---
_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
corr_author: '1'
date_created: 2018-12-11T12:06:10Z
date_published: 2009-11-17T00:00:00Z
date_updated: 2024-10-09T20:53:56Z
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.
corr_author: '1'
date_created: 2018-12-11T12:07:09Z
date_published: 2009-11-05T00:00:00Z
date_updated: 2025-09-30T09:53:09Z
day: '05'
ddc:
- '570'
department:
- _id: NiBa
doi: 10.1086/605958
external_id:
isi:
- '000271021900002'
pmid:
- ' 19788353'
intvolume: ' 174'
isi: 1
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 174
year: '2009'
...
---
OA_type: closed access
_id: '4137'
abstract:
- lang: eng
text: "Why do species have finite ranges in space and time?\r\n\r\nAll species have
limited ecological distributions, and all species eventually become extinct. At
the heart of these distributional limits is the idea of trade-offs: a single population
or species cannot maximize its fitness in all environments (Woodward and Kelly
2003). Each species therefore occupies a limited range of ecological conditions,
or a particular period in history, and interacts in complex ways in ecosystems
consisting of many co-existing species. These interactions may in turn generate
more specialization (Nosil & Harmon, this volume; Schemske, this volume). However,
from an evolutionary biology perspective this explanation is incomplete. Populations
clearly adapt to novel environments in some circumstances, otherwise there would
be no life on land, no mammals in the ocean, and only a few species on oceanic
islands such as Hawaii (Wagner & Funk 1995). What processes, therefore, act to
constrain adaptation to changing environments and continually prevent the expansion
of species into new habitats at the edge of their range?\r\n\r\nUnderstanding
the factors that limit the temporal or spatial persistence of species is of key
practical importance, given ongoing changes in global climate (Root et al. 2003),
coupled with rapid habitat loss and alteration by the introduction of exotic species
of parasites, predators and competitors."
alternative_title:
- ' Ecological Reviews'
article_processing_charge: No
author:
- first_name: Jon
full_name: Bridle, Jon
last_name: Bridle
- first_name: Jitka
full_name: Polechova, Jitka
id: 3BBFB084-F248-11E8-B48F-1D18A9856A87
last_name: Polechova
orcid: 0000-0003-0951-3112
- first_name: Timothy
full_name: Vines, Timothy
last_name: Vines
citation:
ama: 'Bridle J, Polechova J, Vines T. Limits to adaptation and patterns of biodiversity.
In: R. K. Butlin JR, Bridle J, Schluter D, eds. Speciation and Patterns of
Diversity. Cambridge University Press; 2009:77-101. doi:10.1017/CBO9780511815683.007'
apa: Bridle, J., Polechova, J., & Vines, T. (2009). Limits to adaptation and
patterns of biodiversity. In J. R. R. K. Butlin, J. Bridle, & D. Schluter
(Eds.), Speciation and Patterns of Diversity (pp. 77–101). Cambridge University
Press. https://doi.org/10.1017/CBO9780511815683.007
chicago: Bridle, Jon, Jitka Polechova, and Timothy Vines. “Limits to Adaptation
and Patterns of Biodiversity.” In Speciation and Patterns of Diversity,
edited by J.R. R. K. Butlin, Jon Bridle, and D. Schluter, 77–101. Cambridge University
Press, 2009. https://doi.org/10.1017/CBO9780511815683.007.
ieee: J. Bridle, J. Polechova, and T. Vines, “Limits to adaptation and patterns
of biodiversity,” in Speciation and Patterns of Diversity, J. R. R. K.
Butlin, J. Bridle, and D. Schluter, Eds. Cambridge University Press, 2009, pp.
77–101.
ista: 'Bridle J, Polechova J, Vines T. 2009.Limits to adaptation and patterns of
biodiversity. In: Speciation and Patterns of Diversity. Ecological Reviews, ,
77–101.'
mla: Bridle, Jon, et al. “Limits to Adaptation and Patterns of Biodiversity.” Speciation
and Patterns of Diversity, edited by J.R. R. K. Butlin et al., Cambridge University
Press, 2009, pp. 77–101, doi:10.1017/CBO9780511815683.007.
short: J. Bridle, J. Polechova, T. Vines, in:, J.R. R. K. Butlin, J. Bridle, D.
Schluter (Eds.), Speciation and Patterns of Diversity, Cambridge University Press,
2009, pp. 77–101.
date_created: 2018-12-11T12:07:09Z
date_published: 2009-01-01T00:00:00Z
date_updated: 2025-07-02T05:50:01Z
day: '01'
doi: 10.1017/CBO9780511815683.007
editor:
- first_name: J.R.
full_name: R. K. Butlin, J.R.
last_name: R. K. Butlin
- first_name: Jon
full_name: Bridle, Jon
last_name: Bridle
- first_name: D.
full_name: Schluter, D.
last_name: Schluter
extern: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: 77 - 101
publication: Speciation and Patterns of Diversity
publication_identifier:
eissn:
- '9780511815683'
publication_status: published
publisher: Cambridge University Press
publist_id: '1984'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Limits to adaptation and patterns of biodiversity
type: book_chapter
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
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'
...
---
_id: '4206'
abstract:
- lang: eng
text: Dorsal closure (DC), the closure of a hole in the dorsal epidermis of Drosophila
embryos by the joining of opposing epithelial cell sheets, has been used as a
model process to study the molecular and cellular mechanisms underlying epithelial
spreading and wound healing. Recent studies have provided novel insights into
how different tissues function cooperatively in this process. Specifically, they
demonstrate a critical function of the epidermis surrounding the hole in modulating
the behavior of the amnioserosa cells inside. These findings shed light not only
on the mechanisms by which the behavior of different tissues is coordinated during
DC, but also on the general mechanisms by which tissues interact to trigger global
morphogenesis, an essential but yet poorly explored aspect of embryogenesis.
article_processing_charge: No
author:
- 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: 'Heisenberg C-PJ. Dorsal closure in Drosophila: cells cannot get out of the
tight spot. Bioessays : News and Reviews in Molecular, Cellular and Developmental
Biology. 2009;31(12):1284-1287. doi:10.1002/bies.200900109'
apa: 'Heisenberg, C.-P. J. (2009). Dorsal closure in Drosophila: cells cannot get
out of the tight spot. Bioessays : News and Reviews in Molecular, Cellular
and Developmental Biology. Wiley-Blackwell. https://doi.org/10.1002/bies.200900109'
chicago: 'Heisenberg, Carl-Philipp J. “Dorsal Closure in Drosophila: Cells Cannot
Get out of the Tight Spot.” Bioessays : News and Reviews in Molecular, Cellular
and Developmental Biology. Wiley-Blackwell, 2009. https://doi.org/10.1002/bies.200900109.'
ieee: 'C.-P. J. Heisenberg, “Dorsal closure in Drosophila: cells cannot get out
of the tight spot,” Bioessays : News and Reviews in Molecular, Cellular and
Developmental Biology, vol. 31, no. 12. Wiley-Blackwell, pp. 1284–1287, 2009.'
ista: 'Heisenberg C-PJ. 2009. Dorsal closure in Drosophila: cells cannot get out
of the tight spot. Bioessays : News and Reviews in Molecular, Cellular and Developmental
Biology. 31(12), 1284–1287.'
mla: 'Heisenberg, Carl-Philipp J. “Dorsal Closure in Drosophila: Cells Cannot Get
out of the Tight Spot.” Bioessays : News and Reviews in Molecular, Cellular
and Developmental Biology, vol. 31, no. 12, Wiley-Blackwell, 2009, pp. 1284–87,
doi:10.1002/bies.200900109.'
short: 'C.-P.J. Heisenberg, Bioessays : News and Reviews in Molecular, Cellular
and Developmental Biology 31 (2009) 1284–1287.'
date_created: 2018-12-11T12:07:35Z
date_published: 2009-12-01T00:00:00Z
date_updated: 2021-01-12T07:55:17Z
day: '01'
doi: 10.1002/bies.200900109
extern: '1'
intvolume: ' 31'
issue: '12'
language:
- iso: eng
month: '12'
oa_version: None
page: 1284 - 1287
publication: 'Bioessays : News and Reviews in Molecular, Cellular and Developmental
Biology'
publication_status: published
publisher: Wiley-Blackwell
publist_id: '1911'
status: public
title: 'Dorsal closure in Drosophila: cells cannot get out of the tight spot'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 31
year: '2009'
...
---
_id: '4217'
abstract:
- lang: eng
text: Nuclear movements play an essential role in metazoan development. Although
the intracellular transport mechanisms underlying nuclear movements have been
studied in detail, relatively little is known about signals from surrounding cells
and tissues controlling these movements. Here, we show that, in gastrulating zebrafish
embryos, convergence movements of nuclei within the yolk syncytial layer (YSL)
are guided by mesoderm and endoderm progenitors migrating along the surface of
the yolk towards the dorsal side of the developing gastrula. Progenitor cells
direct the convergence movements of internal yolk syncytial nuclei (iYSN) by modulating
cortical flow within the YSL in which the iYSN are entrained. The effect of mesoderm
and endoderm progenitors on the convergence movement of iYSN depends on the expression
of E-cadherin, indicating that adhesive contact between the cells and the YSL
is required for the mesendoderm-modulated YSL cortical flow mediating nuclear
convergence. In summary, our data reveal a crucial function for cortical flow
in the coordination of syncytial nuclear movements with surrounding cells and
tissues during zebrafish gastrulation.
article_processing_charge: No
author:
- first_name: Lara
full_name: Carvalho, Lara
last_name: Carvalho
- first_name: Jan
full_name: Stuehmer, Jan
last_name: Stuehmer
- first_name: Justin
full_name: Bois, Justin
last_name: Bois
- first_name: Yannis
full_name: Kalaidzidis, Yannis
last_name: Kalaidzidis
- first_name: Virginie
full_name: Lecaudey, Virginie
last_name: Lecaudey
- 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: Carvalho L, Stuehmer J, Bois J, Kalaidzidis Y, Lecaudey V, Heisenberg C-PJ.
Control of convergent yolk syncytial layer nuclear movement in zebrafish. Development.
2009;136(8):1305-1315. doi:10.1242/dev.026922
apa: Carvalho, L., Stuehmer, J., Bois, J., Kalaidzidis, Y., Lecaudey, V., &
Heisenberg, C.-P. J. (2009). Control of convergent yolk syncytial layer nuclear
movement in zebrafish. Development. Company of Biologists. https://doi.org/10.1242/dev.026922
chicago: Carvalho, Lara, Jan Stuehmer, Justin Bois, Yannis Kalaidzidis, Virginie
Lecaudey, and Carl-Philipp J Heisenberg. “Control of Convergent Yolk Syncytial
Layer Nuclear Movement in Zebrafish.” Development. Company of Biologists,
2009. https://doi.org/10.1242/dev.026922.
ieee: L. Carvalho, J. Stuehmer, J. Bois, Y. Kalaidzidis, V. Lecaudey, and C.-P.
J. Heisenberg, “Control of convergent yolk syncytial layer nuclear movement in
zebrafish,” Development, vol. 136, no. 8. Company of Biologists, pp. 1305–1315,
2009.
ista: Carvalho L, Stuehmer J, Bois J, Kalaidzidis Y, Lecaudey V, Heisenberg C-PJ.
2009. Control of convergent yolk syncytial layer nuclear movement in zebrafish.
Development. 136(8), 1305–1315.
mla: Carvalho, Lara, et al. “Control of Convergent Yolk Syncytial Layer Nuclear
Movement in Zebrafish.” Development, vol. 136, no. 8, Company of Biologists,
2009, pp. 1305–15, doi:10.1242/dev.026922.
short: L. Carvalho, J. Stuehmer, J. Bois, Y. Kalaidzidis, V. Lecaudey, C.-P.J. Heisenberg,
Development 136 (2009) 1305–1315.
date_created: 2018-12-11T12:07:39Z
date_published: 2009-04-15T00:00:00Z
date_updated: 2021-01-12T07:55:22Z
day: '15'
doi: 10.1242/dev.026922
extern: '1'
intvolume: ' 136'
issue: '8'
language:
- iso: eng
month: '04'
oa_version: None
page: 1305 - 1315
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '1901'
status: public
title: Control of convergent yolk syncytial layer nuclear movement in zebrafish
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 136
year: '2009'
...
---
_id: '4223'
abstract:
- lang: eng
text: 'Both Gram-positive and Gram-negative bacteria contain bactoprenol-dependent
biosynthetic pathways expressing non-essential cell surface polysaccharides that
function as virulence factors. Although these polymers are not required for bacterial
viability in vitro, genes in many of the biosynthetic pathways are conditionally
essential: they cannot be deleted except in strains incapable of initiating polymer
synthesis. We report a cell-based, pathway-specific strategy to screen for small
molecule inhibitors of conditionally essential enzymes. The screen identifies
molecules that prevent the growth of a wildtype bacterial strain but do not affect
the growth of a mutant strain incapable of initiating polymer synthesis. We have
applied this approach to discover inhibitors of wall teichoic acid (WTA) biosynthesis
in Staphylococcus aureus. WTAs are anionic cell surface polysaccharides required
for host colonization that have been suggested as targets for new antimicrobials.
We have identified a small molecule, 7-chloro-N,N-diethyl-3-(phenylsulfonyl)-[1,2,3]triazolo[1,5-a]quinolin-5-amine
(1835F03), that inhibits the growth of a panel of S. aureus strains (MIC = 1−3
μg mL−1), including clinical methicillin-resistant S. aureus (MRSA) isolates.
Using a combination of biochemistry and genetics, we have identified the molecular
target as TarG, the transmembrane component of the ABC transporter that exports
WTAs to the cell surface. We also show that preventing the completion of WTA biosynthesis
once it has been initiated triggers growth arrest. The discovery of 1835F03 validates
our chemical genetics strategy for identifying inhibitors of conditionally essential
enzymes, and the strategy should be applicable to many other bactoprenol-dependent
biosynthetic pathways in the pursuit of novel antibacterials and probes of bacterial
stress responses.'
article_processing_charge: No
author:
- first_name: Jonathan
full_name: Swoboda, Jonathan
last_name: Swoboda
- first_name: Timothy
full_name: Meredith, Timothy
last_name: Meredith
- first_name: Jennifer
full_name: Campbell, Jennifer
last_name: Campbell
- first_name: Stephanie
full_name: Brown, Stephanie
last_name: Brown
- first_name: Takashi
full_name: Suzuki, Takashi
last_name: Suzuki
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Amy
full_name: Malhowski, Amy
last_name: Malhowski
- first_name: Roy
full_name: Kishony, Roy
last_name: Kishony
- first_name: Michael
full_name: Gilmore, Michael
last_name: Gilmore
- first_name: Suzanne
full_name: Walker, Suzanne
last_name: Walker
citation:
ama: Swoboda J, Meredith T, Campbell J, et al. Discovery of a Small Molecule that
Blocks Wall Teichoic Acid Biosynthesis in Staphylococcus aureus. ACS Chemical
Biology. 2009;4(10):875-883. doi:10.1021/cb900151k
apa: Swoboda, J., Meredith, T., Campbell, J., Brown, S., Suzuki, T., Bollenbach,
M. T., … Walker, S. (2009). Discovery of a Small Molecule that Blocks Wall Teichoic
Acid Biosynthesis in Staphylococcus aureus. ACS Chemical Biology. American
Chemical Society. https://doi.org/10.1021/cb900151k
chicago: Swoboda, Jonathan, Timothy Meredith, Jennifer Campbell, Stephanie Brown,
Takashi Suzuki, Mark Tobias Bollenbach, Amy Malhowski, Roy Kishony, Michael Gilmore,
and Suzanne Walker. “Discovery of a Small Molecule That Blocks Wall Teichoic Acid
Biosynthesis in Staphylococcus Aureus.” ACS Chemical Biology. American
Chemical Society, 2009. https://doi.org/10.1021/cb900151k.
ieee: J. Swoboda et al., “Discovery of a Small Molecule that Blocks Wall
Teichoic Acid Biosynthesis in Staphylococcus aureus,” ACS Chemical Biology,
vol. 4, no. 10. American Chemical Society, pp. 875–883, 2009.
ista: Swoboda J, Meredith T, Campbell J, Brown S, Suzuki T, Bollenbach MT, Malhowski
A, Kishony R, Gilmore M, Walker S. 2009. Discovery of a Small Molecule that Blocks
Wall Teichoic Acid Biosynthesis in Staphylococcus aureus. ACS Chemical Biology.
4(10), 875–883.
mla: Swoboda, Jonathan, et al. “Discovery of a Small Molecule That Blocks Wall Teichoic
Acid Biosynthesis in Staphylococcus Aureus.” ACS Chemical Biology, vol.
4, no. 10, American Chemical Society, 2009, pp. 875–83, doi:10.1021/cb900151k.
short: J. Swoboda, T. Meredith, J. Campbell, S. Brown, T. Suzuki, M.T. Bollenbach,
A. Malhowski, R. Kishony, M. Gilmore, S. Walker, ACS Chemical Biology 4 (2009)
875–883.
date_created: 2018-12-11T12:07:41Z
date_published: 2009-08-18T00:00:00Z
date_updated: 2021-01-12T07:55:25Z
day: '18'
doi: 10.1021/cb900151k
extern: '1'
intvolume: ' 4'
issue: '10'
language:
- iso: eng
main_file_link:
- url: 10.1021/cb900151k [doi]
month: '08'
oa_version: None
page: 875 - 883
publication: ACS Chemical Biology
publication_status: published
publisher: American Chemical Society
publist_id: '1894'
status: public
title: Discovery of a Small Molecule that Blocks Wall Teichoic Acid Biosynthesis in
Staphylococcus aureus
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 4
year: '2009'
...
---
_id: '4228'
abstract:
- lang: eng
text: Suppressive drug interactions, in which one antibiotic can actually help bacterial
cells to grow faster in the presence of another, occur between protein and DNA
synthesis inhibitors. Here, we show that this suppression results from nonoptimal
regulation of ribosomal genes in the presence of DNA stress. Using GFP-tagged
transcription reporters in Escherichia coli, we find that ribosomal genes are
not directly regulated by DNA stress, leading to an imbalance between cellular
DNA and protein content. To test whether ribosomal gene expression under DNA stress
is nonoptimal for growth rate, we sequentially deleted up to six of the seven
ribosomal RNA operons. These synthetic manipulations of ribosomal gene expression
correct the protein-DNA imbalance, lead to improved survival and growth, and completely
remove the suppressive drug interaction. A simple mathematical model explains
the nonoptimal regulation in different nutrient environments. These results reveal
the genetic mechanism underlying an important class of suppressive drug interactions.
author:
- first_name: Tobias
full_name: Bollenbach, Tobias
last_name: Bollenbach
- first_name: Selwyn
full_name: Quan, Selwyn
last_name: Quan
- first_name: Remy P
full_name: Remy Chait
id: 3464AE84-F248-11E8-B48F-1D18A9856A87
last_name: Chait
orcid: 0000-0003-0876-3187
- first_name: Roy
full_name: Kishony, Roy
last_name: Kishony
citation:
ama: Bollenbach T, Quan S, Chait RP, Kishony R. Nonoptimal Microbial Response to
Antibiotics Underlies Suppressive Drug Interactions. Cell. 2009;139(4):707-718.
doi:10.1016/j.cell.2009.10.025
apa: Bollenbach, T., Quan, S., Chait, R. P., & Kishony, R. (2009). Nonoptimal
Microbial Response to Antibiotics Underlies Suppressive Drug Interactions. Cell.
Cell Press. https://doi.org/10.1016/j.cell.2009.10.025
chicago: Bollenbach, Tobias, Selwyn Quan, Remy P Chait, and Roy Kishony. “Nonoptimal
Microbial Response to Antibiotics Underlies Suppressive Drug Interactions.” Cell.
Cell Press, 2009. https://doi.org/10.1016/j.cell.2009.10.025.
ieee: T. Bollenbach, S. Quan, R. P. Chait, and R. Kishony, “Nonoptimal Microbial
Response to Antibiotics Underlies Suppressive Drug Interactions,” Cell,
vol. 139, no. 4. Cell Press, pp. 707–718, 2009.
ista: Bollenbach T, Quan S, Chait RP, Kishony R. 2009. Nonoptimal Microbial Response
to Antibiotics Underlies Suppressive Drug Interactions. Cell. 139(4), 707–718.
mla: Bollenbach, Tobias, et al. “Nonoptimal Microbial Response to Antibiotics Underlies
Suppressive Drug Interactions.” Cell, vol. 139, no. 4, Cell Press, 2009,
pp. 707–18, doi:10.1016/j.cell.2009.10.025.
short: T. Bollenbach, S. Quan, R.P. Chait, R. Kishony, Cell 139 (2009) 707–718.
date_created: 2018-12-11T12:07:43Z
date_published: 2009-01-01T00:00:00Z
date_updated: 2021-01-12T07:55:27Z
day: '01'
doi: 10.1016/j.cell.2009.10.025
extern: 1
intvolume: ' 139'
issue: '4'
month: '01'
page: 707 - 718
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '1890'
quality_controlled: 0
status: public
title: Nonoptimal Microbial Response to Antibiotics Underlies Suppressive Drug Interactions
type: journal_article
volume: 139
year: '2009'
...
---
_id: '4231'
abstract:
- lang: eng
text: The evolution of quantitative characters depends on the frequencies of the
alleles involved, yet these frequencies cannot usually be measured. Previous groups
have proposed an approximation to the dynamics of quantitative traits, based on
an analogy with statistical mechanics. We present a modified version of that approach,
which makes the analogy more precise and applies quite generally to describe the
evolution of allele frequencies. We calculate explicitly how the macroscopic quantities
(i.e., quantities that depend on the quantitative trait) depend on evolutionary
forces, in a way that is independent of the microscopic details. We first show
that the stationary distribution of allele frequencies under drift, selection,
and mutation maximizes a certain measure of entropy, subject to constraints on
the expectation of observable quantities. We then approximate the dynamical changes
in these expectations, assuming that the distribution of allele frequencies always
maximizes entropy, conditional on the expected values. When applied to directional
selection on an additive trait, this gives a very good approximation to the evolution
of the trait mean and the genetic variance, when the number of mutations per generation
is sufficiently high (4Nμ > 1). We show how the method can be modified for
small mutation rates (4Nμ → 0). We outline how this method describes epistatic
interactions as, for example, with stabilizing selection.
acknowledgement: "N.B. was supported by the Engineering and Physical Sciences Research
Council (GR/T11753 and GR/T19537) and by the Royal Society.\r\nWe are grateful to
Ellen Baake for helping to initiate this project and for her comments on this manuscript.
We also thank Michael Turelli for his comments on the manuscript and I. Pen for
discussions and support in this project. This project was a result of a collaboration
supported by the European Science Foundation grant “Integrating population genetics
and conservation biology.” "
article_processing_charge: No
author:
- 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: Harold
full_name: De Vladar, Harold
last_name: De Vladar
citation:
ama: Barton NH, De Vladar H. Statistical mechanics and the evolution of polygenic
quantitative traits. Genetics. 2009;181(3):997-1011. doi:10.1534/genetics.108.099309
apa: Barton, N. H., & De Vladar, H. (2009). Statistical mechanics and the evolution
of polygenic quantitative traits. Genetics. Genetics Society of America.
https://doi.org/10.1534/genetics.108.099309
chicago: Barton, Nicholas H, and Harold De Vladar. “Statistical Mechanics and the
Evolution of Polygenic Quantitative Traits.” Genetics. Genetics Society
of America, 2009. https://doi.org/10.1534/genetics.108.099309.
ieee: N. H. Barton and H. De Vladar, “Statistical mechanics and the evolution of
polygenic quantitative traits,” Genetics, vol. 181, no. 3. Genetics Society
of America, pp. 997–1011, 2009.
ista: Barton NH, De Vladar H. 2009. Statistical mechanics and the evolution of polygenic
quantitative traits. Genetics. 181(3), 997–1011.
mla: Barton, Nicholas H., and Harold De Vladar. “Statistical Mechanics and the Evolution
of Polygenic Quantitative Traits.” Genetics, vol. 181, no. 3, Genetics
Society of America, 2009, pp. 997–1011, doi:10.1534/genetics.108.099309.
short: N.H. Barton, H. De Vladar, Genetics 181 (2009) 997–1011.
corr_author: '1'
date_created: 2018-12-11T12:07:44Z
date_published: 2009-03-01T00:00:00Z
date_updated: 2025-09-30T09:52:35Z
day: '01'
department:
- _id: NiBa
doi: 10.1534/genetics.108.099309
external_id:
isi:
- '000270213500018'
intvolume: ' 181'
isi: 1
issue: '3'
language:
- iso: eng
month: '03'
oa_version: None
page: 997 - 1011
publication: Genetics
publication_status: published
publisher: Genetics Society of America
publist_id: '1882'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Statistical mechanics and the evolution of polygenic quantitative traits
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 181
year: '2009'
...
---
_id: '4232'
article_processing_charge: No
author:
- first_name: Harold
full_name: Vladar, Harold
id: 2A181218-F248-11E8-B48F-1D18A9856A87
last_name: Vladar
orcid: 0000-0002-5985-7653
citation:
ama: de Vladar H. Stochasticity and Variability in the dynamics and genetics of
populations. 2009.
apa: de Vladar, H. (2009). Stochasticity and Variability in the dynamics and
genetics of populations. Faculty of mathematical and natural sciences, University
of Groningen.
chicago: Vladar, Harold de. “Stochasticity and Variability in the Dynamics and Genetics
of Populations.” Faculty of mathematical and natural sciences, University of Groningen,
2009.
ieee: H. de Vladar, “Stochasticity and Variability in the dynamics and genetics
of populations,” Faculty of mathematical and natural sciences, University of Groningen,
2009.
ista: de Vladar H. 2009. Stochasticity and Variability in the dynamics and genetics
of populations. Faculty of mathematical and natural sciences, University of Groningen.
mla: de Vladar, Harold. Stochasticity and Variability in the Dynamics and Genetics
of Populations. Faculty of mathematical and natural sciences, University of
Groningen, 2009.
short: H. de Vladar, Stochasticity and Variability in the Dynamics and Genetics
of Populations, Faculty of mathematical and natural sciences, University of Groningen,
2009.
date_created: 2018-12-11T12:07:44Z
date_published: 2009-01-01T00:00:00Z
date_updated: 2025-07-02T06:46:07Z
day: '01'
extern: '1'
language:
- iso: eng
month: '01'
oa_version: None
publication_status: published
publisher: Faculty of mathematical and natural sciences, University of Groningen
publist_id: '1883'
status: public
title: Stochasticity and Variability in the dynamics and genetics of populations
type: dissertation
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2009'
...
---
_id: '4242'
abstract:
- lang: eng
text: 'Felsenstein distinguished two ways by which selection can directly strengthen
isolation. First, a modifier that strengthens prezygotic isolation can be favored
everywhere. This fits with the traditional view of reinforcement as an adaptation
to reduce deleterious hybridization by strengthening assortative mating. Second,
selection can favor association between different incompatibilities, despite recombination.
We generalize this “two allele” model to follow associations among any number
of incompatibilities, which may include both assortment and hybrid inviability.
Our key argument is that this process, of coupling between incompatibilities,
may be quite different from the usual view of reinforcement: strong isolation
can evolve through the coupling of any kind of incompatibility, whether prezygotic
or postzygotic. Single locus incompatibilities become coupled because associations
between them increase the variance in compatibility, which in turn increases mean
fitness if there is positive epistasis. Multiple incompatibilities, each maintained
by epistasis, can become coupled in the same way. In contrast, a single-locus
incompatibility can become coupled with loci that reduce the viability of haploid
hybrids because this reduces harmful recombination. We obtain simple approximations
for the limits of tight linkage, and strong assortment, and show how assortment
alleles can invade through associations with other components of reproductive
isolation.'
acknowledgement: "This work was supported by a Royal Society/Wolfson Research Merit
award, and by a grant from the Natural Environment Research Council.\r\nWe are very
grateful for insightful comments from S. P. Otto, and for helpful suggestions from
the referees and the Associate Editor, Maria Servedio."
article_processing_charge: No
author:
- 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: Maria
full_name: De Cara, Maria
last_name: De Cara
citation:
ama: Barton NH, De Cara M. The evolution of strong reproductive isolation. Evolution;
International Journal of Organic Evolution. 2009;63(5):1171-1190. doi:10.1111/j.1558-5646.2009.00622.x
apa: Barton, N. H., & De Cara, M. (2009). The evolution of strong reproductive
isolation. Evolution; International Journal of Organic Evolution. Wiley.
https://doi.org/10.1111/j.1558-5646.2009.00622.x
chicago: Barton, Nicholas H, and Maria De Cara. “The Evolution of Strong Reproductive
Isolation.” Evolution; International Journal of Organic Evolution. Wiley,
2009. https://doi.org/10.1111/j.1558-5646.2009.00622.x.
ieee: N. H. Barton and M. De Cara, “The evolution of strong reproductive isolation,”
Evolution; International Journal of Organic Evolution, vol. 63, no. 5.
Wiley, pp. 1171–1190, 2009.
ista: Barton NH, De Cara M. 2009. The evolution of strong reproductive isolation.
Evolution; International Journal of Organic Evolution. 63(5), 1171–1190.
mla: Barton, Nicholas H., and Maria De Cara. “The Evolution of Strong Reproductive
Isolation.” Evolution; International Journal of Organic Evolution, vol.
63, no. 5, Wiley, 2009, pp. 1171–90, doi:10.1111/j.1558-5646.2009.00622.x.
short: N.H. Barton, M. De Cara, Evolution; International Journal of Organic Evolution
63 (2009) 1171–1190.
corr_author: '1'
date_created: 2018-12-11T12:07:48Z
date_published: 2009-05-01T00:00:00Z
date_updated: 2025-09-30T09:52:11Z
day: '01'
ddc:
- '570'
department:
- _id: NiBa
doi: 10.1111/j.1558-5646.2009.00622.x
external_id:
isi:
- '000265145800006'
file:
- access_level: open_access
checksum: 1920d2e25ef335833764256c1a47bbfb
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:46Z
date_updated: 2020-07-14T12:46:25Z
file_id: '4903'
file_name: IST-2016-551-v1+1_BartonDeCaraRevNew.pdf
file_size: 720913
relation: main_file
- access_level: open_access
checksum: c1c51bbc10d4f328fc96fc5b0e5dc25d
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:47Z
date_updated: 2020-07-14T12:46:25Z
file_id: '4904'
file_name: IST-2016-551-v1+2_BartonDeCaraRevNewSI.pdf
file_size: 290160
relation: main_file
file_date_updated: 2020-07-14T12:46:25Z
has_accepted_license: '1'
intvolume: ' 63'
isi: 1
issue: '5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Submitted Version
page: 1171 - 1190
publication: Evolution; International Journal of Organic Evolution
publication_status: published
publisher: Wiley
publist_id: '1866'
pubrep_id: '551'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The evolution of strong reproductive isolation
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 63
year: '2009'
...
---
_id: '4357'
abstract:
- lang: eng
text: Parallel evolution is the acquisition of identical adaptive traits in independently
evolving populations. Understanding whether the genetic changes underlying adaptation
to a common selective environment are parallel within and between species is interesting
because it sheds light on the degree of evolutionary constraints. If parallel
evolution is perfect, then the implication is that forces such as functional constraints,
epistasis, and pleiotropy play an important role in shaping the outcomes of adaptive
evolution. In addition, population genetic theory predicts that the probability
of parallel evolution will decline with an increase in the number of adaptive
solutions-if a single adaptive solution exists, then parallel evolution will be
observed among highly divergent species. For this reason, it is predicted that
close relatives-which likely overlap more in the details of their adaptive solutions-will
show more parallel evolution. By adapting three related bacteriophage species
to a novel environment we find (1) a high rate of parallel genetic evolution at
orthologous nucleotide and amino acid residues within species, (2) parallel beneficial
mutations do not occur in a common order in which they fix or appear in an evolving
population, (3) low rates of parallel evolution and convergent evolution between
species, and (4) the probability of parallel and convergent evolution between
species is strongly effected by divergence.
author:
- first_name: Jonathan P
full_name: Jonathan Bollback
id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
last_name: Bollback
orcid: 0000-0002-4624-4612
- first_name: John
full_name: Huelsenbeck, John P
last_name: Huelsenbeck
citation:
ama: Bollback JP, Huelsenbeck J. Parallel genetic evolution within and between bacteriophage
species of varying degrees of divergence. Genetics. 2009;181(1):225-234.
doi:10.1534/genetics.107.085225
apa: Bollback, J. P., & Huelsenbeck, J. (2009). Parallel genetic evolution within
and between bacteriophage species of varying degrees of divergence. Genetics.
Genetics Society of America. https://doi.org/10.1534/genetics.107.085225
chicago: Bollback, Jonathan P, and John Huelsenbeck. “Parallel Genetic Evolution
within and between Bacteriophage Species of Varying Degrees of Divergence.” Genetics.
Genetics Society of America, 2009. https://doi.org/10.1534/genetics.107.085225.
ieee: J. P. Bollback and J. Huelsenbeck, “Parallel genetic evolution within and
between bacteriophage species of varying degrees of divergence,” Genetics,
vol. 181, no. 1. Genetics Society of America, pp. 225–234, 2009.
ista: Bollback JP, Huelsenbeck J. 2009. Parallel genetic evolution within and between
bacteriophage species of varying degrees of divergence. Genetics. 181(1), 225–234.
mla: Bollback, Jonathan P., and John Huelsenbeck. “Parallel Genetic Evolution within
and between Bacteriophage Species of Varying Degrees of Divergence.” Genetics,
vol. 181, no. 1, Genetics Society of America, 2009, pp. 225–34, doi:10.1534/genetics.107.085225.
short: J.P. Bollback, J. Huelsenbeck, Genetics 181 (2009) 225–234.
date_created: 2018-12-11T12:08:26Z
date_published: 2009-01-01T00:00:00Z
date_updated: 2021-01-12T07:56:22Z
day: '01'
doi: 10.1534/genetics.107.085225
extern: 1
intvolume: ' 181'
issue: '1'
month: '01'
page: 225 - 234
publication: Genetics
publication_status: published
publisher: Genetics Society of America
publist_id: '1101'
quality_controlled: 0
status: public
title: Parallel genetic evolution within and between bacteriophage species of varying
degrees of divergence
type: journal_article
volume: 181
year: '2009'
...
---
_id: '4360'
abstract:
- lang: eng
text: 'Motivated by applications in software verification, we explore automated
reasoning about the non-disjoint combination of theories of infinitely many finite
structures, where the theories share set variables and set operations. We prove
a combination theorem and apply it to show the decidability of the satisfiability
problem for a class of formulas obtained by applying propositional connectives
to formulas belonging to: 1) Boolean Algebra with Presburger Arithmetic (with
quantifiers over sets and integers), 2) weak monadic second-order logic over trees
(with monadic second-order quantifiers), 3) two-variable logic with counting quantifiers
(ranging over elements), 4) the Bernays-Schönfinkel-Ramsey class of first-order
logic with equality (with ∃ * ∀ * quantifier prefix), and 5) the quantifier-free
logic of multisets with cardinality constraints.'
alternative_title:
- LNCS
article_processing_charge: No
author:
- first_name: Thomas
full_name: Wies, Thomas
id: 447BFB88-F248-11E8-B48F-1D18A9856A87
last_name: Wies
- first_name: Ruzica
full_name: Piskac, Ruzica
last_name: Piskac
- first_name: Viktor
full_name: Kuncak, Viktor
last_name: Kuncak
citation:
ama: 'Wies T, Piskac R, Kuncak V. Combining theories with shared set operations.
In: 7th International Symposium on Frontiers of Combining Systems. Vol
5749. Springer; 2009:366-382. doi:10.1007/978-3-642-04222-5_23'
apa: 'Wies, T., Piskac, R., & Kuncak, V. (2009). Combining theories with shared
set operations. In 7th International Symposium on Frontiers of Combining Systems
(Vol. 5749, pp. 366–382). Trento, Italy: Springer. https://doi.org/10.1007/978-3-642-04222-5_23'
chicago: Wies, Thomas, Ruzica Piskac, and Viktor Kuncak. “Combining Theories with
Shared Set Operations.” In 7th International Symposium on Frontiers of Combining
Systems, 5749:366–82. Springer, 2009. https://doi.org/10.1007/978-3-642-04222-5_23.
ieee: T. Wies, R. Piskac, and V. Kuncak, “Combining theories with shared set operations,”
in 7th International Symposium on Frontiers of Combining Systems, Trento,
Italy, 2009, vol. 5749, pp. 366–382.
ista: 'Wies T, Piskac R, Kuncak V. 2009. Combining theories with shared set operations.
7th International Symposium on Frontiers of Combining Systems. FroCoS: Frontiers
of Combining Systems, LNCS, vol. 5749, 366–382.'
mla: Wies, Thomas, et al. “Combining Theories with Shared Set Operations.” 7th
International Symposium on Frontiers of Combining Systems, vol. 5749, Springer,
2009, pp. 366–82, doi:10.1007/978-3-642-04222-5_23.
short: T. Wies, R. Piskac, V. Kuncak, in:, 7th International Symposium on Frontiers
of Combining Systems, Springer, 2009, pp. 366–382.
conference:
end_date: 2009-09-18
location: Trento, Italy
name: 'FroCoS: Frontiers of Combining Systems'
start_date: 2009-09-16
date_created: 2018-12-11T12:08:27Z
date_published: 2009-01-01T00:00:00Z
date_updated: 2025-07-02T06:21:09Z
day: '01'
doi: 10.1007/978-3-642-04222-5_23
extern: '1'
intvolume: ' 5749'
language:
- iso: eng
month: '01'
oa_version: None
page: 366 - 382
publication: 7th International Symposium on Frontiers of Combining Systems
publication_status: published
publisher: Springer
publist_id: '1098'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Combining theories with shared set operations
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5749
year: '2009'
...