.pdf
file_size: 7816875
relation: main_file
file_date_updated: 2023-02-21T23:30:39Z
has_accepted_license: '1'
intvolume: ' 221'
isi: 1
issue: '10'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
issn:
- 0021-9525
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Eps15/Pan1p is a master regulator of the late stages of the endocytic pathway
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 221
year: '2022'
...
---
_id: '9363'
abstract:
- lang: eng
text: Optogenetics has been harnessed to shed new mechanistic light on current and
future therapeutic strategies. This has been to date achieved by the regulation
of ion flow and electrical signals in neuronal cells and neural circuits that
are known to be affected by disease. In contrast, the optogenetic delivery of
trophic biochemical signals, which support cell survival and are implicated in
degenerative disorders, has never been demonstrated in an animal model of disease.
Here, we reengineered the human and Drosophila melanogaster REarranged during
Transfection (hRET and dRET) receptors to be activated by light, creating one-component
optogenetic tools termed Opto-hRET and Opto-dRET. Upon blue light stimulation,
these receptors robustly induced the MAPK/ERK proliferative signaling pathway
in cultured cells. In PINK1B9 flies that exhibit loss of PTEN-induced putative
kinase 1 (PINK1), a kinase associated with familial Parkinson’s disease (PD),
light activation of Opto-dRET suppressed mitochondrial defects, tissue degeneration
and behavioral deficits. In human cells with PINK1 loss-of-function, mitochondrial
fragmentation was rescued using Opto-dRET via the PI3K/NF-кB pathway. Our results
demonstrate that a light-activated receptor can ameliorate disease hallmarks in
a genetic model of PD. The optogenetic delivery of trophic signals is cell type-specific
and reversible and thus has the potential to inspire novel strategies towards
a spatio-temporal regulation of tissue repair.
acknowledgement: We thank R. Cagan, A. Whitworth and J. Nagpal for fly lines and advice,
S. Herlitze for provision of a tissue culture illuminator, and Verian Bader for
help with statistical analysis.
article_processing_charge: No
author:
- first_name: Álvaro
full_name: Inglés Prieto, Álvaro
id: 2A9DB292-F248-11E8-B48F-1D18A9856A87
last_name: Inglés Prieto
orcid: 0000-0002-5409-8571
- first_name: Nikolas
full_name: Furthmann, Nikolas
last_name: Furthmann
- first_name: Samuel H.
full_name: Crossman, Samuel H.
last_name: Crossman
- first_name: Alexandra Madelaine
full_name: Tichy, Alexandra Madelaine
last_name: Tichy
- first_name: Nina
full_name: Hoyer, Nina
last_name: Hoyer
- first_name: Meike
full_name: Petersen, Meike
last_name: Petersen
- first_name: Vanessa
full_name: Zheden, Vanessa
id: 39C5A68A-F248-11E8-B48F-1D18A9856A87
last_name: Zheden
- first_name: Julia
full_name: Bicher, Julia
id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87
last_name: Bicher
- first_name: Eva
full_name: Gschaider-Reichhart, Eva
id: 3FEE232A-F248-11E8-B48F-1D18A9856A87
last_name: Gschaider-Reichhart
orcid: 0000-0002-7218-7738
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
- first_name: Peter
full_name: Soba, Peter
last_name: Soba
- first_name: Konstanze F.
full_name: Winklhofer, Konstanze F.
last_name: Winklhofer
- first_name: Harald L
full_name: Janovjak, Harald L
id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
last_name: Janovjak
orcid: 0000-0002-8023-9315
citation:
ama: Inglés Prieto Á, Furthmann N, Crossman SH, et al. Optogenetic delivery of trophic
signals in a genetic model of Parkinson’s disease. PLoS genetics. 2021;17(4):e1009479.
doi:10.1371/journal.pgen.1009479
apa: Inglés Prieto, Á., Furthmann, N., Crossman, S. H., Tichy, A. M., Hoyer, N.,
Petersen, M., … Janovjak, H. L. (2021). Optogenetic delivery of trophic signals
in a genetic model of Parkinson’s disease. PLoS Genetics. Public Library
of Science. https://doi.org/10.1371/journal.pgen.1009479
chicago: Inglés Prieto, Álvaro, Nikolas Furthmann, Samuel H. Crossman, Alexandra
Madelaine Tichy, Nina Hoyer, Meike Petersen, Vanessa Zheden, et al. “Optogenetic
Delivery of Trophic Signals in a Genetic Model of Parkinson’s Disease.” PLoS
Genetics. Public Library of Science, 2021. https://doi.org/10.1371/journal.pgen.1009479.
ieee: Á. Inglés Prieto et al., “Optogenetic delivery of trophic signals in
a genetic model of Parkinson’s disease,” PLoS genetics, vol. 17, no. 4.
Public Library of Science, p. e1009479, 2021.
ista: Inglés Prieto Á, Furthmann N, Crossman SH, Tichy AM, Hoyer N, Petersen M,
Zheden V, Bicher J, Gschaider-Reichhart E, György A, Siekhaus DE, Soba P, Winklhofer
KF, Janovjak HL. 2021. Optogenetic delivery of trophic signals in a genetic model
of Parkinson’s disease. PLoS genetics. 17(4), e1009479.
mla: Inglés Prieto, Álvaro, et al. “Optogenetic Delivery of Trophic Signals in a
Genetic Model of Parkinson’s Disease.” PLoS Genetics, vol. 17, no. 4, Public
Library of Science, 2021, p. e1009479, doi:10.1371/journal.pgen.1009479.
short: Á. Inglés Prieto, N. Furthmann, S.H. Crossman, A.M. Tichy, N. Hoyer, M. Petersen,
V. Zheden, J. Bicher, E. Gschaider-Reichhart, A. György, D.E. Siekhaus, P. Soba,
K.F. Winklhofer, H.L. Janovjak, PLoS Genetics 17 (2021) e1009479.
date_created: 2021-05-02T22:01:29Z
date_published: 2021-04-01T00:00:00Z
date_updated: 2023-08-08T13:17:47Z
day: '01'
ddc:
- '570'
department:
- _id: EM-Fac
- _id: LoSw
- _id: DaSi
doi: 10.1371/journal.pgen.1009479
external_id:
isi:
- '000640606700001'
file:
- access_level: open_access
checksum: 82a74668f863e8dfb22fdd4f845c92ce
content_type: application/pdf
creator: kschuh
date_created: 2021-05-04T09:05:27Z
date_updated: 2021-05-04T09:05:27Z
file_id: '9369'
file_name: 2021_PLOS_Ingles-Prieto.pdf
file_size: 3072764
relation: main_file
success: 1
file_date_updated: 2021-05-04T09:05:27Z
has_accepted_license: '1'
intvolume: ' 17'
isi: 1
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: e1009479
publication: PLoS genetics
publication_identifier:
eissn:
- '15537404'
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: Optogenetic delivery of trophic signals in a genetic model of 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: 17
year: '2021'
...
---
_id: '10536'
abstract:
- lang: eng
text: TGFβ overexpression is commonly detected in cancer patients and correlates
with poor prognosis and metastasis. Cancer progression is often associated with
an enhanced recruitment of myeloid-derived cells to the tumor microenvironment.
Here we show that functional TGFβ-signaling in myeloid cells is required for metastasis
to the lungs and the liver. Myeloid-specific deletion of Tgfbr2 resulted in reduced
spontaneous lung metastasis, which was associated with a reduction of proinflammatory
cytokines in the metastatic microenvironment. Notably, CD8+ T cell depletion in
myeloid-specific Tgfbr2-deficient mice rescued lung metastasis. Myeloid-specific
Tgfbr2-deficiency resulted in reduced liver metastasis with an almost complete
absence of myeloid cells within metastatic foci. On contrary, an accumulation
of Tgfβ-responsive myeloid cells was associated with an increased recruitment
of monocytes and granulocytes and higher proinflammatory cytokine levels in control
mice. Monocytic cells isolated from metastatic livers of Tgfbr2-deficient mice
showed increased polarization towards the M1 phenotype, Tnfα and Il-1β expression,
reduced levels of M2 markers and reduced production of chemokines responsible
for myeloid-cell recruitment. No significant differences in Tgfβ levels were observed
at metastatic sites of any model. These data demonstrate that Tgfβ signaling in
monocytic myeloid cells suppresses CD8+ T cell activity during lung metastasis,
while these cells actively contribute to tumor growth during liver metastasis.
Thus, myeloid cells modulate metastasis through different mechanisms in a tissue-specific
manner.
acknowledgement: The authors acknowledge the assistance of the Laboratory Animal Services
Center (LASC) – UZH, Center for Microscopy and Image Analysis, and the Flow Cytometry
Center of the University of Zurich.
article_number: '765151'
article_processing_charge: No
article_type: original
author:
- first_name: Cristina
full_name: Stefanescu, Cristina
last_name: Stefanescu
- first_name: Merel
full_name: Van Gogh, Merel
last_name: Van Gogh
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: Mathias
full_name: Heikenwalder, Mathias
last_name: Heikenwalder
- first_name: Lubor
full_name: Borsig, Lubor
last_name: Borsig
citation:
ama: Stefanescu C, Van Gogh M, Roblek M, Heikenwalder M, Borsig L. TGFβ signaling
in myeloid cells promotes lung and liver metastasis through different mechanisms.
Frontiers in Oncology. 2021;11. doi:10.3389/fonc.2021.765151
apa: Stefanescu, C., Van Gogh, M., Roblek, M., Heikenwalder, M., & Borsig, L.
(2021). TGFβ signaling in myeloid cells promotes lung and liver metastasis through
different mechanisms. Frontiers in Oncology. Frontiers. https://doi.org/10.3389/fonc.2021.765151
chicago: Stefanescu, Cristina, Merel Van Gogh, Marko Roblek, Mathias Heikenwalder,
and Lubor Borsig. “TGFβ Signaling in Myeloid Cells Promotes Lung and Liver Metastasis
through Different Mechanisms.” Frontiers in Oncology. Frontiers, 2021.
https://doi.org/10.3389/fonc.2021.765151.
ieee: C. Stefanescu, M. Van Gogh, M. Roblek, M. Heikenwalder, and L. Borsig, “TGFβ
signaling in myeloid cells promotes lung and liver metastasis through different
mechanisms,” Frontiers in Oncology, vol. 11. Frontiers, 2021.
ista: Stefanescu C, Van Gogh M, Roblek M, Heikenwalder M, Borsig L. 2021. TGFβ signaling
in myeloid cells promotes lung and liver metastasis through different mechanisms.
Frontiers in Oncology. 11, 765151.
mla: Stefanescu, Cristina, et al. “TGFβ Signaling in Myeloid Cells Promotes Lung
and Liver Metastasis through Different Mechanisms.” Frontiers in Oncology,
vol. 11, 765151, Frontiers, 2021, doi:10.3389/fonc.2021.765151.
short: C. Stefanescu, M. Van Gogh, M. Roblek, M. Heikenwalder, L. Borsig, Frontiers
in Oncology 11 (2021).
date_created: 2021-12-12T23:01:27Z
date_published: 2021-11-18T00:00:00Z
date_updated: 2023-08-17T06:20:32Z
day: '18'
ddc:
- '610'
department:
- _id: DaSi
doi: 10.3389/fonc.2021.765151
external_id:
isi:
- '000726603400001'
pmid:
- '34868988'
file:
- access_level: open_access
checksum: 56cbac80e6891ce750511a30161b7792
content_type: application/pdf
creator: alisjak
date_created: 2021-12-13T13:32:37Z
date_updated: 2021-12-13T13:32:37Z
file_id: '10539'
file_name: 2021_Frontiers_Stefanescu.pdf
file_size: 9245199
relation: main_file
success: 1
file_date_updated: 2021-12-13T13:32:37Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: Frontiers in Oncology
publication_identifier:
eissn:
- 2234-943X
publication_status: published
publisher: Frontiers
quality_controlled: '1'
scopus_import: '1'
status: public
title: TGFβ signaling in myeloid cells promotes lung and liver metastasis through
different mechanisms
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: '2021'
...
---
_id: '8557'
abstract:
- lang: eng
text: The infiltration of immune cells into tissues underlies the establishment
of tissue resident macrophages, and responses to infections and tumors. Yet the
mechanisms immune cells utilize to negotiate tissue barriers in living organisms
are not well understood, and a role for cortical actin has not been examined.
Here we find that the tissue invasion of Drosophila macrophages, also known as
plasmatocytes or hemocytes, utilizes enhanced cortical F-actin levels stimulated
by the Drosophila member of the fos proto oncogene transcription factor family
(Dfos, Kayak). RNA sequencing analysis and live imaging show that Dfos enhances
F-actin levels around the entire macrophage surface by increasing mRNA levels
of the membrane spanning molecular scaffold tetraspanin TM4SF, and the actin cross-linking
filamin Cheerio which are themselves required for invasion. Cortical F-actin levels
are critical as expressing a dominant active form of Diaphanous, a actin polymerizing
Formin, can rescue the Dfos Dominant Negative macrophage invasion defect. In vivo
imaging shows that Dfos is required to enhance the efficiency of the initial phases
of macrophage tissue entry. Genetic evidence argues that this Dfos-induced program
in macrophages counteracts the constraint produced by the tension of surrounding
tissues and buffers the mechanical properties of the macrophage nucleus from affecting
tissue entry. We thus identify tuning the cortical actin cytoskeleton through
Dfos as a key process allowing efficient forward movement of an immune cell into
surrounding tissues.
acknowledged_ssus:
- _id: LifeSc
acknowledgement: 'We thank the following for their contributions: The Drosophila Genomics
Resource Center supported by NIH grant 2P40OD010949-10A1 for plasmids, K. Brueckner.
B. Stramer, M. Uhlirova, O. Schuldiner, the Bloomington Drosophila Stock Center
supported by NIH grant P40OD018537 and the Vienna Drosophila Resource Center for
fly stocks, FlyBase (Thurmond et al., 2019) for essential genomic information, and
the BDGP in situ database for data (Tomancak et al., 2002, 2007). For antibodies,
we thank the Developmental Studies Hybridoma Bank, which was created by the Eunice
Kennedy Shriver National Institute of Child Health and Human Development of the
NIH, and is maintained at the University of Iowa, as well as J. Zeitlinger for her
generous gift of Dfos antibody. We thank the Vienna BioCenter Core Facilities for
RNA sequencing and analysis and the Life Scientific Service Units at IST Austria
for technical support and assistance with microscopy and FACS analysis. We thank
C.P. Heisenberg, P. Martin, M. Sixt and Siekhaus group members for discussions and
T.Hurd, A. Ratheesh and P. Rangan for comments on the manuscript. A.G. was supported
by the Austrian Science Fund (FWF) grant DASI_FWF01_P29638S, D.E.S. by Marie Curie
CIG 334077/IRTIM. M.S. is supported by the FWF, PhD program W1212 915 and the European
Research Council (ERC) Advanced grant (ERC-2015-AdG TNT-Tumors 694883). S.W. is
supported by an OEAW, DOC fellowship.'
article_processing_charge: No
author:
- first_name: Vera
full_name: Belyaeva, Vera
id: 47F080FE-F248-11E8-B48F-1D18A9856A87
last_name: Belyaeva
- first_name: Stephanie
full_name: Wachner, Stephanie
id: 2A95E7B0-F248-11E8-B48F-1D18A9856A87
last_name: Wachner
- first_name: Igor
full_name: Gridchyn, Igor
id: 4B60654C-F248-11E8-B48F-1D18A9856A87
last_name: Gridchyn
orcid: 0000-0002-1807-1929
- first_name: Markus
full_name: Linder, Markus
last_name: Linder
- first_name: Shamsi
full_name: Emtenani, Shamsi
id: 49D32318-F248-11E8-B48F-1D18A9856A87
last_name: Emtenani
orcid: 0000-0001-6981-6938
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Maria
full_name: Sibilia, Maria
last_name: Sibilia
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
citation:
ama: Belyaeva V, Wachner S, Gridchyn I, et al. Cortical actin properties controlled
by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance.
bioRxiv. doi:10.1101/2020.09.18.301481
apa: Belyaeva, V., Wachner, S., Gridchyn, I., Linder, M., Emtenani, S., György,
A., … Siekhaus, D. E. (n.d.). Cortical actin properties controlled by Drosophila
Fos aid macrophage infiltration against surrounding tissue resistance. bioRxiv.
https://doi.org/10.1101/2020.09.18.301481
chicago: Belyaeva, Vera, Stephanie Wachner, Igor Gridchyn, Markus Linder, Shamsi
Emtenani, Attila György, Maria Sibilia, and Daria E Siekhaus. “Cortical Actin
Properties Controlled by Drosophila Fos Aid Macrophage Infiltration against Surrounding
Tissue Resistance.” BioRxiv, n.d. https://doi.org/10.1101/2020.09.18.301481.
ieee: V. Belyaeva et al., “Cortical actin properties controlled by Drosophila
Fos aid macrophage infiltration against surrounding tissue resistance,” bioRxiv.
.
ista: Belyaeva V, Wachner S, Gridchyn I, Linder M, Emtenani S, György A, Sibilia
M, Siekhaus DE. Cortical actin properties controlled by Drosophila Fos aid macrophage
infiltration against surrounding tissue resistance. bioRxiv, 10.1101/2020.09.18.301481.
mla: Belyaeva, Vera, et al. “Cortical Actin Properties Controlled by Drosophila
Fos Aid Macrophage Infiltration against Surrounding Tissue Resistance.” BioRxiv,
doi:10.1101/2020.09.18.301481.
short: V. Belyaeva, S. Wachner, I. Gridchyn, M. Linder, S. Emtenani, A. György,
M. Sibilia, D.E. Siekhaus, BioRxiv (n.d.).
date_created: 2020-09-23T09:36:47Z
date_published: 2020-09-18T00:00:00Z
date_updated: 2024-03-25T23:30:12Z
day: '18'
department:
- _id: DaSi
- _id: JoCs
doi: 10.1101/2020.09.18.301481
ec_funded: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2020.09.18.301481
month: '09'
oa: 1
oa_version: Preprint
project:
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: 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
- _id: 26199CA4-B435-11E9-9278-68D0E5697425
grant_number: '24800'
name: Tissue barrier penetration is crucial for immunity and metastasis
publication: bioRxiv
publication_status: submitted
related_material:
record:
- id: '10614'
relation: later_version
status: public
- id: '8983'
relation: dissertation_contains
status: public
status: public
title: Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration
against surrounding tissue resistance
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '8983'
abstract:
- lang: eng
text: Metabolic adaptation is a critical feature of migrating cells. It tunes the
metabolic programs of migrating cells to allow them to efficiently exert their
crucial roles in development, inflammatory responses and tumor metastasis. Cell
migration through physically challenging contexts requires energy. However, how
the metabolic reprogramming that underlies in vivo cell invasion is controlled
is still unanswered. In my PhD project, I identify a novel conserved metabolic
shift in Drosophila melanogaster immune cells that by modulating their bioenergetic
potential controls developmentally programmed tissue invasion. We show that this
regulation requires a novel conserved nuclear protein, named Atossa. Atossa enhances
the transcription of a set of proteins, including an RNA helicase Porthos and
two metabolic enzymes, each of which increases the tissue invasion of leading
Drosophila macrophages and can rescue the atossa mutant phenotype. Porthos selectively
regulates the translational efficiency of a subset of mRNAs containing a 5’-UTR
cis-regulatory TOP-like sequence. These 5’TOPL mRNA targets encode mitochondrial-related
proteins, including subunits of mitochondrial oxidative phosphorylation (OXPHOS)
components III and V and other metabolic-related proteins. Porthos powers up mitochondrial
OXPHOS to engender a sufficient ATP supply, which is required for tissue invasion
of leading macrophages. Atossa’s two vertebrate orthologs rescue the invasion
defect. In my PhD project, I elucidate that Atossa displays a conserved developmental
metabolic control to modulate metabolic capacities and the cellular energy state,
through altered transcription and translation, to aid the tissue infiltration
of leading cells into energy demanding barriers.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: E-Lib
- _id: CampIT
acknowledgement: Also, I would like to express my appreciation and thanks to the Bioimaging
facility, LSF, GSO, library, and IT people at IST Austria.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Shamsi
full_name: Emtenani, Shamsi
id: 49D32318-F248-11E8-B48F-1D18A9856A87
last_name: Emtenani
orcid: 0000-0001-6981-6938
citation:
ama: Emtenani S. Metabolic regulation of Drosophila macrophage tissue invasion.
2020. doi:10.15479/AT:ISTA:8983
apa: Emtenani, S. (2020). Metabolic regulation of Drosophila macrophage tissue
invasion. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8983
chicago: Emtenani, Shamsi. “Metabolic Regulation of Drosophila Macrophage Tissue
Invasion.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8983.
ieee: S. Emtenani, “Metabolic regulation of Drosophila macrophage tissue invasion,”
Institute of Science and Technology Austria, 2020.
ista: Emtenani S. 2020. Metabolic regulation of Drosophila macrophage tissue invasion.
Institute of Science and Technology Austria.
mla: Emtenani, Shamsi. Metabolic Regulation of Drosophila Macrophage Tissue Invasion.
Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8983.
short: S. Emtenani, Metabolic Regulation of Drosophila Macrophage Tissue Invasion,
Institute of Science and Technology Austria, 2020.
date_created: 2020-12-30T15:41:26Z
date_published: 2020-12-30T00:00:00Z
date_updated: 2023-09-07T13:24:17Z
day: '30'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: DaSi
doi: 10.15479/AT:ISTA:8983
file:
- access_level: open_access
checksum: ec2797ab7a6f253b35df0572b36d1b43
content_type: application/pdf
creator: semtenan
date_created: 2020-12-30T15:34:01Z
date_updated: 2021-12-31T23:30:04Z
embargo: 2021-12-30
file_id: '8984'
file_name: Thesis_Shamsi_Emtenani_pdfA.pdf
file_size: 10848175
relation: main_file
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checksum: cc30e6608a9815414024cf548dff3b3a
content_type: application/pdf
creator: semtenan
date_created: 2020-12-30T15:37:36Z
date_updated: 2021-12-31T23:30:04Z
embargo_to: open_access
file_id: '8985'
file_name: Thesis_Shamsi_Emtenani_source file.pdf
file_size: 10073648
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file_date_updated: 2021-12-31T23:30:04Z
has_accepted_license: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: '141'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '8557'
relation: part_of_dissertation
status: public
- id: '6187'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
title: Metabolic regulation of Drosophila macrophage tissue invasion
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2020'
...
---
_id: '7466'
abstract:
- lang: eng
text: Unpaired ligands are secreted signals that act via a GP130-like receptor,
domeless, to activate JAK/STAT signalling in Drosophila. Like many mammalian cytokines,
unpaireds can be activated by infection and other stresses and can promote insulin
resistance in target tissues. However, the importance of this effect in non-inflammatory
physiology is unknown. Here, we identify a requirement for unpaired-JAK signalling
as a metabolic regulator in healthy adult Drosophila muscle. Adult muscles show
basal JAK-STAT signalling activity in the absence of any immune challenge. Plasmatocytes
(Drosophila macrophages) are an important source of this tonic signal. Loss of
the dome receptor on adult muscles significantly reduces lifespan and causes local
and systemic metabolic pathology. These pathologies result from hyperactivation
of AKT and consequent deregulation of metabolism. Thus, we identify a cytokine
signal that must be received in muscle to control AKT activity and metabolic homeostasis.
article_number: e51595
article_processing_charge: No
article_type: original
author:
- first_name: Katrin
full_name: Kierdorf, Katrin
last_name: Kierdorf
- first_name: Fabian
full_name: Hersperger, Fabian
last_name: Hersperger
- first_name: Jessica
full_name: Sharrock, Jessica
last_name: Sharrock
- first_name: Crystal M.
full_name: Vincent, Crystal M.
last_name: Vincent
- first_name: Pinar
full_name: Ustaoglu, Pinar
last_name: Ustaoglu
- first_name: Jiawen
full_name: Dou, Jiawen
last_name: Dou
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Olaf
full_name: Groß, Olaf
last_name: Groß
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
- first_name: Marc S.
full_name: Dionne, Marc S.
last_name: Dionne
citation:
ama: Kierdorf K, Hersperger F, Sharrock J, et al. Muscle function and homeostasis
require cytokine inhibition of AKT activity in Drosophila. eLife. 2020;9.
doi:10.7554/eLife.51595
apa: Kierdorf, K., Hersperger, F., Sharrock, J., Vincent, C. M., Ustaoglu, P., Dou,
J., … Dionne, M. S. (2020). Muscle function and homeostasis require cytokine inhibition
of AKT activity in Drosophila. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.51595
chicago: Kierdorf, Katrin, Fabian Hersperger, Jessica Sharrock, Crystal M. Vincent,
Pinar Ustaoglu, Jiawen Dou, Attila György, Olaf Groß, Daria E Siekhaus, and Marc
S. Dionne. “Muscle Function and Homeostasis Require Cytokine Inhibition of AKT
Activity in Drosophila.” ELife. eLife Sciences Publications, 2020. https://doi.org/10.7554/eLife.51595.
ieee: K. Kierdorf et al., “Muscle function and homeostasis require cytokine
inhibition of AKT activity in Drosophila,” eLife, vol. 9. eLife Sciences
Publications, 2020.
ista: Kierdorf K, Hersperger F, Sharrock J, Vincent CM, Ustaoglu P, Dou J, György
A, Groß O, Siekhaus DE, Dionne MS. 2020. Muscle function and homeostasis require
cytokine inhibition of AKT activity in Drosophila. eLife. 9, e51595.
mla: Kierdorf, Katrin, et al. “Muscle Function and Homeostasis Require Cytokine
Inhibition of AKT Activity in Drosophila.” ELife, vol. 9, e51595, eLife
Sciences Publications, 2020, doi:10.7554/eLife.51595.
short: K. Kierdorf, F. Hersperger, J. Sharrock, C.M. Vincent, P. Ustaoglu, J. Dou,
A. György, O. Groß, D.E. Siekhaus, M.S. Dionne, ELife 9 (2020).
date_created: 2020-02-09T23:00:51Z
date_published: 2020-01-20T00:00:00Z
date_updated: 2023-08-17T14:36:39Z
day: '20'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.7554/eLife.51595
external_id:
isi:
- '000512304800001'
file:
- access_level: open_access
checksum: 3a072be843f416c7a7d532a51dc0addb
content_type: application/pdf
creator: dernst
date_created: 2020-02-10T08:53:16Z
date_updated: 2020-07-14T12:47:59Z
file_id: '7470'
file_name: 2020_eLife_Kierdorf.pdf
file_size: 4959933
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
project:
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: Drosophila TNFa´s Funktion in Immunzellen
publication: eLife
publication_identifier:
eissn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Muscle function and homeostasis require cytokine inhibition of AKT activity
in Drosophila
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: '8'
abstract:
- lang: eng
text: Despite their different origins, Drosophila glia and hemocytes are related
cell populations that provide an immune function. Drosophila hemocytes patrol
the body cavity and act as macrophages outside the nervous system whereas glia
originate from the neuroepithelium and provide the scavenger population of the
nervous system. Drosophila glia are hence the functional orthologs of vertebrate
microglia, even though the latter are cells of immune origin that subsequently
move into the brain during development. Interestingly, the Drosophila immune cells
within (glia) and outside the nervous system (hemocytes) require the same transcription
factor Glide/Gcm for their development. This raises the issue of how do glia specifically
differentiate in the nervous system and hemocytes in the procephalic mesoderm.
The Repo homeodomain transcription factor and pan-glial direct target of Glide/Gcm
is known to ensure glial terminal differentiation. Here we show that Repo also
takes center stage in the process that discriminates between glia and hemocytes.
First, Repo expression is repressed in the hemocyte anlagen by mesoderm-specific
factors. Second, Repo ectopic activation in the procephalic mesoderm is sufficient
to repress the expression of hemocyte-specific genes. Third, the lack of Repo
triggers the expression of hemocyte markers in glia. Thus, a complex network of
tissue-specific cues biases the potential of Glide/Gcm. These data allow us to
revise the concept of fate determinants and help us understand the bases of cell
specification. Both sexes were analyzed.SIGNIFICANCE STATEMENTDistinct cell types
often require the same pioneer transcription factor, raising the issue of how
does one factor trigger different fates. In Drosophila, glia and hemocytes provide
a scavenger activity within and outside the nervous system, respectively. While
they both require the Glide/Gcm transcription factor, glia originate from the
ectoderm, hemocytes from the mesoderm. Here we show that tissue-specific factors
inhibit the gliogenic potential of Glide/Gcm in the mesoderm by repressing the
expression of the homeodomain protein Repo, a major glial-specific target of Glide/Gcm.
Repo expression in turn inhibits the expression of hemocyte-specific genes in
the nervous system. These cell-specific networks secure the establishment of the
glial fate only in the nervous system and allow cell diversification.
acknowledgement: This work was supported by INSERM, CNRS, UDS, Ligue Régionale contre
le Cancer, Hôpital de Strasbourg, Association pour la Recherche sur le Cancer (ARC)
and Agence Nationale de la Recherche (ANR) grants. P.B.C. was funded by the ANR
and by the ARSEP (Fondation pour l'Aide à la Recherche sur la Sclérose en Plaques),
and G.T. by governmental and ARC fellowships. This work was also supported by grants
from the Ataxia UK (2491) and the NC3R (NC/L000199/1) awarded to M.F. The Institut
de Génétique et de Biologie Moléculaire et Cellulaire was also supported by a French
state fund through the ANR labex. D.E.S. was funded by Marie Curie Grant CIG 334077/IRTIM.
We thank B. Altenhein, K. Brückner, M. Crozatier, L. Waltzer, M. Logan, E. Kurant,
R. Reuter, E. Kurucz, J.L Dimarcq, J. Hoffmann, C. Goodman, the DHSB, and the BDSC
for reagents and flies. We also thank all of the laboratory members for comments
on the manuscript; C. Diebold, C. Delaporte, M. Pezze, the fly, and imaging and
antibody facilities for technical assistance; and D. Dembele for help with statistics.
In addition, we thank Alison Brewer for help with Luciferase assays.
article_processing_charge: No
article_type: original
author:
- first_name: Guillaume
full_name: Trébuchet, Guillaume
last_name: Trébuchet
- first_name: Pierre B
full_name: Cattenoz, Pierre B
last_name: Cattenoz
- first_name: János
full_name: Zsámboki, János
last_name: Zsámboki
- first_name: David
full_name: Mazaud, David
last_name: Mazaud
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
- first_name: Manolis
full_name: Fanto, Manolis
last_name: Fanto
- first_name: Angela
full_name: Giangrande, Angela
last_name: Giangrande
citation:
ama: Trébuchet G, Cattenoz PB, Zsámboki J, et al. The Repo homeodomain transcription
factor suppresses hematopoiesis in Drosophila and preserves the glial fate. Journal
of Neuroscience. 2019;39(2):238-255. doi:10.1523/JNEUROSCI.1059-18.2018
apa: Trébuchet, G., Cattenoz, P. B., Zsámboki, J., Mazaud, D., Siekhaus, D. E.,
Fanto, M., & Giangrande, A. (2019). The Repo homeodomain transcription factor
suppresses hematopoiesis in Drosophila and preserves the glial fate. Journal
of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1059-18.2018
chicago: Trébuchet, Guillaume, Pierre B Cattenoz, János Zsámboki, David Mazaud,
Daria E Siekhaus, Manolis Fanto, and Angela Giangrande. “The Repo Homeodomain
Transcription Factor Suppresses Hematopoiesis in Drosophila and Preserves the
Glial Fate.” Journal of Neuroscience. Society for Neuroscience, 2019. https://doi.org/10.1523/JNEUROSCI.1059-18.2018.
ieee: G. Trébuchet et al., “The Repo homeodomain transcription factor suppresses
hematopoiesis in Drosophila and preserves the glial fate,” Journal of Neuroscience,
vol. 39, no. 2. Society for Neuroscience, pp. 238–255, 2019.
ista: Trébuchet G, Cattenoz PB, Zsámboki J, Mazaud D, Siekhaus DE, Fanto M, Giangrande
A. 2019. The Repo homeodomain transcription factor suppresses hematopoiesis in
Drosophila and preserves the glial fate. Journal of Neuroscience. 39(2), 238–255.
mla: Trébuchet, Guillaume, et al. “The Repo Homeodomain Transcription Factor Suppresses
Hematopoiesis in Drosophila and Preserves the Glial Fate.” Journal of Neuroscience,
vol. 39, no. 2, Society for Neuroscience, 2019, pp. 238–55, doi:10.1523/JNEUROSCI.1059-18.2018.
short: G. Trébuchet, P.B. Cattenoz, J. Zsámboki, D. Mazaud, D.E. Siekhaus, M. Fanto,
A. Giangrande, Journal of Neuroscience 39 (2019) 238–255.
date_created: 2018-12-11T11:44:07Z
date_published: 2019-01-09T00:00:00Z
date_updated: 2023-09-19T10:10:55Z
day: '09'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.1523/JNEUROSCI.1059-18.2018
ec_funded: 1
external_id:
isi:
- '000455189900006'
pmid:
- '30504274'
file:
- access_level: open_access
checksum: 8f6925eb4cd1e8747d8ea25929c68de6
content_type: application/pdf
creator: dernst
date_created: 2020-10-02T09:33:28Z
date_updated: 2020-10-02T09:33:28Z
file_id: '8596'
file_name: 2019_JournNeuroscience_Trebuchet.pdf
file_size: 9455414
relation: main_file
success: 1
file_date_updated: 2020-10-02T09:33:28Z
has_accepted_license: '1'
intvolume: ' 39'
isi: 1
issue: '2'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 238-255
pmid: 1
project:
- _id: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '8048'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila
and preserves the glial fate
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 39
year: '2019'
...
---
_id: '7097'
abstract:
- lang: eng
text: Early endosomes, also called sorting endosomes, are known to mature into late
endosomesvia the Rab5-mediated endolysosomal trafficking pathway. Thus, early
endosome existence isthought to be maintained by the continual fusion of transport
vesicles from the plasmamembrane and thetrans-Golgi network (TGN). Here we show
instead that endocytosis isdispensable and post-Golgi vesicle transport is crucial
for the formation of endosomes andthe subsequent endolysosomal traffic regulated
by yeast Rab5 Vps21p. Fittingly, all threeproteins required for endosomal nucleotide
exchange on Vps21p arefirst recruited to theTGN before transport to the endosome, namely the GEF Vps9p
and the epsin-relatedadaptors Ent3/5p. The TGN recruitment of these components
is distinctly controlled, withVps9p appearing to require the Arf1p GTPase, and
the Rab11s, Ypt31p/32p. These resultsprovide a different view of endosome formation
and identify the TGN as a critical location forregulating progress through the
endolysosomal trafficking pathway.
article_number: '419'
article_processing_charge: No
article_type: original
author:
- first_name: Makoto
full_name: Nagano, Makoto
last_name: Nagano
- first_name: Junko Y.
full_name: Toshima, Junko Y.
last_name: Toshima
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
- first_name: Jiro
full_name: Toshima, Jiro
last_name: Toshima
citation:
ama: Nagano M, Toshima JY, Siekhaus DE, Toshima J. Rab5-mediated endosome formation
is regulated at the trans-Golgi network. Communications Biology. 2019;2(1).
doi:10.1038/s42003-019-0670-5
apa: Nagano, M., Toshima, J. Y., Siekhaus, D. E., & Toshima, J. (2019). Rab5-mediated
endosome formation is regulated at the trans-Golgi network. Communications
Biology. Springer Nature. https://doi.org/10.1038/s42003-019-0670-5
chicago: Nagano, Makoto, Junko Y. Toshima, Daria E Siekhaus, and Jiro Toshima. “Rab5-Mediated
Endosome Formation Is Regulated at the Trans-Golgi Network.” Communications
Biology. Springer Nature, 2019. https://doi.org/10.1038/s42003-019-0670-5.
ieee: M. Nagano, J. Y. Toshima, D. E. Siekhaus, and J. Toshima, “Rab5-mediated endosome
formation is regulated at the trans-Golgi network,” Communications Biology,
vol. 2, no. 1. Springer Nature, 2019.
ista: Nagano M, Toshima JY, Siekhaus DE, Toshima J. 2019. Rab5-mediated endosome
formation is regulated at the trans-Golgi network. Communications Biology. 2(1),
419.
mla: Nagano, Makoto, et al. “Rab5-Mediated Endosome Formation Is Regulated at the
Trans-Golgi Network.” Communications Biology, vol. 2, no. 1, 419, Springer
Nature, 2019, doi:10.1038/s42003-019-0670-5.
short: M. Nagano, J.Y. Toshima, D.E. Siekhaus, J. Toshima, Communications Biology
2 (2019).
date_created: 2019-11-25T07:55:01Z
date_published: 2019-11-15T00:00:00Z
date_updated: 2023-08-30T07:27:55Z
day: '15'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.1038/s42003-019-0670-5
external_id:
isi:
- '000496767800005'
file:
- access_level: open_access
checksum: c63c69a264fc8a0e52f2b0d482f3bdae
content_type: application/pdf
creator: dernst
date_created: 2019-11-25T07:58:05Z
date_updated: 2020-07-14T12:47:49Z
file_id: '7098'
file_name: 2019_CommunicBiology_Nagano.pdf
file_size: 2626069
relation: main_file
file_date_updated: 2020-07-14T12:47:49Z
has_accepted_license: '1'
intvolume: ' 2'
isi: 1
issue: '1'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: Communications Biology
publication_identifier:
issn:
- 2399-3642
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Rab5-mediated endosome formation is regulated at the trans-Golgi network
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: 2
year: '2019'
...
---
_id: '7180'
abstract:
- lang: eng
text: Arabidopsis PIN2 protein directs transport of the phytohormone auxin from
the root tip into the root elongation zone. Variation in hormone transport, which
depends on a delicate interplay between PIN2 sorting to and from polar plasma
membrane domains, determines root growth. By employing a constitutively degraded
version of PIN2, we identify brassinolides as antagonists of PIN2 endocytosis.
This response does not require de novo protein synthesis, but involves early events
in canonical brassinolide signaling. Brassinolide-controlled adjustments in PIN2
sorting and intracellular distribution governs formation of a lateral PIN2 gradient
in gravistimulated roots, coinciding with adjustments in auxin signaling and directional
root growth. Strikingly, simulations indicate that PIN2 gradient formation is
no prerequisite for root bending but rather dampens asymmetric auxin flow and
signaling. Crosstalk between brassinolide signaling and endocytic PIN2 sorting,
thus, appears essential for determining the rate of gravity-induced root curvature
via attenuation of differential cell elongation.
article_number: '5516'
article_processing_charge: No
article_type: original
author:
- first_name: Katarzyna
full_name: Retzer, Katarzyna
last_name: Retzer
- first_name: Maria
full_name: Akhmanova, Maria
id: 3425EC26-F248-11E8-B48F-1D18A9856A87
last_name: Akhmanova
orcid: 0000-0003-1522-3162
- first_name: Nataliia
full_name: Konstantinova, Nataliia
last_name: Konstantinova
- first_name: Kateřina
full_name: Malínská, Kateřina
last_name: Malínská
- first_name: Johannes
full_name: Leitner, Johannes
last_name: Leitner
- first_name: Jan
full_name: Petrášek, Jan
last_name: Petrášek
- first_name: Christian
full_name: Luschnig, Christian
last_name: Luschnig
citation:
ama: Retzer K, Akhmanova M, Konstantinova N, et al. Brassinosteroid signaling delimits
root gravitropism via sorting of the Arabidopsis PIN2 auxin transporter. Nature
Communications. 2019;10. doi:10.1038/s41467-019-13543-1
apa: Retzer, K., Akhmanova, M., Konstantinova, N., Malínská, K., Leitner, J., Petrášek,
J., & Luschnig, C. (2019). Brassinosteroid signaling delimits root gravitropism
via sorting of the Arabidopsis PIN2 auxin transporter. Nature Communications.
Springer Nature. https://doi.org/10.1038/s41467-019-13543-1
chicago: Retzer, Katarzyna, Maria Akhmanova, Nataliia Konstantinova, Kateřina Malínská,
Johannes Leitner, Jan Petrášek, and Christian Luschnig. “Brassinosteroid Signaling
Delimits Root Gravitropism via Sorting of the Arabidopsis PIN2 Auxin Transporter.”
Nature Communications. Springer Nature, 2019. https://doi.org/10.1038/s41467-019-13543-1.
ieee: K. Retzer et al., “Brassinosteroid signaling delimits root gravitropism
via sorting of the Arabidopsis PIN2 auxin transporter,” Nature Communications,
vol. 10. Springer Nature, 2019.
ista: Retzer K, Akhmanova M, Konstantinova N, Malínská K, Leitner J, Petrášek J,
Luschnig C. 2019. Brassinosteroid signaling delimits root gravitropism via sorting
of the Arabidopsis PIN2 auxin transporter. Nature Communications. 10, 5516.
mla: Retzer, Katarzyna, et al. “Brassinosteroid Signaling Delimits Root Gravitropism
via Sorting of the Arabidopsis PIN2 Auxin Transporter.” Nature Communications,
vol. 10, 5516, Springer Nature, 2019, doi:10.1038/s41467-019-13543-1.
short: K. Retzer, M. Akhmanova, N. Konstantinova, K. Malínská, J. Leitner, J. Petrášek,
C. Luschnig, Nature Communications 10 (2019).
date_created: 2019-12-15T23:00:43Z
date_published: 2019-12-01T00:00:00Z
date_updated: 2023-09-06T14:08:21Z
day: '01'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.1038/s41467-019-13543-1
external_id:
isi:
- '000500508100001'
pmid:
- '31797871'
file:
- access_level: open_access
checksum: 77e8720a8e0f3091b98159f85be40893
content_type: application/pdf
creator: dernst
date_created: 2019-12-16T07:37:50Z
date_updated: 2020-07-14T12:47:52Z
file_id: '7184'
file_name: 2019_NatureComm_Retzer.pdf
file_size: 5156533
relation: main_file
file_date_updated: 2020-07-14T12:47:52Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 264CBBAC-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02379
name: Modeling epithelial tissue mechanics during cell invasion
publication: Nature Communications
publication_identifier:
eissn:
- '20411723'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Brassinosteroid signaling delimits root gravitropism via sorting of the Arabidopsis
PIN2 auxin transporter
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: 10
year: '2019'
...
---
_id: '6187'
abstract:
- lang: eng
text: Aberrant display of the truncated core1 O-glycan T-antigen is a common feature
of human cancer cells that correlates with metastasis. Here we show that T-antigen
in Drosophila melanogaster macrophages is involved in their developmentally programmed
tissue invasion. Higher macrophage T-antigen levels require an atypical major
facilitator superfamily (MFS) member that we named Minerva which enables macrophage
dissemination and invasion. We characterize for the first time the T and Tn glycoform
O-glycoproteome of the Drosophila melanogaster embryo, and determine that Minerva
increases the presence of T-antigen on proteins in pathways previously linked
to cancer, most strongly on the sulfhydryl oxidase Qsox1 which we show is required
for macrophage tissue entry. Minerva’s vertebrate ortholog, MFSD1, rescues the
minerva mutant’s migration and T-antigen glycosylation defects. We thus identify
a key conserved regulator that orchestrates O-glycosylation on a protein subset
to activate a program governing migration steps important for both development
and cancer metastasis.
acknowledged_ssus:
- _id: LifeSc
article_number: e41801
article_processing_charge: No
author:
- first_name: Katarina
full_name: Valosková, Katarina
id: 46F146FC-F248-11E8-B48F-1D18A9856A87
last_name: Valosková
- first_name: Julia
full_name: Biebl, Julia
id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87
last_name: Biebl
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: Shamsi
full_name: Emtenani, Shamsi
id: 49D32318-F248-11E8-B48F-1D18A9856A87
last_name: Emtenani
orcid: 0000-0001-6981-6938
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Michaela
full_name: Misova, Michaela
id: 495A3C32-F248-11E8-B48F-1D18A9856A87
last_name: Misova
orcid: 0000-0003-2427-6856
- first_name: Aparna
full_name: Ratheesh, Aparna
id: 2F064CFE-F248-11E8-B48F-1D18A9856A87
last_name: Ratheesh
orcid: 0000-0001-7190-0776
- first_name: Patricia
full_name: Rodrigues, Patricia
id: 2CE4065A-F248-11E8-B48F-1D18A9856A87
last_name: Rodrigues
- first_name: Katerina
full_name: Shkarina, Katerina
last_name: Shkarina
- first_name: Ida Signe Bohse
full_name: Larsen, Ida Signe Bohse
last_name: Larsen
- first_name: Sergey Y
full_name: Vakhrushev, Sergey Y
last_name: Vakhrushev
- first_name: Henrik
full_name: Clausen, Henrik
last_name: Clausen
- 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: Valosková K, Bicher J, Roblek M, et al. A conserved major facilitator superfamily
member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion.
eLife. 2019;8. doi:10.7554/elife.41801
apa: Valosková, K., Bicher, J., Roblek, M., Emtenani, S., György, A., Misova, M.,
… Siekhaus, D. E. (2019). A conserved major facilitator superfamily member orchestrates
a subset of O-glycosylation to aid macrophage tissue invasion. ELife. eLife
Sciences Publications. https://doi.org/10.7554/elife.41801
chicago: Valosková, Katarina, Julia Bicher, Marko Roblek, Shamsi Emtenani, Attila
György, Michaela Misova, Aparna Ratheesh, et al. “A Conserved Major Facilitator
Superfamily Member Orchestrates a Subset of O-Glycosylation to Aid Macrophage
Tissue Invasion.” ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/elife.41801.
ieee: K. Valosková et al., “A conserved major facilitator superfamily member
orchestrates a subset of O-glycosylation to aid macrophage tissue invasion,” eLife,
vol. 8. eLife Sciences Publications, 2019.
ista: Valosková K, Bicher J, Roblek M, Emtenani S, György A, Misova M, Ratheesh
A, Rodrigues P, Shkarina K, Larsen ISB, Vakhrushev SY, Clausen H, Siekhaus DE.
2019. A conserved major facilitator superfamily member orchestrates a subset of
O-glycosylation to aid macrophage tissue invasion. eLife. 8, e41801.
mla: Valosková, Katarina, et al. “A Conserved Major Facilitator Superfamily Member
Orchestrates a Subset of O-Glycosylation to Aid Macrophage Tissue Invasion.” ELife,
vol. 8, e41801, eLife Sciences Publications, 2019, doi:10.7554/elife.41801.
short: K. Valosková, J. Bicher, M. Roblek, S. Emtenani, A. György, M. Misova, A.
Ratheesh, P. Rodrigues, K. Shkarina, I.S.B. Larsen, S.Y. Vakhrushev, H. Clausen,
D.E. Siekhaus, ELife 8 (2019).
date_created: 2019-03-28T13:37:45Z
date_published: 2019-03-26T00:00:00Z
date_updated: 2024-03-25T23:30:15Z
day: '26'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.7554/elife.41801
ec_funded: 1
external_id:
isi:
- '000462530200001'
file:
- access_level: open_access
checksum: cc0d1a512559d52e7e7cb0e9b9854b40
content_type: application/pdf
creator: dernst
date_created: 2019-03-28T14:00:41Z
date_updated: 2020-07-14T12:47:23Z
file_id: '6188'
file_name: 2019_eLife_Valoskova.pdf
file_size: 4496017
relation: main_file
file_date_updated: 2020-07-14T12:47:23Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
project:
- _id: 253CDE40-B435-11E9-9278-68D0E5697425
grant_number: '24283'
name: Examination of the role of a MFS transporter in the migration of Drosophila
immune cells
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: The role of Drosophila TNF alpha in immune cell invasion
- _id: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
- _id: 25388084-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '329540'
name: 'Breaking barriers: Investigating the junctional and mechanobiological changes
underlying the ability of Drosophila immune cells to invade an epithelium'
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/new-gene-potentially-involved-in-metastasis-identified/
record:
- id: '6530'
relation: dissertation_contains
- id: '8983'
relation: dissertation_contains
status: public
- id: '6546'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation
to aid macrophage tissue invasion
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 8
year: '2019'
...
---
_id: '6190'
abstract:
- lang: eng
text: "Increased levels of the chemokine CCL2 in cancer patients are associated
with poor prognosis. Experimental evidence suggests that CCL2 correlates with
inflammatory monocyte recruitment and induction of vascular activation, but the
functionality remains open. Here, we show that endothelial Ccr2 facilitates pulmonary
metastasis using an endothelial-specific Ccr2-deficient mouse model (Ccr2ecKO).
Similar levels of circulating monocytes and equal leukocyte recruitment to metastatic
lesions of Ccr2ecKO and Ccr2fl/fl littermates were observed. The absence of endothelial
Ccr2 strongly reduced pulmonary metastasis, while the primary tumor growth was
unaffected. Despite a comparable cytokine milieu in Ccr2ecKO and Ccr2fl/fl littermates
the absence of vascular permeability induction was observed only in Ccr2ecKO mice.
CCL2 stimulation of pulmonary endothelial cells resulted in increased phosphorylation
of MLC2, endothelial cell retraction, and vascular leakiness that was blocked
by an addition of a CCR2 inhibitor. These data demonstrate that endothelial CCR2
expression is required for tumor cell extravasation and pulmonary metastasis.\r\n\r\nImplications:
The findings provide mechanistic insight into how CCL2–CCR2 signaling in endothelial
cells promotes their activation through myosin light chain phosphorylation, resulting
in endothelial retraction and enhanced tumor cell migration and metastasis."
article_processing_charge: No
article_type: original
author:
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: Darya
full_name: Protsyuk, Darya
last_name: Protsyuk
- first_name: Paul F.
full_name: Becker, Paul F.
last_name: Becker
- first_name: Cristina
full_name: Stefanescu, Cristina
last_name: Stefanescu
- first_name: Christian
full_name: Gorzelanny, Christian
last_name: Gorzelanny
- first_name: Jesus F.
full_name: Glaus Garzon, Jesus F.
last_name: Glaus Garzon
- first_name: Lucia
full_name: Knopfova, Lucia
last_name: Knopfova
- first_name: Mathias
full_name: Heikenwalder, Mathias
last_name: Heikenwalder
- first_name: Bruno
full_name: Luckow, Bruno
last_name: Luckow
- first_name: Stefan W.
full_name: Schneider, Stefan W.
last_name: Schneider
- first_name: Lubor
full_name: Borsig, Lubor
last_name: Borsig
citation:
ama: Roblek M, Protsyuk D, Becker PF, et al. CCL2 is a vascular permeability factor
inducing CCR2-dependent endothelial retraction during lung metastasis. Molecular
Cancer Research. 2019;17(3):783-793. doi:10.1158/1541-7786.MCR-18-0530
apa: Roblek, M., Protsyuk, D., Becker, P. F., Stefanescu, C., Gorzelanny, C., Glaus
Garzon, J. F., … Borsig, L. (2019). CCL2 is a vascular permeability factor inducing
CCR2-dependent endothelial retraction during lung metastasis. Molecular Cancer
Research. AACR. https://doi.org/10.1158/1541-7786.MCR-18-0530
chicago: Roblek, Marko, Darya Protsyuk, Paul F. Becker, Cristina Stefanescu, Christian
Gorzelanny, Jesus F. Glaus Garzon, Lucia Knopfova, et al. “CCL2 Is a Vascular
Permeability Factor Inducing CCR2-Dependent Endothelial Retraction during Lung
Metastasis.” Molecular Cancer Research. AACR, 2019. https://doi.org/10.1158/1541-7786.MCR-18-0530.
ieee: M. Roblek et al., “CCL2 is a vascular permeability factor inducing
CCR2-dependent endothelial retraction during lung metastasis,” Molecular Cancer
Research, vol. 17, no. 3. AACR, pp. 783–793, 2019.
ista: Roblek M, Protsyuk D, Becker PF, Stefanescu C, Gorzelanny C, Glaus Garzon
JF, Knopfova L, Heikenwalder M, Luckow B, Schneider SW, Borsig L. 2019. CCL2 is
a vascular permeability factor inducing CCR2-dependent endothelial retraction
during lung metastasis. Molecular Cancer Research. 17(3), 783–793.
mla: Roblek, Marko, et al. “CCL2 Is a Vascular Permeability Factor Inducing CCR2-Dependent
Endothelial Retraction during Lung Metastasis.” Molecular Cancer Research,
vol. 17, no. 3, AACR, 2019, pp. 783–93, doi:10.1158/1541-7786.MCR-18-0530.
short: M. Roblek, D. Protsyuk, P.F. Becker, C. Stefanescu, C. Gorzelanny, J.F. Glaus
Garzon, L. Knopfova, M. Heikenwalder, B. Luckow, S.W. Schneider, L. Borsig, Molecular
Cancer Research 17 (2019) 783–793.
date_created: 2019-03-31T21:59:12Z
date_published: 2019-03-01T00:00:00Z
date_updated: 2023-08-25T08:57:01Z
day: '01'
department:
- _id: DaSi
doi: 10.1158/1541-7786.MCR-18-0530
external_id:
isi:
- '000460099800012'
pmid:
- '30552233'
intvolume: ' 17'
isi: 1
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1158/1541-7786.MCR-18-0530
month: '03'
oa: 1
oa_version: Published Version
page: 783-793
pmid: 1
publication: Molecular Cancer Research
publication_identifier:
eissn:
- '15573125'
issn:
- '15417786'
publication_status: published
publisher: AACR
quality_controlled: '1'
scopus_import: '1'
status: public
title: CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial
retraction during lung metastasis
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 17
year: '2019'
...
---
_id: '6546'
abstract:
- lang: eng
text: "Invasive migration plays a crucial role not only during development and homeostasis
but also in pathological states, such as tumor metastasis. Drosophila macrophage
migration into the extended germband is an interesting system to study invasive
migration. It carries similarities to immune cell transmigration and cancer cell
invasion, therefore studying this process could also bring new understanding of
invasion in higher organisms. In our work, we uncover a highly conserved member
of the major facilitator family that plays a role in tissue invasion through regulation
of glycosylation on a subgroup of proteins and/or by aiding the precise timing
of DN-Cadherin downregulation. \r\n\r\nAberrant display of the truncated core1
O-glycan T-antigen is a common feature of human cancer cells that correlates with
metastasis. Here we show that T-antigen in Drosophila melanogaster macrophages
is involved in their developmentally programmed tissue invasion. Higher macrophage
T-antigen levels require an atypical major facilitator superfamily (MFS) member
that we named Minerva which enables macrophage dissemination and invasion. We
characterize for the first time the T and Tn glycoform O-glycoproteome of the
Drosophila melanogaster embryo, and determine that Minerva increases the presence
of T-antigen on proteins in pathways previously linked to cancer, most strongly
on the sulfhydryl oxidase Qsox1 which we show is required for macrophage tissue
entry. Minerva’s vertebrate ortholog, MFSD1, rescues the minerva mutant’s migration
and T-antigen glycosylation defects. We thus identify \r\na key conserved regulator
that orchestrates O-glycosylation on a protein subset to activate \r\na program
governing migration steps important for both development and cancer metastasis.
\r\n"
acknowledged_ssus:
- _id: Bio
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Katarina
full_name: Valosková, Katarina
id: 46F146FC-F248-11E8-B48F-1D18A9856A87
last_name: Valosková
citation:
ama: Valosková K. The role of a highly conserved major facilitator superfamily member
in Drosophila embryonic macrophage migration. 2019. doi:10.15479/AT:ISTA:6546
apa: Valosková, K. (2019). The role of a highly conserved major facilitator superfamily
member in Drosophila embryonic macrophage migration. Institute of Science
and Technology Austria. https://doi.org/10.15479/AT:ISTA:6546
chicago: Valosková, Katarina. “The Role of a Highly Conserved Major Facilitator
Superfamily Member in Drosophila Embryonic Macrophage Migration.” Institute of
Science and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6546.
ieee: K. Valosková, “The role of a highly conserved major facilitator superfamily
member in Drosophila embryonic macrophage migration,” Institute of Science and
Technology Austria, 2019.
ista: Valosková K. 2019. The role of a highly conserved major facilitator superfamily
member in Drosophila embryonic macrophage migration. Institute of Science and
Technology Austria.
mla: Valosková, Katarina. The Role of a Highly Conserved Major Facilitator Superfamily
Member in Drosophila Embryonic Macrophage Migration. Institute of Science
and Technology Austria, 2019, doi:10.15479/AT:ISTA:6546.
short: K. Valosková, The Role of a Highly Conserved Major Facilitator Superfamily
Member in Drosophila Embryonic Macrophage Migration, Institute of Science and
Technology Austria, 2019.
date_created: 2019-06-07T12:49:19Z
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name: Examination of the role of a MFS transporter in the migration of Drosophila
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publisher: Institute of Science and Technology Austria
related_material:
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supervisor:
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full_name: Siekhaus, Daria E
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title: The role of a highly conserved major facilitator superfamily member in Drosophila
embryonic macrophage migration
type: dissertation
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...