---
_id: '3948'
abstract:
- lang: eng
text: Inhibiting the alpha(4) subunit of the integrin heterodimers alpha(4)beta(1)
and alpha(4)beta(7) with the monoclonal antibody natalizumab is an effective treatment
for multiple sclerosis (MS). However, the pharmacological action of natalizumab
is not understood conclusively. Previous studies suggested that natalizumab inhibits
activation, proliferation, or extravasation of inflammatory cells. To specify
which mechanisms, cell types, and alpha(4) heterodimers are affected by the antibody
treatment, we studied MS-like experimental autoimmune encephalomyelitis (EAE)
in mice lacking the beta(1)-integrin gene either in all hematopoietic cells or
selectively in T lymphocytes. Our results show that T cells critically rely on
beta(1) integrins to accumulate in the central nervous system (CNS) during EAE,
whereas CNS infiltration of beta(1)-deficient myeloid cells remains unaffected,
suggesting that T cells are the main target of anti-alpha(4)-antibody blockade.
We demonstrate that beta(1)-integrin expression on encephalitogenic T cells is
critical for EAE development, and we therefore exclude alpha(4)beta(7) as a target
integrin of the antibody treatment. T cells lacking beta(1) integrin are unable
to firmly adhere to CNS endothelium in vivo, whereas their priming and expansion
remain unaffected. Collectively, these results suggest that the primary action
of natalizumab is interference with T cell extravasation via inhibition of alpha(4)beta(1)
integrins.
author:
- first_name: Martina
full_name: Bauer, Martina
last_name: Bauer
- first_name: Cord
full_name: Brakebusch, Cord
last_name: Brakebusch
- first_name: Caroline
full_name: Coisne, Caroline
last_name: Coisne
- first_name: Michael K
full_name: Michael Sixt
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Hartmut
full_name: Wekerle, Hartmut
last_name: Wekerle
- first_name: Britta
full_name: Engelhardt, Britta
last_name: Engelhardt
- first_name: Reinhard
full_name: Fässler, Reinhard
last_name: Fässler
citation:
ama: Bauer M, Brakebusch C, Coisne C, et al. β1 integrins differentially control
extravasation of inflammatory cell subsets into the CNS during autoimmunity. PNAS.
2009;106(6):1920-1925. doi:10.1073/pnas.0808909106
apa: Bauer, M., Brakebusch, C., Coisne, C., Sixt, M. K., Wekerle, H., Engelhardt,
B., & Fässler, R. (2009). β1 integrins differentially control extravasation
of inflammatory cell subsets into the CNS during autoimmunity. PNAS. National
Academy of Sciences. https://doi.org/10.1073/pnas.0808909106
chicago: Bauer, Martina, Cord Brakebusch, Caroline Coisne, Michael K Sixt, Hartmut
Wekerle, Britta Engelhardt, and Reinhard Fässler. “Β1 Integrins Differentially
Control Extravasation of Inflammatory Cell Subsets into the CNS during Autoimmunity.”
PNAS. National Academy of Sciences, 2009. https://doi.org/10.1073/pnas.0808909106.
ieee: M. Bauer et al., “β1 integrins differentially control extravasation
of inflammatory cell subsets into the CNS during autoimmunity,” PNAS, vol.
106, no. 6. National Academy of Sciences, pp. 1920–1925, 2009.
ista: Bauer M, Brakebusch C, Coisne C, Sixt MK, Wekerle H, Engelhardt B, Fässler
R. 2009. β1 integrins differentially control extravasation of inflammatory cell
subsets into the CNS during autoimmunity. PNAS. 106(6), 1920–1925.
mla: Bauer, Martina, et al. “Β1 Integrins Differentially Control Extravasation of
Inflammatory Cell Subsets into the CNS during Autoimmunity.” PNAS, vol.
106, no. 6, National Academy of Sciences, 2009, pp. 1920–25, doi:10.1073/pnas.0808909106.
short: M. Bauer, C. Brakebusch, C. Coisne, M.K. Sixt, H. Wekerle, B. Engelhardt,
R. Fässler, PNAS 106 (2009) 1920–1925.
date_created: 2018-12-11T12:06:03Z
date_published: 2009-02-10T00:00:00Z
date_updated: 2021-01-12T07:53:24Z
day: '10'
doi: 10.1073/pnas.0808909106
extern: 1
intvolume: ' 106'
issue: '6'
month: '02'
page: 1920 - 1925
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '2180'
quality_controlled: 0
status: public
title: β1 integrins differentially control extravasation of inflammatory cell subsets
into the CNS during autoimmunity
type: journal_article
volume: 106
year: '2009'
...
---
_id: '3949'
abstract:
- lang: eng
text: Adhesion and motility of mammalian leukocytes are essential requirements for
innate and adaptive immune defense mechanisms. We show here that the guanine nucleotide
exchange factor cytohesin-1, which had previously been demonstrated to be an important
component of beta-2 integrin activation in lymphocytes, regulates the activation
of the small GTPase RhoA in primary dendritic cells (DCs). Cytohesin-1 and RhoA
are both required for the induction of chemokine-dependent conformational changes
of the integrin beta-2 subunit of DCs during adhesion under physiological flow
conditions. Furthermore, use of RNAi in murine bone marrow DCs (BM-DCs) revealed
that interference with cytohesin-1 signaling impairs migration of wild-type dendritic
cells in complex 3D environments and in vivo. This phenotype was not observed
in the complete absence of integrins. We thus demonstrate an essential role of
cytohesin-1/RhoA during ameboid migration in the presence of integrins and further
suggest that DCs without integrins switch to a different migration mode.
author:
- first_name: Thomas
full_name: Quast, Thomas
last_name: Quast
- first_name: Barbara
full_name: Tappertzhofen, Barbara
last_name: Tappertzhofen
- first_name: Cora
full_name: Schild, Cora
last_name: Schild
- first_name: Jessica
full_name: Grell, Jessica
last_name: Grell
- first_name: Niklas
full_name: Czeloth, Niklas
last_name: Czeloth
- first_name: Reinhold
full_name: Förster, Reinhold
last_name: Förster
- first_name: Ronen
full_name: Alon, Ronen
last_name: Alon
- first_name: Line
full_name: Fraemohs, Line
last_name: Fraemohs
- first_name: Katrin
full_name: Dreck, Katrin
last_name: Dreck
- first_name: Christian
full_name: Weber, Christian
last_name: Weber
- first_name: Tim
full_name: Lämmermann, Tim
last_name: Lämmermann
- first_name: Michael K
full_name: Michael Sixt
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Waldemar
full_name: Kolanus, Waldemar
last_name: Kolanus
citation:
ama: Quast T, Tappertzhofen B, Schild C, et al. Cytohesin-1 controls the activation
of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells.
Blood. 2009;113(23):5801-5810. doi:10.1182/blood-2008-08-176123
apa: Quast, T., Tappertzhofen, B., Schild, C., Grell, J., Czeloth, N., Förster,
R., … Kolanus, W. (2009). Cytohesin-1 controls the activation of RhoA and modulates
integrin-dependent adhesion and migration of dendritic cells. Blood. American
Society of Hematology. https://doi.org/10.1182/blood-2008-08-176123
chicago: Quast, Thomas, Barbara Tappertzhofen, Cora Schild, Jessica Grell, Niklas
Czeloth, Reinhold Förster, Ronen Alon, et al. “Cytohesin-1 Controls the Activation
of RhoA and Modulates Integrin-Dependent Adhesion and Migration of Dendritic Cells.”
Blood. American Society of Hematology, 2009. https://doi.org/10.1182/blood-2008-08-176123.
ieee: T. Quast et al., “Cytohesin-1 controls the activation of RhoA and modulates
integrin-dependent adhesion and migration of dendritic cells,” Blood, vol.
113, no. 23. American Society of Hematology, pp. 5801–5810, 2009.
ista: Quast T, Tappertzhofen B, Schild C, Grell J, Czeloth N, Förster R, Alon R,
Fraemohs L, Dreck K, Weber C, Lämmermann T, Sixt MK, Kolanus W. 2009. Cytohesin-1
controls the activation of RhoA and modulates integrin-dependent adhesion and
migration of dendritic cells. Blood. 113(23), 5801–5810.
mla: Quast, Thomas, et al. “Cytohesin-1 Controls the Activation of RhoA and Modulates
Integrin-Dependent Adhesion and Migration of Dendritic Cells.” Blood, vol.
113, no. 23, American Society of Hematology, 2009, pp. 5801–10, doi:10.1182/blood-2008-08-176123.
short: T. Quast, B. Tappertzhofen, C. Schild, J. Grell, N. Czeloth, R. Förster,
R. Alon, L. Fraemohs, K. Dreck, C. Weber, T. Lämmermann, M.K. Sixt, W. Kolanus,
Blood 113 (2009) 5801–5810.
date_created: 2018-12-11T12:06:03Z
date_published: 2009-06-04T00:00:00Z
date_updated: 2021-01-12T07:53:24Z
day: '04'
doi: 10.1182/blood-2008-08-176123
extern: 1
intvolume: ' 113'
issue: '23'
month: '06'
page: 5801 - 5810
publication: Blood
publication_status: published
publisher: American Society of Hematology
publist_id: '2177'
quality_controlled: 0
status: public
title: Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent
adhesion and migration of dendritic cells
type: journal_article
volume: 113
year: '2009'
...
---
_id: '3950'
abstract:
- lang: eng
text: Integrin activation is essential for the function of all blood cells, including
platelets and leukocytes. The blood cell-specific FERM domain protein Kindlin-3
is required for the activation of the beta1 and beta3 integrins on platelets.
Impaired activation of beta1, beta2 and beta3 integrins on platelets and leukocytes
is the hallmark of a rare autosomal recessive leukocyte adhesion deficiency syndrome
in humans called LAD-III, characterized by severe bleeding and impaired adhesion
of leukocytes to inflamed endothelia. Here we show that Kindlin-3 also binds the
beta2 integrin cytoplasmic domain and is essential for neutrophil binding and
spreading on beta2 integrin-dependent ligands such as intercellular adhesion molecule-1
and the complement C3 activation product iC3b. Moreover, loss of Kindlin-3 expression
abolished firm adhesion and arrest of neutrophils on activated endothelial cells
in vitro and in vivo, whereas selectin-mediated rolling was unaffected. Thus,
Kindlin-3 is essential to activate the beta1, beta2 and beta3 integrin classes,
and loss of Kindlin-3 function is sufficient to cause a LAD-III-like phenotype
in mice.
author:
- first_name: Markus
full_name: Moser, Markus
last_name: Moser
- first_name: Martina
full_name: Bauer, Martina
last_name: Bauer
- first_name: Stephan
full_name: Schmid, Stephan
last_name: Schmid
- first_name: Raphael
full_name: Ruppert, Raphael
last_name: Ruppert
- first_name: Sarah
full_name: Schmidt, Sarah
last_name: Schmidt
- first_name: Michael K
full_name: Michael Sixt
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Hao
full_name: Wang, Hao-Ven
last_name: Wang
- first_name: Markus
full_name: Sperandio, Markus
last_name: Sperandio
- first_name: Reinhard
full_name: Fässler, Reinhard
last_name: Fässler
citation:
ama: Moser M, Bauer M, Schmid S, et al. Kindlin-3 is required for β2 integrin-mediated
leukocyte adhesion to endothelial cells. Nature Medicine. 2009;15(3):300-305.
doi:10.1038/nm.1921
apa: Moser, M., Bauer, M., Schmid, S., Ruppert, R., Schmidt, S., Sixt, M. K., …
Fässler, R. (2009). Kindlin-3 is required for β2 integrin-mediated leukocyte adhesion
to endothelial cells. Nature Medicine. Nature Publishing Group. https://doi.org/10.1038/nm.1921
chicago: Moser, Markus, Martina Bauer, Stephan Schmid, Raphael Ruppert, Sarah Schmidt,
Michael K Sixt, Hao Wang, Markus Sperandio, and Reinhard Fässler. “Kindlin-3 Is
Required for Β2 Integrin-Mediated Leukocyte Adhesion to Endothelial Cells.” Nature
Medicine. Nature Publishing Group, 2009. https://doi.org/10.1038/nm.1921.
ieee: M. Moser et al., “Kindlin-3 is required for β2 integrin-mediated leukocyte
adhesion to endothelial cells,” Nature Medicine, vol. 15, no. 3. Nature
Publishing Group, pp. 300–305, 2009.
ista: Moser M, Bauer M, Schmid S, Ruppert R, Schmidt S, Sixt MK, Wang H, Sperandio
M, Fässler R. 2009. Kindlin-3 is required for β2 integrin-mediated leukocyte adhesion
to endothelial cells. Nature Medicine. 15(3), 300–305.
mla: Moser, Markus, et al. “Kindlin-3 Is Required for Β2 Integrin-Mediated Leukocyte
Adhesion to Endothelial Cells.” Nature Medicine, vol. 15, no. 3, Nature
Publishing Group, 2009, pp. 300–05, doi:10.1038/nm.1921.
short: M. Moser, M. Bauer, S. Schmid, R. Ruppert, S. Schmidt, M.K. Sixt, H. Wang,
M. Sperandio, R. Fässler, Nature Medicine 15 (2009) 300–305.
date_created: 2018-12-11T12:06:04Z
date_published: 2009-02-22T00:00:00Z
date_updated: 2021-01-12T07:53:25Z
day: '22'
doi: 10.1038/nm.1921
extern: 1
intvolume: ' 15'
issue: '3'
month: '02'
page: 300 - 305
publication: Nature Medicine
publication_status: published
publisher: Nature Publishing Group
publist_id: '2178'
quality_controlled: 0
status: public
title: Kindlin-3 is required for β2 integrin-mediated leukocyte adhesion to endothelial
cells
type: journal_article
volume: 15
year: '2009'
...
---
_id: '3951'
abstract:
- lang: eng
text: The morphological term 'amoeboid' migration subsumes a number of rather distinct
biophysical modes of cellular locomotion that range from blebbing motility to
entirely actin-polymerization-based gliding. Here, we discuss the diverse principles
of force generation and force transduction that lead to the distinct amoeboid
phenotypes. We argue that shifting the balance between actin protrusion, actomyosin
contraction, and adhesion to the extracellular substrate can explain the different
modes of amoeboid movement and that blebbing and gliding are barely extreme variants
of one common migration strategy. Depending on the cell type, physiological conditions
or experimental manipulation, amoeboid cells can adopt the distinct mechanical
modes of amoeboid migration.
author:
- first_name: Tim
full_name: Lämmermann, Tim
last_name: Lämmermann
- 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, Sixt MK. Mechanical modes of “amoeboid” cell migration. Current
Opinion in Cell Biology. 2009;21(5):636-644. doi:10.1016/j.ceb.2009.05.003
apa: Lämmermann, T., & Sixt, M. K. (2009). Mechanical modes of “amoeboid” cell
migration. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2009.05.003
chicago: Lämmermann, Tim, and Michael K Sixt. “Mechanical Modes of ‘amoeboid’ Cell
Migration.” Current Opinion in Cell Biology. Elsevier, 2009. https://doi.org/10.1016/j.ceb.2009.05.003.
ieee: T. Lämmermann and M. K. Sixt, “Mechanical modes of ‘amoeboid’ cell migration,”
Current Opinion in Cell Biology, vol. 21, no. 5. Elsevier, pp. 636–644,
2009.
ista: Lämmermann T, Sixt MK. 2009. Mechanical modes of ‘amoeboid’ cell migration.
Current Opinion in Cell Biology. 21(5), 636–644.
mla: Lämmermann, Tim, and Michael K. Sixt. “Mechanical Modes of ‘amoeboid’ Cell
Migration.” Current Opinion in Cell Biology, vol. 21, no. 5, Elsevier,
2009, pp. 636–44, doi:10.1016/j.ceb.2009.05.003.
short: T. Lämmermann, M.K. Sixt, Current Opinion in Cell Biology 21 (2009) 636–644.
date_created: 2018-12-11T12:06:04Z
date_published: 2009-10-01T00:00:00Z
date_updated: 2021-01-12T07:53:25Z
day: '01'
doi: 10.1016/j.ceb.2009.05.003
extern: 1
intvolume: ' 21'
issue: '5'
month: '10'
page: 636 - 644
publication: Current Opinion in Cell Biology
publication_status: published
publisher: Elsevier
publist_id: '2176'
quality_controlled: 0
status: public
title: Mechanical modes of 'amoeboid' cell migration
type: journal_article
volume: 21
year: '2009'
...
---
_id: '3952'
abstract:
- lang: eng
text: The mammalian actin-binding protein 1 (mAbp1, Hip-55, SH3P7) is phosphorylated
by the nonreceptor tyrosine kinase Syk that has a fundamental effect for several
beta(2) integrin (CD11/CD18)-mediated neutrophil functions. Live cell imaging
showed a dynamic enrichment of enhanced green fluorescence protein-tagged mAbp1
at the phagocytic cup of neutrophil-like differentiated HL-60 cells during beta(2)
integrin-mediated phagocytosis of serum-opsonized Escherichia coli. The genetic
absence of Syk or its pharmacologic inhibition using piceatannol abrogated the
proper localization of mAbp1 at the phagocytic cup. The genetic absence or down-regulation
of mAbp1 using the RNA interference technique significantly compromised beta(2)
integrin-mediated phagocytosis of serum-opsonized E coli or Salmonella typhimurium
in vitro as well as clearance of S typhimurium infection in vivo. Moreover, the
genetic absence of mAbp1 almost completely abrogated firm neutrophil adhesion
under physiologic shear stress conditions in vitro as well as leukocyte adhesion
and extravasation in inflamed cremaster muscle venules of mice treated with tumor-necrosis
factor alpha. Functional analysis showed that the down-regulation of mAbp1 diminished
the number of beta(2) integrin clusters in the high-affinity conformation under
flow conditions. These unanticipated results define mAbp1 as a novel molecular
player in integrin biology that is critical for phagocytosis and firm neutrophil
adhesion under flow conditions.
author:
- first_name: Jürgen
full_name: Schymeinsky, Jürgen
last_name: Schymeinsky
- first_name: Ronald
full_name: Gerstl, Ronald
last_name: Gerstl
- first_name: Ingrid
full_name: Mannigel, Ingrid
last_name: Mannigel
- first_name: Katy
full_name: Niedung, Katy
last_name: Niedung
- first_name: David
full_name: Frommhold, David
last_name: Frommhold
- first_name: Klaus
full_name: Panthel, Klaus
last_name: Panthel
- first_name: Jürgen
full_name: Heesemann, Jürgen
last_name: Heesemann
- first_name: Michael K
full_name: Michael Sixt
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Thomas
full_name: Quast, Thomas
last_name: Quast
- first_name: Waldemar
full_name: Kolanus, Waldemar
last_name: Kolanus
- first_name: Attila
full_name: Mocsai, Attila
last_name: Mocsai
- first_name: Jürgen
full_name: Wienands, Jürgen
last_name: Wienands
- first_name: Markus
full_name: Sperandio, Markus
last_name: Sperandio
- first_name: Barbara
full_name: Walzog, Barbara
last_name: Walzog
citation:
ama: 'Schymeinsky J, Gerstl R, Mannigel I, et al. A fundamental role of mAbp1 in
neutrophils: impact on β(2) integrin-mediated phagocytosis and adhesion in vivo.
Blood. 2009;114(19):4209-4220. doi:10.1182/blood-2009-02-206169'
apa: 'Schymeinsky, J., Gerstl, R., Mannigel, I., Niedung, K., Frommhold, D., Panthel,
K., … Walzog, B. (2009). A fundamental role of mAbp1 in neutrophils: impact on
β(2) integrin-mediated phagocytosis and adhesion in vivo. Blood. American
Society of Hematology. https://doi.org/10.1182/blood-2009-02-206169'
chicago: 'Schymeinsky, Jürgen, Ronald Gerstl, Ingrid Mannigel, Katy Niedung, David
Frommhold, Klaus Panthel, Jürgen Heesemann, et al. “A Fundamental Role of MAbp1
in Neutrophils: Impact on β(2) Integrin-Mediated Phagocytosis and Adhesion in
Vivo.” Blood. American Society of Hematology, 2009. https://doi.org/10.1182/blood-2009-02-206169.'
ieee: 'J. Schymeinsky et al., “A fundamental role of mAbp1 in neutrophils:
impact on β(2) integrin-mediated phagocytosis and adhesion in vivo,” Blood,
vol. 114, no. 19. American Society of Hematology, pp. 4209–4220, 2009.'
ista: 'Schymeinsky J, Gerstl R, Mannigel I, Niedung K, Frommhold D, Panthel K, Heesemann
J, Sixt MK, Quast T, Kolanus W, Mocsai A, Wienands J, Sperandio M, Walzog B. 2009.
A fundamental role of mAbp1 in neutrophils: impact on β(2) integrin-mediated phagocytosis
and adhesion in vivo. Blood. 114(19), 4209–4220.'
mla: 'Schymeinsky, Jürgen, et al. “A Fundamental Role of MAbp1 in Neutrophils: Impact
on β(2) Integrin-Mediated Phagocytosis and Adhesion in Vivo.” Blood, vol.
114, no. 19, American Society of Hematology, 2009, pp. 4209–20, doi:10.1182/blood-2009-02-206169.'
short: J. Schymeinsky, R. Gerstl, I. Mannigel, K. Niedung, D. Frommhold, K. Panthel,
J. Heesemann, M.K. Sixt, T. Quast, W. Kolanus, A. Mocsai, J. Wienands, M. Sperandio,
B. Walzog, Blood 114 (2009) 4209–4220.
date_created: 2018-12-11T12:06:04Z
date_published: 2009-11-05T00:00:00Z
date_updated: 2021-01-12T07:53:26Z
day: '05'
doi: 10.1182/blood-2009-02-206169
extern: 1
intvolume: ' 114'
issue: '19'
month: '11'
page: 4209 - 4220
publication: Blood
publication_status: published
publisher: American Society of Hematology
publist_id: '2175'
quality_controlled: 0
status: public
title: 'A fundamental role of mAbp1 in neutrophils: impact on β(2) integrin-mediated
phagocytosis and adhesion in vivo'
type: journal_article
volume: 114
year: '2009'
...
---
_id: '3953'
abstract:
- lang: eng
text: CD4(+)CD25(+) regulatory T cell (Treg) entry into secondary lymphoid organs
and local expansion is critical for their immunosuppressive function. Long-term
application of the sphingosine-1 phosphate receptor agonist FTY720 exerts pleiotropic
anti-inflammatory effects, whereas short-term FTY720 boosts antiviral immunity.
In this study, we provide evidence that FTY720 potently inhibits Treg proliferation
in vitro and in vivo without affecting their viability, phenotype, or in vitro
immunosuppression. In contrast, adoptively transferred Treg exposed ex vivo to
FTY720 lost their protective effects in murine models of acute glomerulonephritis
and acute graft-vs-host disease. On a cellular level, FTY720 inhibits IL-2-induced
STAT-5 phosphorylation, paralleled by a loss of FoxP3 expression during Treg expansion
in vitro. Notably, loss of in vivo immunosuppression is not due to impaired migration
to or localization within secondary lymphoid organs. We could even show a selective
trapping of adoptively transferred Treg in inflammatory lymph nodes by FTY720.
Finally, Treg isolated from animals systemically exposed to FTY720 also exhibit
a significantly impaired proliferative response upon restimulation when compared
with Treg isolated from solvent-treated animals. In summary, our data suggest
that sphingosine-1 phosphate receptor-mediated signals induced by FTY720 abrogate
their in vivo immunosuppressive potential by blocking IL-2 induced expansion,
which is indispensable for their in vivo immunosuppressive activity.
author:
- first_name: Anna
full_name: Wolf, Anna Maria
last_name: Wolf
- first_name: Kathrin
full_name: Eller, Kathrin
last_name: Eller
- first_name: Robert
full_name: Zeiser, Robert
last_name: Zeiser
- first_name: Christoph
full_name: Dürr, Christoph
last_name: Dürr
- first_name: Ulrike
full_name: Gerlach, Ulrike V
last_name: Gerlach
- first_name: Michael K
full_name: Michael Sixt
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Lydia
full_name: Markut, Lydia
last_name: Markut
- first_name: Guenther
full_name: Gastl, Guenther
last_name: Gastl
- first_name: Alexander
full_name: Rosenkranz, Alexander R
last_name: Rosenkranz
- first_name: Dominik
full_name: Wolf, Dominik
last_name: Wolf
citation:
ama: Wolf A, Eller K, Zeiser R, et al. The sphingosine 1-phosphate receptor agonist
FTY720 potently inhibits regulatory T cell proliferation in vitro and in vivo.
Journal of Immunology. 2009;183(6):3751-3760. doi:10.4049/jimmunol.0901011
apa: Wolf, A., Eller, K., Zeiser, R., Dürr, C., Gerlach, U., Sixt, M. K., … Wolf,
D. (2009). The sphingosine 1-phosphate receptor agonist FTY720 potently inhibits
regulatory T cell proliferation in vitro and in vivo. Journal of Immunology.
American Association of Immunologists. https://doi.org/10.4049/jimmunol.0901011
chicago: Wolf, Anna, Kathrin Eller, Robert Zeiser, Christoph Dürr, Ulrike Gerlach,
Michael K Sixt, Lydia Markut, Guenther Gastl, Alexander Rosenkranz, and Dominik
Wolf. “The Sphingosine 1-Phosphate Receptor Agonist FTY720 Potently Inhibits Regulatory
T Cell Proliferation in Vitro and in Vivo.” Journal of Immunology. American
Association of Immunologists, 2009. https://doi.org/10.4049/jimmunol.0901011.
ieee: A. Wolf et al., “The sphingosine 1-phosphate receptor agonist FTY720
potently inhibits regulatory T cell proliferation in vitro and in vivo,” Journal
of Immunology, vol. 183, no. 6. American Association of Immunologists, pp.
3751–3760, 2009.
ista: Wolf A, Eller K, Zeiser R, Dürr C, Gerlach U, Sixt MK, Markut L, Gastl G,
Rosenkranz A, Wolf D. 2009. The sphingosine 1-phosphate receptor agonist FTY720
potently inhibits regulatory T cell proliferation in vitro and in vivo. Journal
of Immunology. 183(6), 3751–3760.
mla: Wolf, Anna, et al. “The Sphingosine 1-Phosphate Receptor Agonist FTY720 Potently
Inhibits Regulatory T Cell Proliferation in Vitro and in Vivo.” Journal of
Immunology, vol. 183, no. 6, American Association of Immunologists, 2009,
pp. 3751–60, doi:10.4049/jimmunol.0901011.
short: A. Wolf, K. Eller, R. Zeiser, C. Dürr, U. Gerlach, M.K. Sixt, L. Markut,
G. Gastl, A. Rosenkranz, D. Wolf, Journal of Immunology 183 (2009) 3751–3760.
date_created: 2018-12-11T12:06:05Z
date_published: 2009-09-15T00:00:00Z
date_updated: 2021-01-12T07:53:26Z
day: '15'
doi: 10.4049/jimmunol.0901011
extern: 1
intvolume: ' 183'
issue: '6'
month: '09'
page: 3751 - 3760
publication: Journal of Immunology
publication_status: published
publisher: American Association of Immunologists
publist_id: '2174'
quality_controlled: 0
status: public
title: The sphingosine 1-phosphate receptor agonist FTY720 potently inhibits regulatory
T cell proliferation in vitro and in vivo
type: journal_article
volume: 183
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'
...
---
_id: '3955'
abstract:
- lang: eng
text: Although both processes occur at similar rates, leukocyte extravasation from
the blood circulation is well investigated, whereas intravasation into lymphatic
vessels has hardly been studied. In contrast to a common assumption-that intra-
and extravasation follow similar molecular principles-we previously showed that
lymphatic entry of dendritic cells (DCs) does not require integrin-mediated adhesive
interactions. In this study, we demonstrate that DC-entry is also independent
of pericellular proteolysis, raising the question of whether lymphatic vessels
offer preexisting entry routes. We find that the perilymphatic basement membrane
of initial lymphatic vessels is discontinuous and therefore leaves gaps for entering
cells. Using a newly developed in situ live cell imaging approach that allows
us to dynamically visualize the cells and their extracellular environment, we
demonstrate that DCs enter through these discontinuities, which are transiently
mechanically dilated by the passaging cells. We further show that penetration
of the underlying lymphatic endothelial layer occurs through flap valves lacking
continuous intercellular junctions. Together, we demonstrate free cellular communication
between interstitium and lymphatic lumen.
author:
- first_name: Holger
full_name: Pflicke, Holger
last_name: Pflicke
- first_name: Michael K
full_name: Michael Sixt
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Pflicke H, Sixt MK. Preformed portals facilitate dendritic cell entry into
afferent lymphatic vessels. The Journal of Experimental Medicine. 2009;206(13):2925-2935.
doi:10.1084/jem.20091739
apa: Pflicke, H., & Sixt, M. K. (2009). Preformed portals facilitate dendritic
cell entry into afferent lymphatic vessels. The Journal of Experimental Medicine.
Rockefeller University Press. https://doi.org/10.1084/jem.20091739
chicago: Pflicke, Holger, and Michael K Sixt. “Preformed Portals Facilitate Dendritic
Cell Entry into Afferent Lymphatic Vessels.” The Journal of Experimental Medicine.
Rockefeller University Press, 2009. https://doi.org/10.1084/jem.20091739.
ieee: H. Pflicke and M. K. Sixt, “Preformed portals facilitate dendritic cell entry
into afferent lymphatic vessels,” The Journal of Experimental Medicine,
vol. 206, no. 13. Rockefeller University Press, pp. 2925–2935, 2009.
ista: Pflicke H, Sixt MK. 2009. Preformed portals facilitate dendritic cell entry
into afferent lymphatic vessels. The Journal of Experimental Medicine. 206(13),
2925–2935.
mla: Pflicke, Holger, and Michael K. Sixt. “Preformed Portals Facilitate Dendritic
Cell Entry into Afferent Lymphatic Vessels.” The Journal of Experimental Medicine,
vol. 206, no. 13, Rockefeller University Press, 2009, pp. 2925–35, doi:10.1084/jem.20091739.
short: H. Pflicke, M.K. Sixt, The Journal of Experimental Medicine 206 (2009) 2925–2935.
date_created: 2018-12-11T12:06:05Z
date_published: 2009-12-07T00:00:00Z
date_updated: 2021-01-12T07:53:27Z
day: '07'
doi: 10.1084/jem.20091739
extern: 1
intvolume: ' 206'
issue: '13'
month: '12'
page: 2925 - 2935
publication: The Journal of Experimental Medicine
publication_status: published
publisher: Rockefeller University Press
publist_id: '2172'
quality_controlled: 0
status: public
title: Preformed portals facilitate dendritic cell entry into afferent lymphatic vessels
type: journal_article
volume: 206
year: '2009'
...
---
_id: '3966'
abstract:
- lang: eng
text: 'Persistent homology has proven to be a useful tool in a variety of contexts,
including the recognition and measurement of shape characteristics of surfaces
in ℝ3. Persistence pairs homology classes that are born and die in a filtration
of a topological space, but does not pair its actual homology classes. For the
sublevelset filtration of a surface in ℝ3, persistence has been extended to a
pairing of essential classes using Reeb graphs. In this paper, we give an algebraic
formulation that extends persistence to essential homology for any filtered space,
present an algorithm to calculate it, and describe how it aids our ability to
recognize shape features for codimension 1 submanifolds of Euclidean space. The
extension derives from Poincaré duality but generalizes to nonmanifold spaces.
We prove stability for general triangulated spaces and duality as well as symmetry
for triangulated manifolds. '
acknowledgement: Research by all three authors is partially supported by DARPA under
grant HR0011-05-1-0007. Research by the second author is also partially supported
by NSF under grant CCR-00-86013.
author:
- first_name: David
full_name: Cohen-Steiner, David
last_name: Cohen Steiner
- first_name: Herbert
full_name: Herbert Edelsbrunner
id: 3FB178DA-F248-11E8-B48F-1D18A9856A87
last_name: Edelsbrunner
orcid: 0000-0002-9823-6833
- first_name: John
full_name: Harer, John
last_name: Harer
citation:
ama: Cohen Steiner D, Edelsbrunner H, Harer J. Extending persistence using Poincare
and Lefschetz duality. Foundations of Computational Mathematics. 2009;9(1):79-103.
doi:10.1007/s10208-008-9027-z
apa: Cohen Steiner, D., Edelsbrunner, H., & Harer, J. (2009). Extending persistence
using Poincare and Lefschetz duality. Foundations of Computational Mathematics.
Springer. https://doi.org/10.1007/s10208-008-9027-z
chicago: Cohen Steiner, David, Herbert Edelsbrunner, and John Harer. “Extending
Persistence Using Poincare and Lefschetz Duality.” Foundations of Computational
Mathematics. Springer, 2009. https://doi.org/10.1007/s10208-008-9027-z.
ieee: D. Cohen Steiner, H. Edelsbrunner, and J. Harer, “Extending persistence using
Poincare and Lefschetz duality,” Foundations of Computational Mathematics,
vol. 9, no. 1. Springer, pp. 79–103, 2009.
ista: Cohen Steiner D, Edelsbrunner H, Harer J. 2009. Extending persistence using
Poincare and Lefschetz duality. Foundations of Computational Mathematics. 9(1),
79–103.
mla: Cohen Steiner, David, et al. “Extending Persistence Using Poincare and Lefschetz
Duality.” Foundations of Computational Mathematics, vol. 9, no. 1, Springer,
2009, pp. 79–103, doi:10.1007/s10208-008-9027-z.
short: D. Cohen Steiner, H. Edelsbrunner, J. Harer, Foundations of Computational
Mathematics 9 (2009) 79–103.
date_created: 2018-12-11T12:06:10Z
date_published: 2009-01-01T00:00:00Z
date_updated: 2021-01-12T07:53:32Z
day: '01'
doi: 10.1007/s10208-008-9027-z
extern: 1
intvolume: ' 9'
issue: '1'
month: '01'
page: 79 - 103
publication: Foundations of Computational Mathematics
publication_status: published
publisher: Springer
publist_id: '2162'
quality_controlled: 0
status: public
title: Extending persistence using Poincare and Lefschetz duality
type: journal_article
volume: 9
year: '2009'
...
---
_id: '3967'
abstract:
- lang: eng
text: Motivated by the measurement of local homology and of functions on noisy domains,
we extend the notion of persistent homology to sequences of kernels, images, and
cokernels of maps induced by inclusions in a filtration of pairs of spaces. Specifically,
we note that persistence in this context is well defined, we prove that the persistence
diagrams are stable, and we explain how to compute them.
author:
- first_name: David
full_name: Cohen-Steiner, David
last_name: Cohen Steiner
- first_name: Herbert
full_name: Herbert Edelsbrunner
id: 3FB178DA-F248-11E8-B48F-1D18A9856A87
last_name: Edelsbrunner
orcid: 0000-0002-9823-6833
- first_name: John
full_name: Harer, John
last_name: Harer
- first_name: Dmitriy
full_name: Morozov, Dmitriy
last_name: Morozov
citation:
ama: 'Cohen Steiner D, Edelsbrunner H, Harer J, Morozov D. Persistent homology for
kernels, images, and cokernels. In: SIAM; 2009:1011-1020.'
apa: 'Cohen Steiner, D., Edelsbrunner, H., Harer, J., & Morozov, D. (2009).
Persistent homology for kernels, images, and cokernels (pp. 1011–1020). Presented
at the SODA: Symposium on Discrete Algorithms, SIAM.'
chicago: Cohen Steiner, David, Herbert Edelsbrunner, John Harer, and Dmitriy Morozov.
“Persistent Homology for Kernels, Images, and Cokernels,” 1011–20. SIAM, 2009.
ieee: 'D. Cohen Steiner, H. Edelsbrunner, J. Harer, and D. Morozov, “Persistent
homology for kernels, images, and cokernels,” presented at the SODA: Symposium
on Discrete Algorithms, 2009, pp. 1011–1020.'
ista: 'Cohen Steiner D, Edelsbrunner H, Harer J, Morozov D. 2009. Persistent homology
for kernels, images, and cokernels. SODA: Symposium on Discrete Algorithms, 1011–1020.'
mla: Cohen Steiner, David, et al. Persistent Homology for Kernels, Images, and
Cokernels. SIAM, 2009, pp. 1011–20.
short: D. Cohen Steiner, H. Edelsbrunner, J. Harer, D. Morozov, in:, SIAM, 2009,
pp. 1011–1020.
conference:
name: 'SODA: Symposium on Discrete Algorithms'
date_created: 2018-12-11T12:06:10Z
date_published: 2009-01-01T00:00:00Z
date_updated: 2021-01-12T07:53:32Z
day: '01'
extern: 1
month: '01'
page: 1011 - 1020
publication_status: published
publisher: SIAM
publist_id: '2159'
quality_controlled: 0
status: public
title: Persistent homology for kernels, images, and cokernels
type: conference
year: '2009'
...
---
_id: '3968'
abstract:
- lang: eng
text: We describe an algorithm for segmenting three-dimensional medical imaging
data modeled as a continuous function on a 3-manifold. It is related to watershed
algorithms developed in image processing but is closer to its mathematical roots,
which are Morse theory and homological algebra. It allows for the implicit treatment
of an underlying mesh, thus combining the structural integrity of its mathematical
foundations with the computational efficiency of image processing.
acknowledgement: This research was partially supported by Geomagic, Inc., and by the
Defense Advanced Research Projects Agency (DARPA) under grants HR0011-05-1-0007
and HR0011-05-1-0057.
alternative_title:
- LNCS
author:
- first_name: Herbert
full_name: Edelsbrunner, Herbert
id: 3FB178DA-F248-11E8-B48F-1D18A9856A87
last_name: Edelsbrunner
orcid: 0000-0002-9823-6833
- first_name: John
full_name: Harer, John
last_name: Harer
citation:
ama: 'Edelsbrunner H, Harer J. The persistent Morse complex segmentation of a 3-manifold.
In: Vol 5903. Springer; 2009:36-50. doi:10.1007/978-3-642-10470-1_4'
apa: 'Edelsbrunner, H., & Harer, J. (2009). The persistent Morse complex segmentation
of a 3-manifold (Vol. 5903, pp. 36–50). Presented at the 3DPH: Modelling the Physiological
Human, Zermatt, Switzerland: Springer. https://doi.org/10.1007/978-3-642-10470-1_4'
chicago: Edelsbrunner, Herbert, and John Harer. “The Persistent Morse Complex Segmentation
of a 3-Manifold,” 5903:36–50. Springer, 2009. https://doi.org/10.1007/978-3-642-10470-1_4.
ieee: 'H. Edelsbrunner and J. Harer, “The persistent Morse complex segmentation
of a 3-manifold,” presented at the 3DPH: Modelling the Physiological Human, Zermatt,
Switzerland, 2009, vol. 5903, pp. 36–50.'
ista: 'Edelsbrunner H, Harer J. 2009. The persistent Morse complex segmentation
of a 3-manifold. 3DPH: Modelling the Physiological Human, LNCS, vol. 5903, 36–50.'
mla: Edelsbrunner, Herbert, and John Harer. The Persistent Morse Complex Segmentation
of a 3-Manifold. Vol. 5903, Springer, 2009, pp. 36–50, doi:10.1007/978-3-642-10470-1_4.
short: H. Edelsbrunner, J. Harer, in:, Springer, 2009, pp. 36–50.
conference:
end_date: 2009-12-02
location: Zermatt, Switzerland
name: '3DPH: Modelling the Physiological Human'
start_date: 2009-11-29
date_created: 2018-12-11T12:06:10Z
date_published: 2009-11-17T00:00:00Z
date_updated: 2021-01-12T07:53:32Z
day: '17'
ddc:
- '000'
department:
- _id: HeEd
doi: 10.1007/978-3-642-10470-1_4
file:
- access_level: open_access
checksum: 11fc85bcc19bab1f020e706a4b8a4660
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:33Z
date_updated: 2020-07-14T12:46:21Z
file_id: '4694'
file_name: IST-2016-535-v1+1_2009-P-04-3ManifoldSegmentation.pdf
file_size: 165090
relation: main_file
file_date_updated: 2020-07-14T12:46:21Z
has_accepted_license: '1'
intvolume: ' 5903'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Submitted Version
page: 36 - 50
publication_status: published
publisher: Springer
publist_id: '2160'
pubrep_id: '535'
quality_controlled: '1'
scopus_import: 1
status: public
title: The persistent Morse complex segmentation of a 3-manifold
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5903
year: '2009'
...
---
_id: '4136'
abstract:
- lang: eng
text: 'Populations living in a spatially and temporally changing environment can
adapt to the changing optimum and/or migrate toward favorable habitats. Here we
extend previous analyses with a static optimum to allow the environment to vary
in time as well as in space. The model follows both population dynamics and the
trait mean under stabilizing selection, and the outcomes can be understood by
comparing the loads due to genetic variance, dispersal, and temporal change. With
fixed genetic variance, we obtain two regimes: (1) adaptation that is uniform
along the environmental gradient and that responds to the moving optimum as expected
for panmictic populations and when the spatial gradient is sufficiently steep,
and (2) a population with limited range that adapts more slowly than the environmental
optimum changes in both time and space; the population therefore becomes locally
extinct and migrates toward suitable habitat. We also use a population‐genetic
model with many loci to allow genetic variance to evolve, and we show that the
only solution now has uniform adaptation.'
article_processing_charge: No
article_type: original
author:
- first_name: Jitka
full_name: Polechova, Jitka
id: 3BBFB084-F248-11E8-B48F-1D18A9856A87
last_name: Polechova
orcid: 0000-0003-0951-3112
- first_name: Nicholas H
full_name: Barton, Nicholas H
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
- first_name: Glenn
full_name: Marion, Glenn
last_name: Marion
citation:
ama: 'Polechova J, Barton NH, Marion G. Species’ range: Adaptation in space and
time. American Naturalist. 2009;174(5):E186-E204. doi:10.1086/605958'
apa: 'Polechova, J., Barton, N. H., & Marion, G. (2009). Species’ range: Adaptation
in space and time. American Naturalist. University of Chicago Press. https://doi.org/10.1086/605958'
chicago: 'Polechova, Jitka, Nicholas H Barton, and Glenn Marion. “Species’ Range:
Adaptation in Space and Time.” American Naturalist. University of Chicago
Press, 2009. https://doi.org/10.1086/605958.'
ieee: 'J. Polechova, N. H. Barton, and G. Marion, “Species’ range: Adaptation in
space and time,” American Naturalist, vol. 174, no. 5. University of Chicago
Press, pp. E186–E204, 2009.'
ista: 'Polechova J, Barton NH, Marion G. 2009. Species’ range: Adaptation in space
and time. American Naturalist. 174(5), E186–E204.'
mla: 'Polechova, Jitka, et al. “Species’ Range: Adaptation in Space and Time.” American
Naturalist, vol. 174, no. 5, University of Chicago Press, 2009, pp. E186–204,
doi:10.1086/605958.'
short: J. Polechova, N.H. Barton, G. Marion, American Naturalist 174 (2009) E186–E204.
date_created: 2018-12-11T12:07:09Z
date_published: 2009-11-05T00:00:00Z
date_updated: 2021-01-12T07:54:46Z
day: '05'
ddc:
- '570'
department:
- _id: NiBa
doi: 10.1086/605958
external_id:
pmid:
- ' 19788353'
intvolume: ' 174'
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.doi.org/10.1086/605958
month: '11'
oa: 1
oa_version: Published Version
page: E186 - E204
pmid: 1
publication: American Naturalist
publication_status: published
publisher: University of Chicago Press
publist_id: '1986'
pubrep_id: '552'
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1086/659642
scopus_import: 1
status: public
title: 'Species'' range: Adaptation in space and time'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 174
year: '2009'
...
---
_id: '4143'
abstract:
- lang: eng
text: 'The migration of single cells and epithelial sheets is of great importance
for gastrulation and organ formation in developing embryos and, if misregulated,
can have dire consequences e.g. during cancer metastasis. A keystone of cell migration
is the regulation of adhesive contacts, which are dynamically assembled and disassembled
via endocytosis. Here, we discuss some of the basic concepts about the function
of endocytic trafficking during cell migration: transport of integrins from the
cell rear to the leading edge in fibroblasts; confinement of signalling to the
front of single cells by endocytic transport of growth factors; regulation of
movement coherence in multicellular sheets by cadherin turnover; and shaping of
extracellular chemokine gradients. Taken together, endocytosis enables migrating
cells and tissues to dynamically modulate their adhesion and signalling, allowing
them to efficiently migrate through their extracellular environment.'
article_processing_charge: No
author:
- first_name: Florian
full_name: Ulrich, Florian
last_name: Ulrich
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Ulrich F, Heisenberg C-PJ. Trafficking and cell migration. Traffic.
2009;10(7):811-818. doi:10.1111/j.1600-0854.2009.00929.x
apa: Ulrich, F., & Heisenberg, C.-P. J. (2009). Trafficking and cell migration.
Traffic. Wiley-Blackwell. https://doi.org/10.1111/j.1600-0854.2009.00929.x
chicago: Ulrich, Florian, and Carl-Philipp J Heisenberg. “Trafficking and Cell Migration.”
Traffic. Wiley-Blackwell, 2009. https://doi.org/10.1111/j.1600-0854.2009.00929.x.
ieee: F. Ulrich and C.-P. J. Heisenberg, “Trafficking and cell migration,” Traffic,
vol. 10, no. 7. Wiley-Blackwell, pp. 811–818, 2009.
ista: Ulrich F, Heisenberg C-PJ. 2009. Trafficking and cell migration. Traffic.
10(7), 811–818.
mla: Ulrich, Florian, and Carl-Philipp J. Heisenberg. “Trafficking and Cell Migration.”
Traffic, vol. 10, no. 7, Wiley-Blackwell, 2009, pp. 811–18, doi:10.1111/j.1600-0854.2009.00929.x.
short: F. Ulrich, C.-P.J. Heisenberg, Traffic 10 (2009) 811–818.
date_created: 2018-12-11T12:07:12Z
date_published: 2009-05-20T00:00:00Z
date_updated: 2021-01-12T07:54:49Z
day: '20'
doi: 10.1111/j.1600-0854.2009.00929.x
extern: '1'
intvolume: ' 10'
issue: '7'
language:
- iso: eng
month: '05'
oa_version: None
page: 811 - 818
publication: Traffic
publication_status: published
publisher: Wiley-Blackwell
publist_id: '1976'
status: public
title: Trafficking and cell migration
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 10
year: '2009'
...
---
_id: '4149'
abstract:
- lang: eng
text: "An important step in the formation of all epithelial organs is the coordinated
polarisation of their constituent cells. One of the factors thought to be crucial
for this process is the extracellular matrix (ECM), which provides positional
information for cells and directs polarity specification and epithelial cyst formation
in 3D culture. However, in vivo evidence for the role of the ECM in epithelial
tissue polarisation is scarce.\r\n\r\nTo gain insight in the factors involved
in establishing cell polarity during organogenesis, we are studying a group of
epithelial cells called the Dorsal Forerunner Cells (DFCs) in zebrafish embryos.
These cells migrate as a cluster towards the vegetal pole of the developing embryo,
where they involute. During this process they polarise, and make foci that open
up to form a ciliated lumen called Kupffer’s vesicle.\r\n\r\nWe find that interfering
with the deposition of components of the extracellular matrix, or with the intracellular
anchors of the cells to the matrix, impairs the polarisation of the DFC’s and
leads to subsequent defects in lumen formation. In addition, we have developed
a method to culture the DFCs ex vivo, allowing us to precisely manipulate the
extracellular environment. The possibility of combining the genetic study of Kupffer’s
vesicle formation in the live embryo with cell biological techniques in organ
culture make this system uniquely relevant for studying the role of the ECM in
polarisation during organogenesis.\r\n"
article_processing_charge: No
author:
- first_name: Gwen
full_name: Soete, Gwen
last_name: Soete
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Soete G, Heisenberg C-PJ. The role of the extracellular matrix in Kupffer’s
vesicle formation in zebrafish. Mechanisms of Development. 2009;126:S168-S168.
doi:10.1016/j.mod.2009.06.391
apa: Soete, G., & Heisenberg, C.-P. J. (2009). The role of the extracellular
matrix in Kupffer’s vesicle formation in zebrafish. Mechanisms of Development.
Elsevier. https://doi.org/10.1016/j.mod.2009.06.391
chicago: Soete, Gwen, and Carl-Philipp J Heisenberg. “The Role of the Extracellular
Matrix in Kupffer’s Vesicle Formation in Zebrafish.” Mechanisms of Development.
Elsevier, 2009. https://doi.org/10.1016/j.mod.2009.06.391.
ieee: G. Soete and C.-P. J. Heisenberg, “The role of the extracellular matrix in
Kupffer’s vesicle formation in zebrafish,” Mechanisms of Development, vol.
126. Elsevier, pp. S168–S168, 2009.
ista: Soete G, Heisenberg C-PJ. 2009. The role of the extracellular matrix in Kupffer’s
vesicle formation in zebrafish. Mechanisms of Development. 126, S168–S168.
mla: Soete, Gwen, and Carl-Philipp J. Heisenberg. “The Role of the Extracellular
Matrix in Kupffer’s Vesicle Formation in Zebrafish.” Mechanisms of Development,
vol. 126, Elsevier, 2009, pp. S168–S168, doi:10.1016/j.mod.2009.06.391.
short: G. Soete, C.-P.J. Heisenberg, Mechanisms of Development 126 (2009) S168–S168.
date_created: 2018-12-11T12:07:14Z
date_published: 2009-08-01T00:00:00Z
date_updated: 2021-01-12T07:54:52Z
day: '01'
doi: 10.1016/j.mod.2009.06.391
extern: '1'
intvolume: ' 126'
language:
- iso: eng
month: '08'
oa_version: None
page: S168 - S168
publication: Mechanisms of Development
publication_status: published
publisher: Elsevier
publist_id: '1970'
status: public
title: The role of the extracellular matrix in Kupffer's vesicle formation in zebrafish
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 126
year: '2009'
...
---
_id: '4158'
abstract:
- lang: eng
text: Together with cell growth, division and death, changes in cell shape are of
central importance for tissue morphogenesis during development. Cell shape is
the product of a cell's material and active properties balanced by external forces.
Control of cell shape, therefore, relies on both tight regulation of intracellular
mechanics and the cell's physical interaction with its environment. In this review,
we first discuss the biological and physical mechanisms of cell shape control.
We next examine a number of develop mental processes in which cell shape change
- either individually or in a coordinated manner - drives embryonic morphogenesis
and discuss how cell shape is controlled in these processes. Finally, we emphasize
that cell shape control during tissue morphogenesis can only be fully understood
by using a combination of cellular, molecular, developmental and biophysical approaches.
article_processing_charge: No
author:
- first_name: Ewa
full_name: Paluch, Ewa
last_name: Paluch
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Paluch E, Heisenberg C-PJ. Biology and physics of cell shape changes in development.
Current Biology. 2009;19(17):R790-R799. doi:10.1016/j.cub.2009.07.029
apa: Paluch, E., & Heisenberg, C.-P. J. (2009). Biology and physics of cell
shape changes in development. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2009.07.029
chicago: Paluch, Ewa, and Carl-Philipp J Heisenberg. “Biology and Physics of Cell
Shape Changes in Development.” Current Biology. Cell Press, 2009. https://doi.org/10.1016/j.cub.2009.07.029.
ieee: E. Paluch and C.-P. J. Heisenberg, “Biology and physics of cell shape changes
in development,” Current Biology, vol. 19, no. 17. Cell Press, pp. R790–R799,
2009.
ista: Paluch E, Heisenberg C-PJ. 2009. Biology and physics of cell shape changes
in development. Current Biology. 19(17), R790–R799.
mla: Paluch, Ewa, and Carl-Philipp J. Heisenberg. “Biology and Physics of Cell Shape
Changes in Development.” Current Biology, vol. 19, no. 17, Cell Press,
2009, pp. R790–99, doi:10.1016/j.cub.2009.07.029.
short: E. Paluch, C.-P.J. Heisenberg, Current Biology 19 (2009) R790–R799.
date_created: 2018-12-11T12:07:17Z
date_published: 2009-09-15T00:00:00Z
date_updated: 2021-01-12T07:54:56Z
day: '15'
doi: 10.1016/j.cub.2009.07.029
extern: '1'
intvolume: ' 19'
issue: '17'
language:
- iso: eng
month: '09'
oa_version: None
page: R790 - R799
publication: Current Biology
publication_status: published
publisher: Cell Press
publist_id: '1960'
status: public
title: Biology and physics of cell shape changes in development
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2009'
...
---
_id: '4159'
abstract:
- lang: eng
text: Apical cell contraction triggers tissue folding and invagination in epithelia.
During Drosophila gastrulation, ventral furrow formation was thought to be driven
by smooth, purse-string-like constriction of an actomyosin belt underlying adherens
junctions. Now Martin et al. report in Nature that ventral furrow formation is
triggered by asynchronous pulsed contractions of the apical acto-myosin cortex
in individual cells.
article_processing_charge: No
author:
- first_name: Ewa
full_name: Paluch, Ewa
last_name: Paluch
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: 'Paluch E, Heisenberg C-PJ. Chaos begets order: Asynchronous cell contractions
drive epithelial morphogenesis. Developmental Cell. 2009;16(1):4-6. doi:10.1016/j.devcel.2008.12.011'
apa: 'Paluch, E., & Heisenberg, C.-P. J. (2009). Chaos begets order: Asynchronous
cell contractions drive epithelial morphogenesis. Developmental Cell. Cell
Press. https://doi.org/10.1016/j.devcel.2008.12.011'
chicago: 'Paluch, Ewa, and Carl-Philipp J Heisenberg. “Chaos Begets Order: Asynchronous
Cell Contractions Drive Epithelial Morphogenesis.” Developmental Cell.
Cell Press, 2009. https://doi.org/10.1016/j.devcel.2008.12.011.'
ieee: 'E. Paluch and C.-P. J. Heisenberg, “Chaos begets order: Asynchronous cell
contractions drive epithelial morphogenesis,” Developmental Cell, vol.
16, no. 1. Cell Press, pp. 4–6, 2009.'
ista: 'Paluch E, Heisenberg C-PJ. 2009. Chaos begets order: Asynchronous cell contractions
drive epithelial morphogenesis. Developmental Cell. 16(1), 4–6.'
mla: 'Paluch, Ewa, and Carl-Philipp J. Heisenberg. “Chaos Begets Order: Asynchronous
Cell Contractions Drive Epithelial Morphogenesis.” Developmental Cell,
vol. 16, no. 1, Cell Press, 2009, pp. 4–6, doi:10.1016/j.devcel.2008.12.011.'
short: E. Paluch, C.-P.J. Heisenberg, Developmental Cell 16 (2009) 4–6.
date_created: 2018-12-11T12:07:18Z
date_published: 2009-01-20T00:00:00Z
date_updated: 2021-01-12T07:54:56Z
day: '20'
doi: 10.1016/j.devcel.2008.12.011
extern: '1'
intvolume: ' 16'
issue: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: 4 - 6
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '1961'
status: public
title: 'Chaos begets order: Asynchronous cell contractions drive epithelial morphogenesis'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 16
year: '2009'
...
---
_id: '4160'
abstract:
- lang: eng
text: While the function of patterning in organogenesis is being extensively studied,
considerably less is known of reverse effects that organ formation imposes on
patterning. In zebrafish, the Kupffer’s vesicle (KV) and parapineal (PP) are embryonic
struc- tures that share mechanisms of organogenesis and whose func- tion is essential
for normal patterning along the left–right axis. Early morphogenesis of KV and
PP organs involve the compaction of progenitor cells into a tight cluster within
which three-dimen- sional cellular rosettes are formed. Organisation into rosettes
pre- cedes the detachment of progenitor cells from neighbouring tissue and thus
represents a key step towards organ formation. Such morphogenetic event is essential
for organ function and its disruption has profound effects on left–right patterning.
acknowledgement: 'Grant sponsors: HHMI, CONICYT (PBCT ACT47, PBCT Red6), ICM P04-048-F,
EU FP6-2004-NEST-PATH EDCBNL, DAAD.'
article_processing_charge: No
author:
- first_name: Pablo
full_name: Oteíza, Pablo
last_name: Oteíza
- first_name: Carmen
full_name: Lemus, Carmen
last_name: Lemus
- first_name: Mathias
full_name: Köppen, Mathias
last_name: Köppen
- first_name: Karina
full_name: Palma, Karina
last_name: Palma
- first_name: Michael
full_name: Krieg, Michael
last_name: Krieg
- first_name: Cristina
full_name: Melo, Cristina
last_name: Melo
- first_name: Cecilia
full_name: Farias, Cecilia
last_name: Farias
- first_name: Eduardo
full_name: Pulgar, Eduardo
last_name: Pulgar
- first_name: Steffen
full_name: Preibisch, Steffen
last_name: Preibisch
- first_name: Steffen
full_name: Hartel, Steffen
last_name: Hartel
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Miguel
full_name: Concha, Miguel
last_name: Concha
citation:
ama: Oteíza P, Lemus C, Köppen M, et al. Linking organ formation to left-right patterning
in the embryonic zebrafish. Mechanisms of Development. 2009;126(Supplement
1):S11-S11. doi:10.1016/j.mod.2009.06.970
apa: Oteíza, P., Lemus, C., Köppen, M., Palma, K., Krieg, M., Melo, C., … Concha,
M. (2009). Linking organ formation to left-right patterning in the embryonic zebrafish.
Mechanisms of Development. Elsevier. https://doi.org/10.1016/j.mod.2009.06.970
chicago: Oteíza, Pablo, Carmen Lemus, Mathias Köppen, Karina Palma, Michael Krieg,
Cristina Melo, Cecilia Farias, et al. “Linking Organ Formation to Left-Right Patterning
in the Embryonic Zebrafish.” Mechanisms of Development. Elsevier, 2009.
https://doi.org/10.1016/j.mod.2009.06.970.
ieee: P. Oteíza et al., “Linking organ formation to left-right patterning
in the embryonic zebrafish,” Mechanisms of Development, vol. 126, no. Supplement
1. Elsevier, pp. S11–S11, 2009.
ista: Oteíza P, Lemus C, Köppen M, Palma K, Krieg M, Melo C, Farias C, Pulgar E,
Preibisch S, Hartel S, Heisenberg C-PJ, Concha M. 2009. Linking organ formation
to left-right patterning in the embryonic zebrafish. Mechanisms of Development.
126(Supplement 1), S11–S11.
mla: Oteíza, Pablo, et al. “Linking Organ Formation to Left-Right Patterning in
the Embryonic Zebrafish.” Mechanisms of Development, vol. 126, no. Supplement
1, Elsevier, 2009, pp. S11–S11, doi:10.1016/j.mod.2009.06.970.
short: P. Oteíza, C. Lemus, M. Köppen, K. Palma, M. Krieg, C. Melo, C. Farias, E.
Pulgar, S. Preibisch, S. Hartel, C.-P.J. Heisenberg, M. Concha, Mechanisms of
Development 126 (2009) S11–S11.
date_created: 2018-12-11T12:07:18Z
date_published: 2009-08-05T00:00:00Z
date_updated: 2021-01-12T07:54:57Z
day: '05'
doi: 10.1016/j.mod.2009.06.970
extern: '1'
intvolume: ' 126'
issue: Supplement 1
language:
- iso: eng
month: '08'
oa_version: None
page: S11 - S11
publication: Mechanisms of Development
publication_status: published
publisher: Elsevier
publist_id: '1959'
status: public
title: Linking organ formation to left-right patterning in the embryonic zebrafish
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 126
year: '2009'
...
---
_id: '4162'
abstract:
- lang: eng
text: Organ formation requires the precise assembly of progenitor cells into a functional
unit. Mechanical forces are likely to play a critical role in this process, but
it is unclear how these are molecularly controlled during development. Here, we
show that Wnt11/ Pk1a-mediated planar cell polarity (PCP) signalling coordinates
formation of the zebrafish laterality organ (Kupffer’s vesicle, KV) by regulating
adhesion forces between organ progenitor cells (the dorsal forerunner cells, DFCs).
article_processing_charge: No
author:
- first_name: Pablo
full_name: Oteíza, Pablo
last_name: Oteíza
- first_name: Mathias
full_name: Köppen, Mathias
last_name: Köppen
- first_name: Michael
full_name: Krieg, Michael
last_name: Krieg
- first_name: Steffen
full_name: Preibisch, Steffen
last_name: Preibisch
- first_name: Steffen
full_name: Haertel, Steffen
last_name: Haertel
- first_name: Daniel
full_name: Müller, Daniel
last_name: Müller
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Miguel
full_name: Concha, Miguel
last_name: Concha
citation:
ama: Oteíza P, Köppen M, Krieg M, et al. Wnt11/Pk1a-mediated planar cell polarity
signalling orchestrates epithelial organ morphogenesis by regulating N-cadherin
dependent cell adhesion forces. Mechanisms of Development. 2009;126(Supplement
1):S80-S80. doi:10.1016/j.mod.2009.06.098
apa: Oteíza, P., Köppen, M., Krieg, M., Preibisch, S., Haertel, S., Müller, D.,
… Concha, M. (2009). Wnt11/Pk1a-mediated planar cell polarity signalling orchestrates
epithelial organ morphogenesis by regulating N-cadherin dependent cell adhesion
forces. Mechanisms of Development. Elsevier. https://doi.org/10.1016/j.mod.2009.06.098
chicago: Oteíza, Pablo, Mathias Köppen, Michael Krieg, Steffen Preibisch, Steffen
Haertel, Daniel Müller, Carl-Philipp J Heisenberg, and Miguel Concha. “Wnt11/Pk1a-Mediated
Planar Cell Polarity Signalling Orchestrates Epithelial Organ Morphogenesis by
Regulating N-Cadherin Dependent Cell Adhesion Forces.” Mechanisms of Development.
Elsevier, 2009. https://doi.org/10.1016/j.mod.2009.06.098.
ieee: P. Oteíza et al., “Wnt11/Pk1a-mediated planar cell polarity signalling
orchestrates epithelial organ morphogenesis by regulating N-cadherin dependent
cell adhesion forces,” Mechanisms of Development, vol. 126, no. Supplement
1. Elsevier, pp. S80–S80, 2009.
ista: Oteíza P, Köppen M, Krieg M, Preibisch S, Haertel S, Müller D, Heisenberg
C-PJ, Concha M. 2009. Wnt11/Pk1a-mediated planar cell polarity signalling orchestrates
epithelial organ morphogenesis by regulating N-cadherin dependent cell adhesion
forces. Mechanisms of Development. 126(Supplement 1), S80–S80.
mla: Oteíza, Pablo, et al. “Wnt11/Pk1a-Mediated Planar Cell Polarity Signalling
Orchestrates Epithelial Organ Morphogenesis by Regulating N-Cadherin Dependent
Cell Adhesion Forces.” Mechanisms of Development, vol. 126, no. Supplement
1, Elsevier, 2009, pp. S80–S80, doi:10.1016/j.mod.2009.06.098.
short: P. Oteíza, M. Köppen, M. Krieg, S. Preibisch, S. Haertel, D. Müller, C.-P.J.
Heisenberg, M. Concha, Mechanisms of Development 126 (2009) S80–S80.
date_created: 2018-12-11T12:07:19Z
date_published: 2009-08-05T00:00:00Z
date_updated: 2021-01-12T07:54:58Z
day: '05'
doi: 10.1016/j.mod.2009.06.098
extern: '1'
intvolume: ' 126'
issue: Supplement 1
language:
- iso: eng
month: '08'
oa_version: None
page: S80 - S80
publication: Mechanisms of Development
publication_status: published
publisher: Elsevier
publist_id: '1957'
status: public
title: Wnt11/Pk1a-mediated planar cell polarity signalling orchestrates epithelial
organ morphogenesis by regulating N-cadherin dependent cell adhesion forces
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 126
year: '2009'
...
---
_id: '4165'
abstract:
- lang: eng
text: The tissues of a developing embryo are simultaneously patterned, moved and
differentiated according to an exchange of information between their constituent
cells. We argue that these complex self-organizing phenomena can only be fully
understood with quantitative mathematical frameworks that allow specific hypotheses
to be formulated and tested. The quantitative and dynamic imaging of growing embryos
at the molecular, cellular and tissue level is the key experimental advance required
to achieve this interaction between theory and experiment. Here we describe how
mathematical modelling has become an invaluable method to integrate quantitative
biological information across temporal and spatial scales, serving to connect
the activity of regulatory molecules with the morphological development of organisms.
article_processing_charge: No
author:
- first_name: Andrew
full_name: Oates, Andrew
last_name: Oates
- first_name: Nicole
full_name: Gorfinkiel, Nicole
last_name: Gorfinkiel
- first_name: Marcos
full_name: Gonzalez Gaitan, Marcos
last_name: Gonzalez Gaitan
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Oates A, Gorfinkiel N, Gonzalez Gaitan M, Heisenberg C-PJ. Quantitative approaches
in developmental biology. Nature Reviews Genetics. 2009;10(8):517-530.
doi:10.1038/nrg2548
apa: Oates, A., Gorfinkiel, N., Gonzalez Gaitan, M., & Heisenberg, C.-P. J.
(2009). Quantitative approaches in developmental biology. Nature Reviews Genetics.
Nature Publishing Group. https://doi.org/10.1038/nrg2548
chicago: Oates, Andrew, Nicole Gorfinkiel, Marcos Gonzalez Gaitan, and Carl-Philipp
J Heisenberg. “Quantitative Approaches in Developmental Biology.” Nature Reviews
Genetics. Nature Publishing Group, 2009. https://doi.org/10.1038/nrg2548.
ieee: A. Oates, N. Gorfinkiel, M. Gonzalez Gaitan, and C.-P. J. Heisenberg, “Quantitative
approaches in developmental biology,” Nature Reviews Genetics, vol. 10,
no. 8. Nature Publishing Group, pp. 517–530, 2009.
ista: Oates A, Gorfinkiel N, Gonzalez Gaitan M, Heisenberg C-PJ. 2009. Quantitative
approaches in developmental biology. Nature Reviews Genetics. 10(8), 517–530.
mla: Oates, Andrew, et al. “Quantitative Approaches in Developmental Biology.” Nature
Reviews Genetics, vol. 10, no. 8, Nature Publishing Group, 2009, pp. 517–30,
doi:10.1038/nrg2548.
short: A. Oates, N. Gorfinkiel, M. Gonzalez Gaitan, C.-P.J. Heisenberg, Nature Reviews
Genetics 10 (2009) 517–530.
date_created: 2018-12-11T12:07:20Z
date_published: 2009-08-01T00:00:00Z
date_updated: 2021-01-12T07:54:59Z
day: '01'
doi: 10.1038/nrg2548
extern: '1'
intvolume: ' 10'
issue: '8'
language:
- iso: eng
month: '08'
oa_version: None
page: 517 - 530
publication: Nature Reviews Genetics
publication_status: published
publisher: Nature Publishing Group
publist_id: '1953'
status: public
title: Quantitative approaches in developmental biology
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 10
year: '2009'
...
---
_id: '4192'
abstract:
- lang: eng
text: "During vertebrate gastrulation, the body axis is established by a variety
of co-ordinated and directed movements of cells. One of these movements is convergence
and extension (CE), which is regulated by a non-canonical Wnt/planar cell polarity
(PCP) pathway. From our forward genetic screen, we have identified 3-hydroxy-3-methyglutaryl-coenzyme
A reductase 1b (hmgcr1b) gene as a dominant enhancer of the silberblick (slb)/wnt11
CE phenotype. hmgcr1b mutant embryos exhibit only very mild CE phenotype during
gastrulation while showing a thicker yolk extension at pharyngula stages. Notably,
abrogation of hmgcr1b also enhances the CE defects of other core PCP mutants/morphants.
The prenylation pathway is one of branches downstream of HMGCR, and has been implicated
for lipid modification at the C-terminus of proteins. To test the possibility
that the prenylation pathway regulates activities of the PCP pathway, we abrogated
farnesyl transferase (FT) or geranylgeranyl transferase (GGT) function using morpholinos
on PCP mutant/morphant backgrounds. Consistent with the notion that FT preferentially
performs lipid modification on to proteins with the CAAX motif including the core
PCP protein Prickle (Pk), abrogation of FT, but not GGT, enhances the pk1a or
pk1b morphant CE phenotype, suggesting the specif icity for targets of the prenylation
enzymes.\r\n"
article_processing_charge: No
author:
- first_name: Masatake
full_name: Kai, Masatake
last_name: Kai
- first_name: Nina
full_name: Buchan, Nina
last_name: Buchan
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Masazumi
full_name: Tada, Masazumi
last_name: Tada
citation:
ama: Kai M, Buchan N, Heisenberg C-PJ, Tada M. Regulation of planar cell polarity
signalling by the prenylation pathway. Mechanisms of Development. 2009;126(Supplement
1):S132-S132. doi:10.1016/j.mod.2009.06.269
apa: Kai, M., Buchan, N., Heisenberg, C.-P. J., & Tada, M. (2009). Regulation
of planar cell polarity signalling by the prenylation pathway. Mechanisms of
Development. Elsevier. https://doi.org/10.1016/j.mod.2009.06.269
chicago: Kai, Masatake, Nina Buchan, Carl-Philipp J Heisenberg, and Masazumi Tada.
“Regulation of Planar Cell Polarity Signalling by the Prenylation Pathway.” Mechanisms
of Development. Elsevier, 2009. https://doi.org/10.1016/j.mod.2009.06.269.
ieee: M. Kai, N. Buchan, C.-P. J. Heisenberg, and M. Tada, “Regulation of planar
cell polarity signalling by the prenylation pathway,” Mechanisms of Development,
vol. 126, no. Supplement 1. Elsevier, pp. S132–S132, 2009.
ista: Kai M, Buchan N, Heisenberg C-PJ, Tada M. 2009. Regulation of planar cell
polarity signalling by the prenylation pathway. Mechanisms of Development. 126(Supplement
1), S132–S132.
mla: Kai, Masatake, et al. “Regulation of Planar Cell Polarity Signalling by the
Prenylation Pathway.” Mechanisms of Development, vol. 126, no. Supplement
1, Elsevier, 2009, pp. S132–S132, doi:10.1016/j.mod.2009.06.269.
short: M. Kai, N. Buchan, C.-P.J. Heisenberg, M. Tada, Mechanisms of Development
126 (2009) S132–S132.
date_created: 2018-12-11T12:07:30Z
date_published: 2009-08-05T00:00:00Z
date_updated: 2021-01-12T07:55:11Z
day: '05'
doi: 10.1016/j.mod.2009.06.269
extern: '1'
intvolume: ' 126'
issue: Supplement 1
language:
- iso: eng
month: '08'
oa_version: None
page: S132 - S132
publication: Mechanisms of Development
publication_status: published
publisher: Elsevier
publist_id: '1927'
status: public
title: Regulation of planar cell polarity signalling by the prenylation pathway
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 126
year: '2009'
...