---
_id: '4155'
abstract:
- lang: eng
text: During vertebrate gastrulation, progenitor cells of different germ layers
acquire specific adhesive properties that contribute to germ layer formation and
separation. Wnt signals have been suggested to function in this process by modulating
the different levels of adhesion between the germ layers, however, direct evidence
for this is still lacking. Here we show that Wnt11, a key signal regulating gastrulation
movements, is needed for the adhesion of zebrafish mesendodermal progenitor cells
to fibronectin, an abundant extracellular matrix component during gastrulation.
To measure this effect, we developed an assay to quantify the adhesion of single
zebrafish primary mesendodermal progenitors using atomic-force microscopy (AFM).
We observed significant differences in detachment force and work between cultured
mesendodermal progenitors from wild-type embryos and from slb/wit11 mutant embryos,
which carry a loss-of-function mutation in the wnt11 gene, when tested on fibronectin-coated
substrates. These differences were probably due to reduced adhesion to the fibronectin
substrate as neither the overall cell morphology nor the cell elasticity grossly
differed between wild-type and mutant cells. Furthermore, in the presence of inhibitors
of fibronectin-integrin binding, such as RGD peptides, the adhesion force and
work were strongly decreased, indicating that integrins are involved in the binding
of mesendodermal progenitors in our assay. These findings demonstrate that AFM
can be used to quantitatively determine the substrate-adhesion of cultured primary
gastrulating cells and provide insight into the role of Wnt11 signalling in modulating
cell adhesion at the single cell scale.
article_processing_charge: No
author:
- first_name: Pierre
full_name: Puech, Pierre
last_name: Puech
- first_name: Anna
full_name: Taubenberger, Anna
last_name: Taubenberger
- first_name: Florian
full_name: Ulrich, Florian
last_name: Ulrich
- first_name: Michael
full_name: Krieg, Michael
last_name: Krieg
- first_name: Daniel
full_name: Mueller, Daniel
last_name: Mueller
- 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: Puech P, Taubenberger A, Ulrich F, Krieg M, Mueller D, Heisenberg C-PJ. Measuring
cell adhesion forces of primary gastrulating cells from zebrafish using atomic
force microscopy. Journal of Cell Science. 2005;118(18):4199-4206. doi:10.1242/jcs.02547
apa: Puech, P., Taubenberger, A., Ulrich, F., Krieg, M., Mueller, D., & Heisenberg,
C.-P. J. (2005). Measuring cell adhesion forces of primary gastrulating cells
from zebrafish using atomic force microscopy. Journal of Cell Science.
Company of Biologists. https://doi.org/10.1242/jcs.02547
chicago: Puech, Pierre, Anna Taubenberger, Florian Ulrich, Michael Krieg, Daniel
Mueller, and Carl-Philipp J Heisenberg. “Measuring Cell Adhesion Forces of Primary
Gastrulating Cells from Zebrafish Using Atomic Force Microscopy.” Journal of
Cell Science. Company of Biologists, 2005. https://doi.org/10.1242/jcs.02547.
ieee: P. Puech, A. Taubenberger, F. Ulrich, M. Krieg, D. Mueller, and C.-P. J. Heisenberg,
“Measuring cell adhesion forces of primary gastrulating cells from zebrafish using
atomic force microscopy,” Journal of Cell Science, vol. 118, no. 18. Company
of Biologists, pp. 4199–4206, 2005.
ista: Puech P, Taubenberger A, Ulrich F, Krieg M, Mueller D, Heisenberg C-PJ. 2005.
Measuring cell adhesion forces of primary gastrulating cells from zebrafish using
atomic force microscopy. Journal of Cell Science. 118(18), 4199–4206.
mla: Puech, Pierre, et al. “Measuring Cell Adhesion Forces of Primary Gastrulating
Cells from Zebrafish Using Atomic Force Microscopy.” Journal of Cell Science,
vol. 118, no. 18, Company of Biologists, 2005, pp. 4199–206, doi:10.1242/jcs.02547.
short: P. Puech, A. Taubenberger, F. Ulrich, M. Krieg, D. Mueller, C.-P.J. Heisenberg,
Journal of Cell Science 118 (2005) 4199–4206.
date_created: 2018-12-11T12:07:16Z
date_published: 2005-01-01T00:00:00Z
date_updated: 2021-01-12T07:54:54Z
day: '01'
doi: 10.1242/jcs.02547
extern: '1'
intvolume: ' 118'
issue: '18'
language:
- iso: eng
month: '01'
oa_version: None
page: 4199 - 4206
publication: Journal of Cell Science
publication_status: published
publisher: Company of Biologists
publist_id: '1964'
status: public
title: Measuring cell adhesion forces of primary gastrulating cells from zebrafish
using atomic force microscopy
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 118
year: '2005'
...
---
_id: '4171'
abstract:
- lang: eng
text: During vertebrate gastrulation, the three germ layers, ectoderm, mesoderm
and endoderm are formed, and the resulting progenitor cells are brought into the
positions from which they will later contribute more complex tissues and organs.
A core element in this process is the internalization of mesodermal and endodermal
progenitors at the onset of gastrulation. Although many of the molecules that
induce mesendoderm have been identified, much less is known about the cellular
mechanisms underlying mesendodermal cell internalization and germ layer formation.
Here we show that at the onset of zebrafish gastrulation, mesendodermal progenitors
in dorsal/axial regions of the germ ring internalize by single cell delamination.
Once internalized, mesendodermal progenitors upregulate ECadherin (Cadherin 1)
expression, become increasingly motile and eventually migrate along the overlying
epiblast (ectodermal) cell layer towards the animal pole of the gastrula. When
E-Cadherin function is compromised, mesendodermal progenitors still internalize,
but, with gastrulation proceeding, fail to elongate and efficiently migrate along
the epiblast, whereas epiblast cells themselves exhibit reduced radial cell intercalation
movements. This indicates that cadherin-mediated cell-cell adhesion is needed
within the forming shield for both epiblast cell intercalation, and mesendodermal
progenitor cell elongation and migration during zebrafish gastrulation. Our data
provide insight into the cellular mechanisms underlying mesendodermal progenitor
cell internalization and subsequent migration during zebrafish gastrulation, and
the role of cadherin-mediated cell-cell adhesion in these processes.
article_processing_charge: No
author:
- first_name: Juan
full_name: Montero, Juan
last_name: Montero
- first_name: Lara
full_name: Carvalho, Lara
last_name: Carvalho
- first_name: Michaela
full_name: Wilsch Bräuninger, Michaela
last_name: Wilsch Bräuninger
- first_name: Beate
full_name: Kilian, Beate
last_name: Kilian
- first_name: Chigdem
full_name: Mustafa, Chigdem
last_name: Mustafa
- 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: Montero J, Carvalho L, Wilsch Bräuninger M, Kilian B, Mustafa C, Heisenberg
C-PJ. Shield formation at the onset of zebrafish gastrulation. Development.
2005;132(6):1187-1198. doi:10.1242/dev.01667
apa: Montero, J., Carvalho, L., Wilsch Bräuninger, M., Kilian, B., Mustafa, C.,
& Heisenberg, C.-P. J. (2005). Shield formation at the onset of zebrafish
gastrulation. Development. Company of Biologists. https://doi.org/10.1242/dev.01667
chicago: Montero, Juan, Lara Carvalho, Michaela Wilsch Bräuninger, Beate Kilian,
Chigdem Mustafa, and Carl-Philipp J Heisenberg. “Shield Formation at the Onset
of Zebrafish Gastrulation.” Development. Company of Biologists, 2005. https://doi.org/10.1242/dev.01667.
ieee: J. Montero, L. Carvalho, M. Wilsch Bräuninger, B. Kilian, C. Mustafa, and
C.-P. J. Heisenberg, “Shield formation at the onset of zebrafish gastrulation,”
Development, vol. 132, no. 6. Company of Biologists, pp. 1187–1198, 2005.
ista: Montero J, Carvalho L, Wilsch Bräuninger M, Kilian B, Mustafa C, Heisenberg
C-PJ. 2005. Shield formation at the onset of zebrafish gastrulation. Development.
132(6), 1187–1198.
mla: Montero, Juan, et al. “Shield Formation at the Onset of Zebrafish Gastrulation.”
Development, vol. 132, no. 6, Company of Biologists, 2005, pp. 1187–98,
doi:10.1242/dev.01667.
short: J. Montero, L. Carvalho, M. Wilsch Bräuninger, B. Kilian, C. Mustafa, C.-P.J.
Heisenberg, Development 132 (2005) 1187–1198.
date_created: 2018-12-11T12:07:22Z
date_published: 2005-03-15T00:00:00Z
date_updated: 2021-01-12T07:55:02Z
day: '15'
doi: 10.1242/dev.01667
extern: '1'
intvolume: ' 132'
issue: '6'
language:
- iso: eng
month: '03'
oa_version: None
page: 1187 - 1198
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '1947'
status: public
title: Shield formation at the onset of zebrafish gastrulation
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 132
year: '2005'
...
---
_id: '4249'
abstract:
- lang: eng
text: We examined causes of speciation in asexual populations in both sympatry and
parapatry, providing an alternative explanation for the speciation patterns reported
by Dieckmann and Doebeli (1999) and Doebeli and Dieckmann (2003). Both in sympatry
and parapatry, they find that speciation occurs relatively easily. We reveal that
in the sympatric clonal model, the equilibrium distribution is continuous and
the disruptive selection driving evolution of discrete clusters is only transient.
Hence, if discrete phenotypes are to remain stable in the sympatric sexual model,
there should be some source of nontransient disruptive selection that will drive
evolution of assortment. We analyze sexually reproducing populations using the
Bulmer’s infinitesimal model and show that cost-free assortment alone leads to
speciation and disruptive selection only arises when the optimal distribution
cannot be matched—in this example, because the phenotypic range is limited. In
addition, Doebeli and Dieckmann’s analyses assumed a high genetic variance and
a high mutation rate. Thus, these theoretical models do not support the conclusion
that sympatric speciation is a likely outcome of competition for resources. In
their parapatric model (Doebeli and Dieckmann 2003), clustering into distinct
phenotypes is driven by edge effects, rather than by frequency-dependent competition.
author:
- first_name: Jitka
full_name: Jitka Polechova
id: 3BBFB084-F248-11E8-B48F-1D18A9856A87
last_name: Polechova
orcid: 0000-0003-0951-3112
- first_name: Nicholas H
full_name: Nicholas Barton
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
citation:
ama: 'Polechova J, Barton NH. Speciation through competition: A critical review.
Evolution; International Journal of Organic Evolution. 2005;59(6):1194-1210.
doi:10.1111/j.0014-3820.2005.tb01771.x'
apa: 'Polechova, J., & Barton, N. H. (2005). Speciation through competition:
A critical review. Evolution; International Journal of Organic Evolution.
Wiley-Blackwell. https://doi.org/10.1111/j.0014-3820.2005.tb01771.x'
chicago: 'Polechova, Jitka, and Nicholas H Barton. “Speciation through Competition:
A Critical Review.” Evolution; International Journal of Organic Evolution.
Wiley-Blackwell, 2005. https://doi.org/10.1111/j.0014-3820.2005.tb01771.x.'
ieee: 'J. Polechova and N. H. Barton, “Speciation through competition: A critical
review,” Evolution; International Journal of Organic Evolution, vol. 59,
no. 6. Wiley-Blackwell, pp. 1194–1210, 2005.'
ista: 'Polechova J, Barton NH. 2005. Speciation through competition: A critical
review. Evolution; International Journal of Organic Evolution. 59(6), 1194–1210.'
mla: 'Polechova, Jitka, and Nicholas H. Barton. “Speciation through Competition:
A Critical Review.” Evolution; International Journal of Organic Evolution,
vol. 59, no. 6, Wiley-Blackwell, 2005, pp. 1194–210, doi:10.1111/j.0014-3820.2005.tb01771.x.'
short: J. Polechova, N.H. Barton, Evolution; International Journal of Organic Evolution
59 (2005) 1194–1210.
date_created: 2018-12-11T12:07:50Z
date_published: 2005-06-01T00:00:00Z
date_updated: 2021-01-12T07:55:36Z
day: '01'
doi: 10.1111/j.0014-3820.2005.tb01771.x
extern: 1
intvolume: ' 59'
issue: '6'
month: '06'
page: 1194 - 1210
publication: Evolution; International Journal of Organic Evolution
publication_status: published
publisher: Wiley-Blackwell
publist_id: '1849'
quality_controlled: 0
status: public
title: 'Speciation through competition: A critical review'
type: journal_article
volume: 59
year: '2005'
...
---
_id: '4251'
abstract:
- lang: eng
text: In finite populations subject to selection, genetic drift generates negative
linkage disequilibrium, on average, even if selection acts independently (i.e.
multiplicatively) upon all loci. Negative disequilibrium reduces the variance
in fitness and hence, by FISHER's Fundamental Theorem (1930), slows the rate of
increase in mean fitness. Modifiers that increase recombination eliminate the
negative disequilibria that impede selection and consequently increase in frequency
by 'hitch-hiking'. In addition, recombinant progeny are more fit on average than
non-recombinant progeny when there is negative linkage disequilibrium and loci
interact multiplicatively. For both these reasons, stochastic fluctuations in
linkage disequilibrium in finite populations favor the evolution of increased
rates of recombination, even in the absence of epistatic interactions among loci
and even when disequilibrium is initially absent. The method developed within
this paper quantifies the strength of selection on a modifier allele that increases
recombination due to stochastically generated linkage disequilibria. The analysis
indicates that, in a population subject to multiplicative selection, genetic associations
generated by drift do select for increased recombination, a result that is confirmed
by Monte Carlo simulations. Selection for a modifier that increases recombination
is highest when linkage among all loci is tight, when beneficial alleles rise
from low to high frequency, and when the population size is small.
author:
- first_name: Nicholas H
full_name: Nicholas Barton
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
- first_name: Sarah
full_name: Otto, Sarah P
last_name: Otto
citation:
ama: Barton NH, Otto S. Evolution of recombination due to random drift. Genetics.
2005;169(4):2353-2370. doi:10.1534/genetics.104.032821
apa: Barton, N. H., & Otto, S. (2005). Evolution of recombination due to random
drift. Genetics. Genetics Society of America. https://doi.org/10.1534/genetics.104.032821
chicago: Barton, Nicholas H, and Sarah Otto. “Evolution of Recombination Due to
Random Drift.” Genetics. Genetics Society of America, 2005. https://doi.org/10.1534/genetics.104.032821.
ieee: N. H. Barton and S. Otto, “Evolution of recombination due to random drift,”
Genetics, vol. 169, no. 4. Genetics Society of America, pp. 2353–2370,
2005.
ista: Barton NH, Otto S. 2005. Evolution of recombination due to random drift. Genetics.
169(4), 2353–2370.
mla: Barton, Nicholas H., and Sarah Otto. “Evolution of Recombination Due to Random
Drift.” Genetics, vol. 169, no. 4, Genetics Society of America, 2005, pp.
2353–70, doi:10.1534/genetics.104.032821.
short: N.H. Barton, S. Otto, Genetics 169 (2005) 2353–2370.
date_created: 2018-12-11T12:07:51Z
date_published: 2005-03-01T00:00:00Z
date_updated: 2021-01-12T07:55:37Z
day: '01'
doi: 10.1534/genetics.104.032821
extern: 1
intvolume: ' 169'
issue: '4'
month: '03'
page: 2353 - 2370
publication: Genetics
publication_status: published
publisher: Genetics Society of America
publist_id: '1846'
quality_controlled: 0
status: public
title: Evolution of recombination due to random drift
type: journal_article
volume: 169
year: '2005'
...
---
_id: '4252'
abstract:
- lang: eng
text: Empirical studies of quantitative genetic variation have revealed robust patterns
that are observed both across traits and across species. However, these patterns
have no compelling explanation, and some of the observations even appear to be
mutually incompatible. We review and extend a major class of theoretical models,
‘mutation–selection models’, that have been proposed to explain quantitative genetic
variation. We also briefly review an alternative class of ‘balancing selection
models’. We consider to what extent the models are compatible with the general
observations, and argue that a key issue is understanding and modelling pleiotropy.
We discuss some
author:
- first_name: Toby
full_name: Johnson, Toby
last_name: Johnson
- first_name: Nicholas H
full_name: Nicholas Barton
id: 4880FE40-F248-11E8-B48F-1D18A9856A87
last_name: Barton
orcid: 0000-0002-8548-5240
citation:
ama: Johnson T, Barton NH. Theoretical models of selection and mutationon quantitative
traits. Philosophical Transactions of the Royal Society of London Series B,
Biological Sciences. 2005;360(1459):1411-1425. doi:10.1098/rstb.2005.1667
apa: Johnson, T., & Barton, N. H. (2005). Theoretical models of selection and
mutationon quantitative traits. Philosophical Transactions of the Royal Society
of London. Series B, Biological Sciences. Royal Society, The. https://doi.org/10.1098/rstb.2005.1667
chicago: Johnson, Toby, and Nicholas H Barton. “Theoretical Models of Selection
and Mutationon Quantitative Traits.” Philosophical Transactions of the Royal
Society of London. Series B, Biological Sciences. Royal Society, The, 2005.
https://doi.org/10.1098/rstb.2005.1667.
ieee: T. Johnson and N. H. Barton, “Theoretical models of selection and mutationon
quantitative traits,” Philosophical Transactions of the Royal Society of London.
Series B, Biological Sciences, vol. 360, no. 1459. Royal Society, The, pp.
1411–1425, 2005.
ista: Johnson T, Barton NH. 2005. Theoretical models of selection and mutationon
quantitative traits. Philosophical Transactions of the Royal Society of London.
Series B, Biological Sciences. 360(1459), 1411–1425.
mla: Johnson, Toby, and Nicholas H. Barton. “Theoretical Models of Selection and
Mutationon Quantitative Traits.” Philosophical Transactions of the Royal Society
of London. Series B, Biological Sciences, vol. 360, no. 1459, Royal Society,
The, 2005, pp. 1411–25, doi:10.1098/rstb.2005.1667.
short: T. Johnson, N.H. Barton, Philosophical Transactions of the Royal Society
of London. Series B, Biological Sciences 360 (2005) 1411–1425.
date_created: 2018-12-11T12:07:51Z
date_published: 2005-07-29T00:00:00Z
date_updated: 2021-01-12T07:55:38Z
day: '29'
doi: 10.1098/rstb.2005.1667
extern: 1
intvolume: ' 360'
issue: '1459'
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1569515/
month: '07'
oa: 1
page: 1411 - 1425
publication: Philosophical Transactions of the Royal Society of London. Series B,
Biological Sciences
publication_status: published
publisher: Royal Society, The
publist_id: '1847'
quality_controlled: 0
status: public
title: Theoretical models of selection and mutationon quantitative traits
type: journal_article
volume: 360
year: '2005'
...