---
_id: '13342'
abstract:
- lang: eng
text: Motile cells moving in multicellular organisms encounter microenvironments
of locally heterogeneous mechanochemical composition. Individual compositional
parameters like chemotactic signals, adhesiveness, and pore sizes are well known
to be sensed by motile cells, providing individual guidance cues for cellular
pathfinding. However, motile cells encounter diverse mechanochemical signals at
the same time, raising the question of how cells respond to locally diverse and
potentially competing signals on their migration routes. Here, we reveal that
motile amoeboid cells require nuclear repositioning, termed nucleokinesis, for
adaptive pathfinding in heterogeneous mechanochemical microenvironments. Using
mammalian immune cells and the amoebaDictyostelium discoideum,
we discover that frequent, rapid and long-distance nucleokinesis is a basic component
of amoeboid pathfinding, enabling cells to reorientate quickly between locally
competing cues. Amoeboid nucleokinesis comprises a two-step cell polarity switch
and is driven by myosin II-forces, sliding the nucleus from a ‘losing’ to the
‘winning’ leading edge to re-adjust the nuclear to the cellular path. Impaired
nucleokinesis distorts fast path adaptions and causes cellular arrest in the microenvironment.
Our findings establish that nucleokinesis is required for amoeboid cell navigation.
Given that motile single-cell amoebae, many immune cells, and some cancer cells
utilize an amoeboid migration strategy, these results suggest that amoeboid nucleokinesis
underlies cellular navigation during unicellular biology, immunity, and disease.
acknowledgement: We thank Christoph Mayr and Bingzhi Wang for initial experiments
on amoeboid nucleokinesis, Ana-Maria Lennon-Duménil and Aline Yatim for bone marrow
from MyoIIA-Flox*CD11c-Cre mice, Michael Sixt and Aglaja Kopf for EMTB-mCherry,
EB3-mCherry, Lifeact-GFP, Lfc knockout, and Myh9-GFP expressing HoxB8 cells, Malte
Benjamin Braun, Mauricio Ruiz, and Madeleine T. Schmitt for critical reading of
the manuscript, and the Core Facility Bioimaging, the Core Facility Flow Cytometry,
and the Animal Core Facility of the Biomedical Center (BMC) for excellent support.
This study was supported by the Peter Hans Hofschneider Professorship of the foundation
“Stiftung Experimentelle Biomedizin” (to JR), the LMU Institutional Strategy LMU-Excellent
within the framework of the German Excellence Initiative (to JR), and the Deutsche
Forschungsgemeinschaft (DFG; German Research Foundation; SFB914 project A12, to
JR), and the CZI grant DAF2020-225401 (https://doi.org/10.37921/120055ratwvi) from
the Chan Zuckerberg Initiative DAF (to RH; an advised fund of Silicon Valley Community
Foundation (funder https://doi.org/10.13039/100014989)). Open Access funding enabled
and organized by Projekt DEAL.
article_number: e114557
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Janina
full_name: Kroll, Janina
last_name: Kroll
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Arthur
full_name: Kuznetcov, Arthur
last_name: Kuznetcov
- first_name: Kasia
full_name: Stefanowski, Kasia
last_name: Stefanowski
- first_name: Monika D.
full_name: Hermann, Monika D.
last_name: Hermann
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Lubuna B
full_name: Shafeek, Lubuna B
id: 3CD37A82-F248-11E8-B48F-1D18A9856A87
last_name: Shafeek
orcid: 0000-0001-7180-6050
- first_name: Annette
full_name: Müller-Taubenberger, Annette
last_name: Müller-Taubenberger
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
citation:
ama: Kroll J, Hauschild R, Kuznetcov A, et al. Adaptive pathfinding by nucleokinesis
during amoeboid migration. EMBO Journal. 2023. doi:10.15252/embj.2023114557
apa: Kroll, J., Hauschild, R., Kuznetcov, A., Stefanowski, K., Hermann, M. D., Merrin,
J., … Renkawitz, J. (2023). Adaptive pathfinding by nucleokinesis during amoeboid
migration. EMBO Journal. Embo Press. https://doi.org/10.15252/embj.2023114557
chicago: Kroll, Janina, Robert Hauschild, Arthur Kuznetcov, Kasia Stefanowski, Monika
D. Hermann, Jack Merrin, Lubuna B Shafeek, Annette Müller-Taubenberger, and Jörg
Renkawitz. “Adaptive Pathfinding by Nucleokinesis during Amoeboid Migration.”
EMBO Journal. Embo Press, 2023. https://doi.org/10.15252/embj.2023114557.
ieee: J. Kroll et al., “Adaptive pathfinding by nucleokinesis during amoeboid
migration,” EMBO Journal. Embo Press, 2023.
ista: Kroll J, Hauschild R, Kuznetcov A, Stefanowski K, Hermann MD, Merrin J, Shafeek
LB, Müller-Taubenberger A, Renkawitz J. 2023. Adaptive pathfinding by nucleokinesis
during amoeboid migration. EMBO Journal., e114557.
mla: Kroll, Janina, et al. “Adaptive Pathfinding by Nucleokinesis during Amoeboid
Migration.” EMBO Journal, e114557, Embo Press, 2023, doi:10.15252/embj.2023114557.
short: J. Kroll, R. Hauschild, A. Kuznetcov, K. Stefanowski, M.D. Hermann, J. Merrin,
L.B. Shafeek, A. Müller-Taubenberger, J. Renkawitz, EMBO Journal (2023).
date_created: 2023-08-01T08:59:06Z
date_published: 2023-11-21T00:00:00Z
date_updated: 2023-11-27T08:47:45Z
day: '21'
ddc:
- '570'
department:
- _id: NanoFab
- _id: Bio
doi: 10.15252/embj.2023114557
external_id:
pmid:
- '37987147'
file:
- access_level: open_access
checksum: 6261d0041c7e8d284c39712c40079730
content_type: application/pdf
creator: dernst
date_created: 2023-11-27T08:45:56Z
date_updated: 2023-11-27T08:45:56Z
file_id: '14611'
file_name: 2023_EmboJournal_Kroll.pdf
file_size: 4862497
relation: main_file
success: 1
file_date_updated: 2023-11-27T08:45:56Z
has_accepted_license: '1'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: EMBO Journal
publication_identifier:
eissn:
- 1460-2075
issn:
- 0261-4189
publication_status: published
publisher: Embo Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Adaptive pathfinding by nucleokinesis during amoeboid migration
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '11182'
abstract:
- lang: eng
text: Immune cells are constantly on the move through multicellular organisms to
explore and respond to pathogens and other harmful insults. While moving, immune
cells efficiently traverse microenvironments composed of tissue cells and extracellular
fibers, which together form complex environments of various porosity, stiffness,
topography, and chemical composition. In this protocol we describe experimental
procedures to investigate immune cell migration through microenvironments of heterogeneous
porosity. In particular, we describe micro-channels, micro-pillars, and collagen
networks as cell migration paths with alternative pore size choices. Employing
micro-channels or micro-pillars that divide at junctions into alternative paths
with initially differentially sized pores allows us to precisely (1) measure the
cellular translocation time through these porous path junctions, (2) quantify
the cellular preference for individual pore sizes, and (3) image cellular components
like the nucleus and the cytoskeleton. This reductionistic experimental setup
thus can elucidate how immune cells perform decisions in complex microenvironments
of various porosity like the interstitium. The setup further allows investigation
of the underlying forces of cellular squeezing and the consequences of cellular
deformation on the integrity of the cell and its organelles. As a complementary
approach that does not require any micro-engineering expertise, we describe the
usage of three-dimensional collagen networks with different pore sizes. Whereas
we here focus on dendritic cells as a model for motile immune cells, the described
protocols are versatile as they are also applicable for other immune cell types
like neutrophils and non-immune cell types such as mesenchymal and cancer cells.
In summary, we here describe protocols to identify the mechanisms and principles
of cellular probing, decision making, and squeezing during cellular movement through
microenvironments of heterogeneous porosity.
acknowledgement: "We thank Kasia Stefanowski for excellent technical assistance, and
the Core Facility Bioimaging of the Biomedical Center (BMC) of the Ludwig-Maximilian
University for excellent support. We gratefully acknowledge financial support from
the Peter Hans Hofschneider Professorship of the Stiftung Experimentelle Biomedizin
(to J.R), from the DFG (Collaborative Research Center SFB914, project A12; and Priority
Programme SPP2332, project 492014049; both to J.R) and from the LMU Institutional
Strategy LMU-Excellent within the framework of the German Excellence Initiative
(to J.R).\r\nOpen access funding enabled and organized by Projekt DEAL."
article_number: e407
article_processing_charge: No
article_type: original
author:
- first_name: Janina
full_name: Kroll, Janina
last_name: Kroll
- first_name: Mauricio J.A.
full_name: Ruiz-Fernandez, Mauricio J.A.
last_name: Ruiz-Fernandez
- first_name: Malte B.
full_name: Braun, Malte B.
last_name: Braun
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
citation:
ama: Kroll J, Ruiz-Fernandez MJA, Braun MB, Merrin J, Renkawitz J. Quantifying the
probing and selection of microenvironmental pores by motile immune cells. Current
Protocols. 2022;2(4). doi:10.1002/cpz1.407
apa: Kroll, J., Ruiz-Fernandez, M. J. A., Braun, M. B., Merrin, J., & Renkawitz,
J. (2022). Quantifying the probing and selection of microenvironmental pores by
motile immune cells. Current Protocols. Wiley. https://doi.org/10.1002/cpz1.407
chicago: Kroll, Janina, Mauricio J.A. Ruiz-Fernandez, Malte B. Braun, Jack Merrin,
and Jörg Renkawitz. “Quantifying the Probing and Selection of Microenvironmental
Pores by Motile Immune Cells.” Current Protocols. Wiley, 2022. https://doi.org/10.1002/cpz1.407.
ieee: J. Kroll, M. J. A. Ruiz-Fernandez, M. B. Braun, J. Merrin, and J. Renkawitz,
“Quantifying the probing and selection of microenvironmental pores by motile immune
cells,” Current Protocols, vol. 2, no. 4. Wiley, 2022.
ista: Kroll J, Ruiz-Fernandez MJA, Braun MB, Merrin J, Renkawitz J. 2022. Quantifying
the probing and selection of microenvironmental pores by motile immune cells.
Current Protocols. 2(4), e407.
mla: Kroll, Janina, et al. “Quantifying the Probing and Selection of Microenvironmental
Pores by Motile Immune Cells.” Current Protocols, vol. 2, no. 4, e407,
Wiley, 2022, doi:10.1002/cpz1.407.
short: J. Kroll, M.J.A. Ruiz-Fernandez, M.B. Braun, J. Merrin, J. Renkawitz, Current
Protocols 2 (2022).
date_created: 2022-04-17T22:01:46Z
date_published: 2022-04-05T00:00:00Z
date_updated: 2022-05-02T08:18:00Z
day: '05'
ddc:
- '570'
department:
- _id: NanoFab
doi: 10.1002/cpz1.407
external_id:
pmid:
- '35384410'
file:
- access_level: open_access
checksum: 72152d005c367777f6cf2f6a477f0d52
content_type: application/pdf
creator: dernst
date_created: 2022-05-02T08:16:10Z
date_updated: 2022-05-02T08:16:10Z
file_id: '11347'
file_name: 2022_CurrentProtocols_Kroll.pdf
file_size: 2142703
relation: main_file
success: 1
file_date_updated: 2022-05-02T08:16:10Z
has_accepted_license: '1'
intvolume: ' 2'
issue: '4'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
publication: Current Protocols
publication_identifier:
eissn:
- 2691-1299
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Quantifying the probing and selection of microenvironmental pores by motile
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: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 2
year: '2022'
...
---
_id: '7875'
abstract:
- lang: eng
text: 'Cells navigating through complex tissues face a fundamental challenge: while
multiple protrusions explore different paths, the cell needs to avoid entanglement.
How a cell surveys and then corrects its own shape is poorly understood. Here,
we demonstrate that spatially distinct microtubule dynamics regulate amoeboid
cell migration by locally promoting the retraction of protrusions. In migrating
dendritic cells, local microtubule depolymerization within protrusions remote
from the microtubule organizing center triggers actomyosin contractility controlled
by RhoA and its exchange factor Lfc. Depletion of Lfc leads to aberrant myosin
localization, thereby causing two effects that rate-limit locomotion: (1) impaired
cell edge coordination during path finding and (2) defective adhesion resolution.
Compromised shape control is particularly hindering in geometrically complex microenvironments,
where it leads to entanglement and ultimately fragmentation of the cell body.
We thus demonstrate that microtubules can act as a proprioceptive device: they
sense cell shape and control actomyosin retraction to sustain cellular coherence.'
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
- _id: PreCl
acknowledgement: "The authors thank the Scientific Service Units (Life Sciences, Bioimaging,
Preclinical) of the Institute of Science and Technology Austria for excellent support.
This work was funded by the European Research Council (ERC StG 281556 and CoG 724373),
two grants from the Austrian\r\nScience Fund (FWF; P29911 and DK Nanocell W1250-B20
to M. Sixt) and by the German Research Foundation (DFG SFB1032 project B09) to O.
Thorn-Seshold and D. Trauner. J. Renkawitz was supported by ISTFELLOW funding from
the People Program (Marie Curie Actions) of the European Union’s Seventh Framework
Programme (FP7/2007-2013) under the Research Executive Agency grant agreement (291734)
and a European Molecular Biology Organization long-term fellowship (ALTF 1396-2014)
co-funded by the European Commission (LTFCOFUND2013, GA-2013-609409), E. Kiermaier
by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany’s
Excellence Strategy—EXC 2151—390873048, and H. Hacker by the American Lebanese Syrian
Associated ¨Charities. K.-D. Fischer was supported by the Analysis, Imaging and
Modelling of Neuronal and Inflammatory Processes graduate school funded by the Ministry
of Economics, Science, and Digitisation of the State Saxony-Anhalt and by the European
Funds for Social and Regional Development."
article_number: e201907154
article_processing_charge: No
article_type: original
author:
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Irute
full_name: Girkontaite, Irute
last_name: Girkontaite
- first_name: Kerry
full_name: Tedford, Kerry
last_name: Tedford
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Oliver
full_name: Thorn-Seshold, Oliver
last_name: Thorn-Seshold
- first_name: Dirk
full_name: Trauner, Dirk
id: E8F27F48-3EBA-11E9-92A1-B709E6697425
last_name: Trauner
- first_name: Hans
full_name: Häcker, Hans
last_name: Häcker
- first_name: Klaus Dieter
full_name: Fischer, Klaus Dieter
last_name: Fischer
- first_name: Eva
full_name: Kiermaier, Eva
id: 3EB04B78-F248-11E8-B48F-1D18A9856A87
last_name: Kiermaier
orcid: 0000-0001-6165-5738
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Kopf A, Renkawitz J, Hauschild R, et al. Microtubules control cellular shape
and coherence in amoeboid migrating cells. The Journal of Cell Biology.
2020;219(6). doi:10.1083/jcb.201907154
apa: Kopf, A., Renkawitz, J., Hauschild, R., Girkontaite, I., Tedford, K., Merrin,
J., … Sixt, M. K. (2020). Microtubules control cellular shape and coherence in
amoeboid migrating cells. The Journal of Cell Biology. Rockefeller University
Press. https://doi.org/10.1083/jcb.201907154
chicago: Kopf, Aglaja, Jörg Renkawitz, Robert Hauschild, Irute Girkontaite, Kerry
Tedford, Jack Merrin, Oliver Thorn-Seshold, et al. “Microtubules Control Cellular
Shape and Coherence in Amoeboid Migrating Cells.” The Journal of Cell Biology.
Rockefeller University Press, 2020. https://doi.org/10.1083/jcb.201907154.
ieee: A. Kopf et al., “Microtubules control cellular shape and coherence
in amoeboid migrating cells,” The Journal of Cell Biology, vol. 219, no.
6. Rockefeller University Press, 2020.
ista: Kopf A, Renkawitz J, Hauschild R, Girkontaite I, Tedford K, Merrin J, Thorn-Seshold
O, Trauner D, Häcker H, Fischer KD, Kiermaier E, Sixt MK. 2020. Microtubules control
cellular shape and coherence in amoeboid migrating cells. The Journal of Cell
Biology. 219(6), e201907154.
mla: Kopf, Aglaja, et al. “Microtubules Control Cellular Shape and Coherence in
Amoeboid Migrating Cells.” The Journal of Cell Biology, vol. 219, no. 6,
e201907154, Rockefeller University Press, 2020, doi:10.1083/jcb.201907154.
short: A. Kopf, J. Renkawitz, R. Hauschild, I. Girkontaite, K. Tedford, J. Merrin,
O. Thorn-Seshold, D. Trauner, H. Häcker, K.D. Fischer, E. Kiermaier, M.K. Sixt,
The Journal of Cell Biology 219 (2020).
date_created: 2020-05-24T22:00:56Z
date_published: 2020-06-01T00:00:00Z
date_updated: 2023-08-21T06:28:17Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
- _id: NanoFab
doi: 10.1083/jcb.201907154
ec_funded: 1
external_id:
isi:
- '000538141100020'
pmid:
- '32379884'
file:
- access_level: open_access
checksum: cb0b9c77842ae1214caade7b77e4d82d
content_type: application/pdf
creator: dernst
date_created: 2020-11-24T13:25:13Z
date_updated: 2020-11-24T13:25:13Z
file_id: '8801'
file_name: 2020_JCellBiol_Kopf.pdf
file_size: 7536712
relation: main_file
success: 1
file_date_updated: 2020-11-24T13:25:13Z
has_accepted_license: '1'
intvolume: ' 219'
isi: 1
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
- _id: 26018E70-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29911
name: Mechanical adaptation of lamellipodial actin
- _id: 252C3B08-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W 1250-B20
name: Nano-Analytics of Cellular Systems
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25A48D24-B435-11E9-9278-68D0E5697425
grant_number: ALTF 1396-2014
name: Molecular and system level view of immune cell migration
publication: The Journal of Cell Biology
publication_identifier:
eissn:
- 1540-8140
publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Microtubules control cellular shape and coherence in amoeboid migrating cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 219
year: '2020'
...
---
_id: '6328'
abstract:
- lang: eng
text: During metazoan development, immune surveillance and cancer dissemination,
cells migrate in complex three-dimensional microenvironments1,2,3. These spaces
are crowded by cells and extracellular matrix, generating mazes with differently
sized gaps that are typically smaller than the diameter of the migrating cell4,5.
Most mesenchymal and epithelial cells and some—but not all—cancer cells actively
generate their migratory path using pericellular tissue proteolysis6. By contrast,
amoeboid cells such as leukocytes use non-destructive strategies of locomotion7,
raising the question how these extremely fast cells navigate through dense tissues.
Here we reveal that leukocytes sample their immediate vicinity for large pore
sizes, and are thereby able to choose the path of least resistance. This allows
them to circumnavigate local obstacles while effectively following global directional
cues such as chemotactic gradients. Pore-size discrimination is facilitated by
frontward positioning of the nucleus, which enables the cells to use their bulkiest
compartment as a mechanical gauge. Once the nucleus and the closely associated
microtubule organizing centre pass the largest pore, cytoplasmic protrusions still
lingering in smaller pores are retracted. These retractions are coordinated by
dynamic microtubules; when microtubules are disrupted, migrating cells lose coherence
and frequently fragment into migratory cytoplasmic pieces. As nuclear positioning
in front of the microtubule organizing centre is a typical feature of amoeboid
migration, our findings link the fundamental organization of cellular polarity
to the strategy of locomotion.
acknowledged_ssus:
- _id: SSU
article_processing_charge: No
article_type: letter_note
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- first_name: Julian A
full_name: Stopp, Julian A
id: 489E3F00-F248-11E8-B48F-1D18A9856A87
last_name: Stopp
- first_name: Ingrid
full_name: de Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: de Vries
- first_name: Meghan K.
full_name: Driscoll, Meghan K.
last_name: Driscoll
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Erik S.
full_name: Welf, Erik S.
last_name: Welf
- first_name: Gaudenz
full_name: Danuser, Gaudenz
last_name: Danuser
- first_name: Reto
full_name: Fiolka, Reto
last_name: Fiolka
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Renkawitz J, Kopf A, Stopp JA, et al. Nuclear positioning facilitates amoeboid
migration along the path of least resistance. Nature. 2019;568:546-550.
doi:10.1038/s41586-019-1087-5
apa: Renkawitz, J., Kopf, A., Stopp, J. A., de Vries, I., Driscoll, M. K., Merrin,
J., … Sixt, M. K. (2019). Nuclear positioning facilitates amoeboid migration along
the path of least resistance. Nature. Springer Nature. https://doi.org/10.1038/s41586-019-1087-5
chicago: Renkawitz, Jörg, Aglaja Kopf, Julian A Stopp, Ingrid de Vries, Meghan K.
Driscoll, Jack Merrin, Robert Hauschild, et al. “Nuclear Positioning Facilitates
Amoeboid Migration along the Path of Least Resistance.” Nature. Springer
Nature, 2019. https://doi.org/10.1038/s41586-019-1087-5.
ieee: J. Renkawitz et al., “Nuclear positioning facilitates amoeboid migration
along the path of least resistance,” Nature, vol. 568. Springer Nature,
pp. 546–550, 2019.
ista: Renkawitz J, Kopf A, Stopp JA, de Vries I, Driscoll MK, Merrin J, Hauschild
R, Welf ES, Danuser G, Fiolka R, Sixt MK. 2019. Nuclear positioning facilitates
amoeboid migration along the path of least resistance. Nature. 568, 546–550.
mla: Renkawitz, Jörg, et al. “Nuclear Positioning Facilitates Amoeboid Migration
along the Path of Least Resistance.” Nature, vol. 568, Springer Nature,
2019, pp. 546–50, doi:10.1038/s41586-019-1087-5.
short: J. Renkawitz, A. Kopf, J.A. Stopp, I. de Vries, M.K. Driscoll, J. Merrin,
R. Hauschild, E.S. Welf, G. Danuser, R. Fiolka, M.K. Sixt, Nature 568 (2019) 546–550.
date_created: 2019-04-17T06:52:28Z
date_published: 2019-04-25T00:00:00Z
date_updated: 2024-03-25T23:30:22Z
day: '25'
department:
- _id: MiSi
- _id: NanoFab
- _id: Bio
doi: 10.1038/s41586-019-1087-5
ec_funded: 1
external_id:
isi:
- '000465594200050'
pmid:
- '30944468'
intvolume: ' 568'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217284/
month: '04'
oa: 1
oa_version: Submitted Version
page: 546-550
pmid: 1
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
- _id: 265FAEBA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W01250-B20
name: Nano-Analytics of Cellular Systems
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25A48D24-B435-11E9-9278-68D0E5697425
grant_number: ALTF 1396-2014
name: Molecular and system level view of immune cell migration
publication: Nature
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/leukocytes-use-their-nucleus-as-a-ruler-to-choose-path-of-least-resistance/
record:
- id: '14697'
relation: dissertation_contains
status: public
- id: '6891'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Nuclear positioning facilitates amoeboid migration along the path of least
resistance
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 568
year: '2019'
...
---
_id: '276'
abstract:
- lang: eng
text: Directed migration of cells relies on their ability to sense directional guidance
cues and to interact with pericellular structures in order to transduce contractile
cytoskeletal- into mechanical forces. These biomechanical processes depend highly
on microenvironmental factors such as exposure to 2D surfaces or 3D matrices.
In vivo, the majority of cells are exposed to 3D environments. Data on 3D cell
migration are mostly derived from intravital microscopy or collagen-based in vitro
assays. Both approaches offer only limited controlla-bility of experimental conditions.
Here, we developed an automated microfluidic system that allows positioning of
cells in 3D microenvironments containing highly controlled diffusion-based chemokine
gradients. Tracking migration in such gradients was feasible in real time at the
single cell level. Moreover, the setup allowed on-chip immunocytochemistry and
thus linking of functional with phenotypical properties in individual cells. Spatially
defined retrieval of cells from the device allows down-stream off-chip analysis.
Using dendritic cells as a model, our setup specifically allowed us for the first
time to quantitate key migration characteristics of cells exposed to identical
gradients of the chemokine CCL19 yet placed on 2D vs in 3D environments. Migration
properties between 2D and 3D migration were distinct. Morphological features of
cells migrating in an in vitro 3D environment were similar to those of cells migrating
in animal tissues, but different from cells migrating on a surface. Our system
thus offers a highly controllable in vitro-mimic of a 3D environment that cells
traffic in vivo.
acknowledgement: This work was supported by the Swiss National Science Foundation
(MD-PhD fellowships, 323530_164221 to C.F.; and 323630_151483 to A.J.; grant PZ00P3_144863
to M.R, grant 31003A_156431 to T.S.; PZ00P3_148000 to C.T.B.; PZ00P3_154733 to M.M.),
a Novartis “FreeNovation” grant to M.M. and T.S. and an EMBO long-term fellowship
(ALTF 1396-2014) co-funded by the European Commission (LTFCOFUND2013, GA-2013-609409)
to J.R.. M.R. was supported by the Gebert Rüf Foundation (GRS 058/14). The funders
had no role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
article_number: e0198330
article_processing_charge: No
article_type: original
author:
- first_name: Corina
full_name: Frick, Corina
last_name: Frick
- first_name: Philip
full_name: Dettinger, Philip
last_name: Dettinger
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Annaïse
full_name: Jauch, Annaïse
last_name: Jauch
- first_name: Christoph
full_name: Berger, Christoph
last_name: Berger
- first_name: Mike
full_name: Recher, Mike
last_name: Recher
- first_name: Timm
full_name: Schroeder, Timm
last_name: Schroeder
- first_name: Matthias
full_name: Mehling, Matthias
last_name: Mehling
citation:
ama: Frick C, Dettinger P, Renkawitz J, et al. Nano-scale microfluidics to study
3D chemotaxis at the single cell level. PLoS One. 2018;13(6). doi:10.1371/journal.pone.0198330
apa: Frick, C., Dettinger, P., Renkawitz, J., Jauch, A., Berger, C., Recher, M.,
… Mehling, M. (2018). Nano-scale microfluidics to study 3D chemotaxis at the single
cell level. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0198330
chicago: Frick, Corina, Philip Dettinger, Jörg Renkawitz, Annaïse Jauch, Christoph
Berger, Mike Recher, Timm Schroeder, and Matthias Mehling. “Nano-Scale Microfluidics
to Study 3D Chemotaxis at the Single Cell Level.” PLoS One. Public Library
of Science, 2018. https://doi.org/10.1371/journal.pone.0198330.
ieee: C. Frick et al., “Nano-scale microfluidics to study 3D chemotaxis at
the single cell level,” PLoS One, vol. 13, no. 6. Public Library of Science,
2018.
ista: Frick C, Dettinger P, Renkawitz J, Jauch A, Berger C, Recher M, Schroeder
T, Mehling M. 2018. Nano-scale microfluidics to study 3D chemotaxis at the single
cell level. PLoS One. 13(6), e0198330.
mla: Frick, Corina, et al. “Nano-Scale Microfluidics to Study 3D Chemotaxis at the
Single Cell Level.” PLoS One, vol. 13, no. 6, e0198330, Public Library
of Science, 2018, doi:10.1371/journal.pone.0198330.
short: C. Frick, P. Dettinger, J. Renkawitz, A. Jauch, C. Berger, M. Recher, T.
Schroeder, M. Mehling, PLoS One 13 (2018).
date_created: 2018-12-11T11:45:34Z
date_published: 2018-06-07T00:00:00Z
date_updated: 2023-09-13T09:00:15Z
day: '07'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1371/journal.pone.0198330
external_id:
isi:
- '000434384900031'
file:
- access_level: open_access
checksum: 95fc5dc3938b3ad3b7697d10c83cc143
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T14:10:32Z
date_updated: 2020-07-14T12:45:45Z
file_id: '5709'
file_name: 2018_Plos_Frick.pdf
file_size: 7682167
relation: main_file
file_date_updated: 2020-07-14T12:45:45Z
has_accepted_license: '1'
intvolume: ' 13'
isi: 1
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '7626'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nano-scale microfluidics to study 3D chemotaxis at the single cell level
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: 13
year: '2018'
...
---
_id: '15'
abstract:
- lang: eng
text: Although much is known about the physiological framework of T cell motility,
and numerous rate-limiting molecules have been identified through loss-of-function
approaches, an integrated functional concept of T cell motility is lacking. Here,
we used in vivo precision morphometry together with analysis of cytoskeletal dynamics
in vitro to deconstruct the basic mechanisms of T cell migration within lymphatic
organs. We show that the contributions of the integrin LFA-1 and the chemokine
receptor CCR7 are complementary rather than positioned in a linear pathway, as
they are during leukocyte extravasation from the blood vasculature. Our data demonstrate
that CCR7 controls cortical actin flows, whereas integrins mediate substrate friction
that is sufficient to drive locomotion in the absence of considerable surface
adhesions and plasma membrane flux.
acknowledged_ssus:
- _id: SSU
acknowledgement: This work was funded by grants from the European Research Council
(ERC StG 281556 and CoG 724373) and the Austrian Science Foundation (FWF) to M.S.
and by Swiss National Foundation (SNF) project grants 31003A_135649, 31003A_153457
and CR23I3_156234 to J.V.S. F.G. received funding from the European Union’s Horizon
2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement
no. 747687, and J.R. was funded by an EMBO long-term fellowship (ALTF 1396-2014).
article_processing_charge: No
author:
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Hons M, Kopf A, Hauschild R, et al. Chemokines and integrins independently
tune actin flow and substrate friction during intranodal migration of T cells.
Nature Immunology. 2018;19(6):606-616. doi:10.1038/s41590-018-0109-z
apa: Hons, M., Kopf, A., Hauschild, R., Leithner, A. F., Gärtner, F. R., Abe, J.,
… Sixt, M. K. (2018). Chemokines and integrins independently tune actin flow and
substrate friction during intranodal migration of T cells. Nature Immunology.
Nature Publishing Group. https://doi.org/10.1038/s41590-018-0109-z
chicago: Hons, Miroslav, Aglaja Kopf, Robert Hauschild, Alexander F Leithner, Florian
R Gärtner, Jun Abe, Jörg Renkawitz, Jens Stein, and Michael K Sixt. “Chemokines
and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal
Migration of T Cells.” Nature Immunology. Nature Publishing Group, 2018.
https://doi.org/10.1038/s41590-018-0109-z.
ieee: M. Hons et al., “Chemokines and integrins independently tune actin
flow and substrate friction during intranodal migration of T cells,” Nature
Immunology, vol. 19, no. 6. Nature Publishing Group, pp. 606–616, 2018.
ista: Hons M, Kopf A, Hauschild R, Leithner AF, Gärtner FR, Abe J, Renkawitz J,
Stein J, Sixt MK. 2018. Chemokines and integrins independently tune actin flow
and substrate friction during intranodal migration of T cells. Nature Immunology.
19(6), 606–616.
mla: Hons, Miroslav, et al. “Chemokines and Integrins Independently Tune Actin Flow
and Substrate Friction during Intranodal Migration of T Cells.” Nature Immunology,
vol. 19, no. 6, Nature Publishing Group, 2018, pp. 606–16, doi:10.1038/s41590-018-0109-z.
short: M. Hons, A. Kopf, R. Hauschild, A.F. Leithner, F.R. Gärtner, J. Abe, J. Renkawitz,
J. Stein, M.K. Sixt, Nature Immunology 19 (2018) 606–616.
date_created: 2018-12-11T11:44:10Z
date_published: 2018-05-18T00:00:00Z
date_updated: 2024-03-25T23:30:22Z
day: '18'
department:
- _id: MiSi
- _id: Bio
doi: 10.1038/s41590-018-0109-z
ec_funded: 1
external_id:
isi:
- '000433041500026'
pmid:
- '29777221'
intvolume: ' 19'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/29777221
month: '05'
oa: 1
oa_version: Published Version
page: 606 - 616
pmid: 1
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
- _id: 25A48D24-B435-11E9-9278-68D0E5697425
grant_number: ALTF 1396-2014
name: Molecular and system level view of immune cell migration
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '8040'
quality_controlled: '1'
related_material:
record:
- id: '6891'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Chemokines and integrins independently tune actin flow and substrate friction
during intranodal migration of T cells
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 19
year: '2018'
...
---
_id: '153'
abstract:
- lang: eng
text: Cells migrating in multicellular organisms steadily traverse complex three-dimensional
(3D) environments. To decipher the underlying cell biology, current experimental
setups either use simplified 2D, tissue-mimetic 3D (e.g., collagen matrices) or
in vivo environments. While only in vivo experiments are truly physiological,
they do not allow for precise manipulation of environmental parameters. 2D in
vitro experiments do allow mechanical and chemical manipulations, but increasing
evidence demonstrates substantial differences of migratory mechanisms in 2D and
3D. Here, we describe simple, robust, and versatile “pillar forests” to investigate
cell migration in complex but fully controllable 3D environments. Pillar forests
are polydimethylsiloxane-based setups, in which two closely adjacent surfaces
are interconnected by arrays of micrometer-sized pillars. Changing the pillar
shape, size, height and the inter-pillar distance precisely manipulates microenvironmental
parameters (e.g., pore sizes, micro-geometry, micro-topology), while being easily
combined with chemotactic cues, surface coatings, diverse cell types and advanced
imaging techniques. Thus, pillar forests combine the advantages of 2D cell migration
assays with the precise definition of 3D environmental parameters.
article_processing_charge: No
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Renkawitz J, Reversat A, Leithner AF, Merrin J, Sixt MK. Micro-engineered
“pillar forests” to study cell migration in complex but controlled 3D environments.
In: Methods in Cell Biology. Vol 147. Academic Press; 2018:79-91. doi:10.1016/bs.mcb.2018.07.004'
apa: Renkawitz, J., Reversat, A., Leithner, A. F., Merrin, J., & Sixt, M. K.
(2018). Micro-engineered “pillar forests” to study cell migration in complex but
controlled 3D environments. In Methods in Cell Biology (Vol. 147, pp. 79–91).
Academic Press. https://doi.org/10.1016/bs.mcb.2018.07.004
chicago: Renkawitz, Jörg, Anne Reversat, Alexander F Leithner, Jack Merrin, and
Michael K Sixt. “Micro-Engineered ‘Pillar Forests’ to Study Cell Migration in
Complex but Controlled 3D Environments.” In Methods in Cell Biology, 147:79–91.
Academic Press, 2018. https://doi.org/10.1016/bs.mcb.2018.07.004.
ieee: J. Renkawitz, A. Reversat, A. F. Leithner, J. Merrin, and M. K. Sixt, “Micro-engineered
‘pillar forests’ to study cell migration in complex but controlled 3D environments,”
in Methods in Cell Biology, vol. 147, Academic Press, 2018, pp. 79–91.
ista: 'Renkawitz J, Reversat A, Leithner AF, Merrin J, Sixt MK. 2018.Micro-engineered
“pillar forests” to study cell migration in complex but controlled 3D environments.
In: Methods in Cell Biology. vol. 147, 79–91.'
mla: Renkawitz, Jörg, et al. “Micro-Engineered ‘Pillar Forests’ to Study Cell Migration
in Complex but Controlled 3D Environments.” Methods in Cell Biology, vol.
147, Academic Press, 2018, pp. 79–91, doi:10.1016/bs.mcb.2018.07.004.
short: J. Renkawitz, A. Reversat, A.F. Leithner, J. Merrin, M.K. Sixt, in:, Methods
in Cell Biology, Academic Press, 2018, pp. 79–91.
date_created: 2018-12-11T11:44:54Z
date_published: 2018-07-27T00:00:00Z
date_updated: 2023-09-13T08:56:35Z
day: '27'
department:
- _id: MiSi
- _id: NanoFab
doi: 10.1016/bs.mcb.2018.07.004
external_id:
isi:
- '000452412300006'
pmid:
- '30165964'
intvolume: ' 147'
isi: 1
language:
- iso: eng
month: '07'
oa_version: None
page: 79 - 91
pmid: 1
publication: Methods in Cell Biology
publication_identifier:
issn:
- 0091679X
publication_status: published
publisher: Academic Press
publist_id: '7768'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Micro-engineered “pillar forests” to study cell migration in complex but controlled
3D environments
type: book_chapter
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 147
year: '2018'
...
---
_id: '437'
abstract:
- lang: eng
text: Dendritic cells (DCs) are sentinels of the adaptive immune system that reside
in peripheral organs of mammals. Upon pathogen encounter, they undergo maturation
and up-regulate the chemokine receptor CCR7 that guides them along gradients of
its chemokine ligands CCL19 and 21 to the next draining lymph node. There, DCs
present peripherally acquired antigen to naïve T cells, thereby triggering adaptive
immunity.
acknowledged_ssus:
- _id: SSU
acknowledgement: "This work was supported by grants of the European Research Council
(ERC CoG 724373) and the Austrian Science Fund (FWF) to M.S. We thank the scientific
support units at IST Austria for excellent technical support.\r\nWe thank the scientific
\ support units at IST Austria for excellent technical support. "
article_processing_charge: Yes (via OA deal)
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Hans
full_name: Haecker, Hans
last_name: Haecker
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Leithner AF, Renkawitz J, de Vries I, Hauschild R, Haecker H, Sixt MK. Fast
and efficient genetic engineering of hematopoietic precursor cells for the study
of dendritic cell migration. European Journal of Immunology. 2018;48(6):1074-1077.
doi:10.1002/eji.201747358
apa: Leithner, A. F., Renkawitz, J., de Vries, I., Hauschild, R., Haecker, H., &
Sixt, M. K. (2018). Fast and efficient genetic engineering of hematopoietic precursor
cells for the study of dendritic cell migration. European Journal of Immunology.
Wiley-Blackwell. https://doi.org/10.1002/eji.201747358
chicago: Leithner, Alexander F, Jörg Renkawitz, Ingrid de Vries, Robert Hauschild,
Hans Haecker, and Michael K Sixt. “Fast and Efficient Genetic Engineering of Hematopoietic
Precursor Cells for the Study of Dendritic Cell Migration.” European Journal
of Immunology. Wiley-Blackwell, 2018. https://doi.org/10.1002/eji.201747358.
ieee: A. F. Leithner, J. Renkawitz, I. de Vries, R. Hauschild, H. Haecker, and M.
K. Sixt, “Fast and efficient genetic engineering of hematopoietic precursor cells
for the study of dendritic cell migration,” European Journal of Immunology,
vol. 48, no. 6. Wiley-Blackwell, pp. 1074–1077, 2018.
ista: Leithner AF, Renkawitz J, de Vries I, Hauschild R, Haecker H, Sixt MK. 2018.
Fast and efficient genetic engineering of hematopoietic precursor cells for the
study of dendritic cell migration. European Journal of Immunology. 48(6), 1074–1077.
mla: Leithner, Alexander F., et al. “Fast and Efficient Genetic Engineering of Hematopoietic
Precursor Cells for the Study of Dendritic Cell Migration.” European Journal
of Immunology, vol. 48, no. 6, Wiley-Blackwell, 2018, pp. 1074–77, doi:10.1002/eji.201747358.
short: A.F. Leithner, J. Renkawitz, I. de Vries, R. Hauschild, H. Haecker, M.K.
Sixt, European Journal of Immunology 48 (2018) 1074–1077.
date_created: 2018-12-11T11:46:28Z
date_published: 2018-02-13T00:00:00Z
date_updated: 2023-09-11T14:01:18Z
day: '13'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
doi: 10.1002/eji.201747358
ec_funded: 1
external_id:
isi:
- '000434963700016'
file:
- access_level: open_access
checksum: 9d5b74cd016505aeb9a4c2d33bbedaeb
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:56Z
date_updated: 2020-07-14T12:46:27Z
file_id: '5044'
file_name: IST-2018-1067-v1+2_Leithner_et_al-2018-European_Journal_of_Immunology.pdf
file_size: 590106
relation: main_file
file_date_updated: 2020-07-14T12:46:27Z
has_accepted_license: '1'
intvolume: ' 48'
isi: 1
issue: '6'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 1074 - 1077
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
publication: European Journal of Immunology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '7386'
pubrep_id: '1067'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Fast and efficient genetic engineering of hematopoietic precursor cells for
the study of dendritic cell migration
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 48
year: '2018'
...
---
_id: '677'
abstract:
- lang: eng
text: The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler
that acts in transcription, replication, and genome stability. It is required
for resistance against genotoxic agents and is involved in the repair of DNA double-strand
breaks (DSBs) by homologous recombination (HR). However, the causes of the HR
defect in INO80-C mutant cells are controversial. Here, we unite previous findings
using a system to study HR with high spatial resolution in budding yeast. We find
that INO80-C has at least two distinct functions during HR—DNA end resection and
presynaptic filament formation. Importantly, the second function is linked to
the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation
and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic
filament formation is the crucial INO80-C function during HR.
author:
- first_name: Claudio
full_name: Lademann, Claudio
last_name: Lademann
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Boris
full_name: Pfander, Boris
last_name: Pfander
- first_name: Stefan
full_name: Jentsch, Stefan
last_name: Jentsch
citation:
ama: Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z
to promote presynaptic filament formation during homologous recombination. Cell
Reports. 2017;19(7):1294-1303. doi:10.1016/j.celrep.2017.04.051
apa: Lademann, C., Renkawitz, J., Pfander, B., & Jentsch, S. (2017). The INO80
complex removes H2A.Z to promote presynaptic filament formation during homologous
recombination. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.051
chicago: Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The
INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous
Recombination.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.051.
ieee: C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex
removes H2A.Z to promote presynaptic filament formation during homologous recombination,”
Cell Reports, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017.
ista: Lademann C, Renkawitz J, Pfander B, Jentsch S. 2017. The INO80 complex removes
H2A.Z to promote presynaptic filament formation during homologous recombination.
Cell Reports. 19(7), 1294–1303.
mla: Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic
Filament Formation during Homologous Recombination.” Cell Reports, vol.
19, no. 7, Cell Press, 2017, pp. 1294–303, doi:10.1016/j.celrep.2017.04.051.
short: C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017)
1294–1303.
date_created: 2018-12-11T11:47:52Z
date_published: 2017-05-16T00:00:00Z
date_updated: 2021-01-12T08:08:57Z
day: '16'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.celrep.2017.04.051
file:
- access_level: open_access
checksum: efc7287d9c6354983cb151880e9ad72a
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:48Z
date_updated: 2020-07-14T12:47:40Z
file_id: '5171'
file_name: IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf
file_size: 3005610
relation: main_file
file_date_updated: 2020-07-14T12:47:40Z
has_accepted_license: '1'
intvolume: ' 19'
issue: '7'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 1294 - 1303
publication: Cell Reports
publication_identifier:
issn:
- '22111247'
publication_status: published
publisher: Cell Press
publist_id: '7046'
pubrep_id: '899'
quality_controlled: '1'
scopus_import: 1
status: public
title: The INO80 complex removes H2A.Z to promote presynaptic filament formation during
homologous recombination
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2017'
...
---
_id: '1150'
abstract:
- lang: eng
text: When neutrophils infiltrate a site of inflammation, they have to stop at the
right place to exert their effector function. In this issue of Developmental Cell,
Wang et al. (2016) show that neutrophils sense reactive oxygen species via the
TRPM2 channel to arrest migration at their target site. © 2016 Elsevier Inc.
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Renkawitz J, Sixt MK. A Radical Break Restraining Neutrophil Migration. Developmental
Cell. 2016;38(5):448-450. doi:10.1016/j.devcel.2016.08.017
apa: Renkawitz, J., & Sixt, M. K. (2016). A Radical Break Restraining Neutrophil
Migration. Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2016.08.017
chicago: Renkawitz, Jörg, and Michael K Sixt. “A Radical Break Restraining Neutrophil
Migration.” Developmental Cell. Cell Press, 2016. https://doi.org/10.1016/j.devcel.2016.08.017.
ieee: J. Renkawitz and M. K. Sixt, “A Radical Break Restraining Neutrophil Migration,”
Developmental Cell, vol. 38, no. 5. Cell Press, pp. 448–450, 2016.
ista: Renkawitz J, Sixt MK. 2016. A Radical Break Restraining Neutrophil Migration.
Developmental Cell. 38(5), 448–450.
mla: Renkawitz, Jörg, and Michael K. Sixt. “A Radical Break Restraining Neutrophil
Migration.” Developmental Cell, vol. 38, no. 5, Cell Press, 2016, pp. 448–50,
doi:10.1016/j.devcel.2016.08.017.
short: J. Renkawitz, M.K. Sixt, Developmental Cell 38 (2016) 448–450.
date_created: 2018-12-11T11:50:25Z
date_published: 2016-09-12T00:00:00Z
date_updated: 2021-01-12T06:48:39Z
day: '12'
department:
- _id: MiSi
doi: 10.1016/j.devcel.2016.08.017
intvolume: ' 38'
issue: '5'
language:
- iso: eng
month: '09'
oa_version: None
page: 448 - 450
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '6208'
quality_controlled: '1'
scopus_import: 1
status: public
title: A Radical Break Restraining Neutrophil Migration
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 38
year: '2016'
...
---
_id: '1201'
abstract:
- lang: eng
text: In this issue of Cell, Skau et al. show that the formin FMN2 organizes a perinuclear
actin cytoskeleton that protects the nucleus and its genomic content of migrating
cells squeezing through small spaces.
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Renkawitz J, Sixt MK. Formin’ a nuclear protection. Cell. 2016;167(6):1448-1449.
doi:10.1016/j.cell.2016.11.024
apa: Renkawitz, J., & Sixt, M. K. (2016). Formin’ a nuclear protection. Cell.
Cell Press. https://doi.org/10.1016/j.cell.2016.11.024
chicago: Renkawitz, Jörg, and Michael K Sixt. “Formin’ a Nuclear Protection.” Cell.
Cell Press, 2016. https://doi.org/10.1016/j.cell.2016.11.024.
ieee: J. Renkawitz and M. K. Sixt, “Formin’ a nuclear protection,” Cell,
vol. 167, no. 6. Cell Press, pp. 1448–1449, 2016.
ista: Renkawitz J, Sixt MK. 2016. Formin’ a nuclear protection. Cell. 167(6), 1448–1449.
mla: Renkawitz, Jörg, and Michael K. Sixt. “Formin’ a Nuclear Protection.” Cell,
vol. 167, no. 6, Cell Press, 2016, pp. 1448–49, doi:10.1016/j.cell.2016.11.024.
short: J. Renkawitz, M.K. Sixt, Cell 167 (2016) 1448–1449.
date_created: 2018-12-11T11:50:41Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2021-01-12T06:49:03Z
day: '01'
department:
- _id: MiSi
doi: 10.1016/j.cell.2016.11.024
intvolume: ' 167'
issue: '6'
language:
- iso: eng
month: '12'
oa_version: None
page: 1448 - 1449
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '6149'
quality_controlled: '1'
scopus_import: 1
status: public
title: Formin’ a nuclear protection
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 167
year: '2016'
...
---
_id: '2215'
abstract:
- lang: eng
text: Homologous recombination is crucial for genome stability and for genetic exchange.
Although our knowledge of the principle steps in recombination and its machinery
is well advanced, homology search, the critical step of exploring the genome for
homologous sequences to enable recombination, has remained mostly enigmatic. However,
recent methodological advances have provided considerable new insights into this
fundamental step in recombination that can be integrated into a mechanistic model.
These advances emphasize the importance of genomic proximity and nuclear organization
for homology search and the critical role of homology search mediators in this
process. They also aid our understanding of how homology search might lead to
unwanted and potentially disease-promoting recombination events.
acknowledgement: J.R. was supported by a Boehringer Ingelheim Fonds PhD stipend.
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Claudio
full_name: Lademann, Claudio
last_name: Lademann
- first_name: Stefan
full_name: Jentsch, Stefan
last_name: Jentsch
citation:
ama: Renkawitz J, Lademann C, Jentsch S. Mechanisms and principles of homology search
during recombination. Nature Reviews Molecular Cell Biology. 2014;15(6):369-383.
doi:10.1038/nrm3805
apa: Renkawitz, J., Lademann, C., & Jentsch, S. (2014). Mechanisms and principles
of homology search during recombination. Nature Reviews Molecular Cell Biology.
Nature Publishing Group. https://doi.org/10.1038/nrm3805
chicago: Renkawitz, Jörg, Claudio Lademann, and Stefan Jentsch. “Mechanisms and
Principles of Homology Search during Recombination.” Nature Reviews Molecular
Cell Biology. Nature Publishing Group, 2014. https://doi.org/10.1038/nrm3805.
ieee: J. Renkawitz, C. Lademann, and S. Jentsch, “Mechanisms and principles of homology
search during recombination,” Nature Reviews Molecular Cell Biology, vol.
15, no. 6. Nature Publishing Group, pp. 369–383, 2014.
ista: Renkawitz J, Lademann C, Jentsch S. 2014. Mechanisms and principles of homology
search during recombination. Nature Reviews Molecular Cell Biology. 15(6), 369–383.
mla: Renkawitz, Jörg, et al. “Mechanisms and Principles of Homology Search during
Recombination.” Nature Reviews Molecular Cell Biology, vol. 15, no. 6,
Nature Publishing Group, 2014, pp. 369–83, doi:10.1038/nrm3805.
short: J. Renkawitz, C. Lademann, S. Jentsch, Nature Reviews Molecular Cell Biology
15 (2014) 369–383.
date_created: 2018-12-11T11:56:22Z
date_published: 2014-05-14T00:00:00Z
date_updated: 2021-01-12T06:56:03Z
day: '14'
department:
- _id: MiSi
doi: 10.1038/nrm3805
intvolume: ' 15'
issue: '6'
language:
- iso: eng
month: '05'
oa_version: None
page: 369 - 383
publication: Nature Reviews Molecular Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '4755'
quality_controlled: '1'
scopus_import: 1
status: public
title: Mechanisms and principles of homology search during recombination
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 15
year: '2014'
...
---
_id: '3961'
abstract:
- lang: eng
text: For innate and adaptive immune responses it is essential that inflammatory
cells use quick and flexible locomotion strategies. Accordingly, most leukocytes
can efficiently infiltrate and traverse almost every physiological or artificial
environment. Here, we review how leukocytes might achieve this task mechanistically,
and summarize recent findings on the principles of cytoskeletal force generation
and transduction at the leading edge of leukocytes. We propose a model in which
the cells switch between adhesion-receptor-mediated force transmission and locomotion
modes that are based on cellular deformations, but independent of adhesion receptors.
This plasticity in migration strategies allows leukocytes to adapt to the geometry
and molecular composition of their environment.
acknowledgement: We are grateful to Michele Weber for critical comments on the manuscript.
Work in the laboratory of M.S. is supported by the German Research Foundation, the
Peter Hans Hofschneider Foundation for Experimental Biomedicine and the Max Planck
Society. J.R. is supported by a PhD fellowship of the Böhringer Ingelheim Fond.
We thank Reinhard Fässler and Stefan Jentsch for their continuous support.
author:
- first_name: Jörg
full_name: Jörg Renkawitz
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Michael K
full_name: Michael Sixt
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Renkawitz J, Sixt MK. Mechanisms of force generation and force transmission
during interstitial leukocyte migration. EMBO Reports. 2010;11(10):744-750.
doi:10.1038/embor.2010.147
apa: Renkawitz, J., & Sixt, M. K. (2010). Mechanisms of force generation and
force transmission during interstitial leukocyte migration. EMBO Reports.
Wiley-Blackwell. https://doi.org/10.1038/embor.2010.147
chicago: Renkawitz, Jörg, and Michael K Sixt. “Mechanisms of Force Generation and
Force Transmission during Interstitial Leukocyte Migration.” EMBO Reports.
Wiley-Blackwell, 2010. https://doi.org/10.1038/embor.2010.147.
ieee: J. Renkawitz and M. K. Sixt, “Mechanisms of force generation and force transmission
during interstitial leukocyte migration,” EMBO Reports, vol. 11, no. 10.
Wiley-Blackwell, pp. 744–750, 2010.
ista: Renkawitz J, Sixt MK. 2010. Mechanisms of force generation and force transmission
during interstitial leukocyte migration. EMBO Reports. 11(10), 744–750.
mla: Renkawitz, Jörg, and Michael K. Sixt. “Mechanisms of Force Generation and Force
Transmission during Interstitial Leukocyte Migration.” EMBO Reports, vol.
11, no. 10, Wiley-Blackwell, 2010, pp. 744–50, doi:10.1038/embor.2010.147.
short: J. Renkawitz, M.K. Sixt, EMBO Reports 11 (2010) 744–750.
date_created: 2018-12-11T12:06:08Z
date_published: 2010-09-24T00:00:00Z
date_updated: 2021-01-12T07:53:30Z
day: '24'
doi: 10.1038/embor.2010.147
extern: 1
intvolume: ' 11'
issue: '10'
month: '09'
page: 744 - 750
publication: EMBO Reports
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2166'
quality_controlled: 0
status: public
title: Mechanisms of force generation and force transmission during interstitial leukocyte
migration
type: journal_article
volume: 11
year: '2010'
...
---
_id: '3947'
abstract:
- lang: eng
text: Mature dendritic cells (DCs) moving from the skin to the lymph node are a
prototypic example of rapidly migrating amoeboid leukocytes. Interstitial DC migration
is directionally guided by chemokines, but independent of specific adhesive interactions
with the tissue as well as pericellular proteolysis. Instead, the protrusive flow
of the actin cytoskeleton directly drives a basal mode of locomotion that is occasionally
supported by actomyosin contractions at the trailing edge to propel the cell's
rigid nucleus. We here delete the small GTPase Cdc42 in DCs and find that actin
flow and actomyosin contraction are still initiated in response to chemotactic
cues. Accordingly, the cells are able to polarize and form protrusions. However,
in the absence of Cdc42 the protrusions are temporally and spatially dysregulated,
which leads to impaired leading edge coordination. Although this defect still
allows the cells to move on 2-dimensional surfaces, their in vivo motility is
completely abrogated. We show that this difference is entirely caused by the geometric
complexity of the environment, as multiple competing protrusions lead to instantaneous
entanglement within 3-dimensional extracellular matrix scaffolds. This demonstrates
that the decisive factor for migrating DCs is not specific interaction with the
extracellular environment, but adequate coordination of cytoskeletal flow.
acknowledgement: |-
We thank Sylvia Cremer for help with statistics and critical reading of the paper and Reinhard Fässler for continuous support.
This work was supported by the German Research Foundation (Bonn, Germany), the Peter Hans Hofschneider Foundation for Experimental Biomedicine (Zürich, Switzerland), and the Max Planck Society (Munich, Germany).
author:
- first_name: Tim
full_name: Lämmermann, Tim
last_name: Lämmermann
- first_name: Jörg
full_name: Jörg Renkawitz
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Xunwei
full_name: Wu, Xunwei
last_name: Wu
- first_name: Karin
full_name: Hirsch, Karin
last_name: Hirsch
- first_name: Cord
full_name: Brakebusch, Cord
last_name: Brakebusch
- first_name: Michael K
full_name: Michael Sixt
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Lämmermann T, Renkawitz J, Wu X, Hirsch K, Brakebusch C, Sixt MK. Cdc42-dependent
leading edge coordination is essential for interstitial dendritic cell migration
(Plenary Paper). Blood. 2009;113(23):5703-5710. doi:10.1182/blood-2008-11-191882
apa: Lämmermann, T., Renkawitz, J., Wu, X., Hirsch, K., Brakebusch, C., & Sixt,
M. K. (2009). Cdc42-dependent leading edge coordination is essential for interstitial
dendritic cell migration (Plenary Paper). Blood. American Society of Hematology.
https://doi.org/10.1182/blood-2008-11-191882
chicago: Lämmermann, Tim, Jörg Renkawitz, Xunwei Wu, Karin Hirsch, Cord Brakebusch,
and Michael K Sixt. “Cdc42-Dependent Leading Edge Coordination Is Essential for
Interstitial Dendritic Cell Migration (Plenary Paper).” Blood. American
Society of Hematology, 2009. https://doi.org/10.1182/blood-2008-11-191882.
ieee: T. Lämmermann, J. Renkawitz, X. Wu, K. Hirsch, C. Brakebusch, and M. K. Sixt,
“Cdc42-dependent leading edge coordination is essential for interstitial dendritic
cell migration (Plenary Paper),” Blood, vol. 113, no. 23. American Society
of Hematology, pp. 5703–5710, 2009.
ista: Lämmermann T, Renkawitz J, Wu X, Hirsch K, Brakebusch C, Sixt MK. 2009. Cdc42-dependent
leading edge coordination is essential for interstitial dendritic cell migration
(Plenary Paper). Blood. 113(23), 5703–5710.
mla: Lämmermann, Tim, et al. “Cdc42-Dependent Leading Edge Coordination Is Essential
for Interstitial Dendritic Cell Migration (Plenary Paper).” Blood, vol.
113, no. 23, American Society of Hematology, 2009, pp. 5703–10, doi:10.1182/blood-2008-11-191882.
short: T. Lämmermann, J. Renkawitz, X. Wu, K. Hirsch, C. Brakebusch, M.K. Sixt,
Blood 113 (2009) 5703–5710.
date_created: 2018-12-11T12:06:03Z
date_published: 2009-06-04T00:00:00Z
date_updated: 2021-01-12T07:53:23Z
day: '04'
doi: 10.1182/blood-2008-11-191882
extern: 1
intvolume: ' 113'
issue: '23'
month: '06'
page: 5703 - 5710
publication: Blood
publication_status: published
publisher: American Society of Hematology
publist_id: '2179'
quality_controlled: 0
status: public
title: Cdc42-dependent leading edge coordination is essential for interstitial dendritic
cell migration (Plenary Paper)
type: journal_article
volume: 113
year: '2009'
...
---
_id: '3954'
abstract:
- lang: eng
text: The leading front of a cell can either protrude as an actin-free membrane
bleb that is inflated by actomyosin-driven contractile forces, or as an actin-rich
pseudopodium, a site where polymerizing actin filaments push out the membrane.
Pushing filaments can only cause the membrane to protrude if the expanding actin
network experiences a retrograde counter-force, which is usually provided by transmembrane
receptors of the integrin family. Here we show that chemotactic dendritic cells
mechanically adapt to the adhesive properties of their substrate by switching
between integrin-mediated and integrin-independent locomotion. We found that on
engaging the integrin-actin clutch, actin polymerization was entirely turned into
protrusion, whereas on disengagement actin underwent slippage and retrograde flow.
Remarkably, accelerated retrograde flow was balanced by an increased actin polymerization
rate; therefore, cell shape and protrusion velocity remained constant on alternating
substrates. Due to this adaptive response in polymerization dynamics, tracks of
adhesive substrate did not dictate the path of the cells. Instead, directional
guidance was exclusively provided by a soluble gradient of chemoattractant, which
endowed these 'amoeboid' cells with extraordinary flexibility, enabling them to
traverse almost every type of tissue.
acknowledgement: We thank S. Cremer for statistical analysis, K. Hirsch for technical
assistance, D. Critchley for talin1-deficient mice and R. Fässler for integrindeficient
mice, discussions and critical reading of the manuscript. This work was supported
by the German Research Foundation, the Peter Hans Hofschneider Foundation for Experimental
Biomedicine, the Max Planck Society, the Alexander von Humboldt Foundation and the
allergology programme of the Landesstiftung Baden-Württemberg.
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Kathrin
full_name: Schumann, Kathrin
id: F44D762E-4F9D-11E9-B64C-9EB26CEFFB5F
last_name: Schumann
- first_name: Michele
full_name: Weber, Michele
id: 3A3FC708-F248-11E8-B48F-1D18A9856A87
last_name: Weber
- first_name: Tim
full_name: Lämmermann, Tim
last_name: Lämmermann
- first_name: Holger
full_name: Pflicke, Holger
last_name: Pflicke
- first_name: Matthieu
full_name: Piel, Matthieu
last_name: Piel
- first_name: Julien
full_name: Polleux, Julien
last_name: Polleux
- first_name: Joachim
full_name: Spatz, Joachim
last_name: Spatz
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Renkawitz J, Schumann K, Weber M, et al. Adaptive force transmission in amoeboid
cell migration. Nature Cell Biology. 2009;11(12):1438-1443. doi:10.1038/ncb1992
apa: Renkawitz, J., Schumann, K., Weber, M., Lämmermann, T., Pflicke, H., Piel,
M., … Sixt, M. K. (2009). Adaptive force transmission in amoeboid cell migration.
Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb1992
chicago: Renkawitz, Jörg, Kathrin Schumann, Michele Weber, Tim Lämmermann, Holger
Pflicke, Matthieu Piel, Julien Polleux, Joachim Spatz, and Michael K Sixt. “Adaptive
Force Transmission in Amoeboid Cell Migration.” Nature Cell Biology. Nature
Publishing Group, 2009. https://doi.org/10.1038/ncb1992.
ieee: J. Renkawitz et al., “Adaptive force transmission in amoeboid cell
migration,” Nature Cell Biology, vol. 11, no. 12. Nature Publishing Group,
pp. 1438–1443, 2009.
ista: Renkawitz J, Schumann K, Weber M, Lämmermann T, Pflicke H, Piel M, Polleux
J, Spatz J, Sixt MK. 2009. Adaptive force transmission in amoeboid cell migration.
Nature Cell Biology. 11(12), 1438–1443.
mla: Renkawitz, Jörg, et al. “Adaptive Force Transmission in Amoeboid Cell Migration.”
Nature Cell Biology, vol. 11, no. 12, Nature Publishing Group, 2009, pp.
1438–43, doi:10.1038/ncb1992.
short: J. Renkawitz, K. Schumann, M. Weber, T. Lämmermann, H. Pflicke, M. Piel,
J. Polleux, J. Spatz, M.K. Sixt, Nature Cell Biology 11 (2009) 1438–1443.
date_created: 2018-12-11T12:06:05Z
date_published: 2009-11-15T00:00:00Z
date_updated: 2021-01-12T07:53:27Z
day: '15'
doi: 10.1038/ncb1992
extern: '1'
intvolume: ' 11'
issue: '12'
language:
- iso: eng
month: '11'
oa_version: None
page: 1438 - 1443
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '2173'
status: public
title: Adaptive force transmission in amoeboid cell migration
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 11
year: '2009'
...