@article{4155, abstract = {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.}, author = {Puech, Pierre and Taubenberger, Anna and Ulrich, Florian and Krieg, Michael and Mueller, Daniel and Heisenberg, Carl-Philipp J}, journal = {Journal of Cell Science}, number = {18}, pages = {4199 -- 4206}, publisher = {Company of Biologists}, title = {{Measuring cell adhesion forces of primary gastrulating cells from zebrafish using atomic force microscopy}}, doi = {10.1242/​jcs.02547}, volume = {118}, year = {2005}, } @article{4171, abstract = {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.}, author = {Montero, Juan and Carvalho, Lara and Wilsch Bräuninger, Michaela and Kilian, Beate and Mustafa, Chigdem and Heisenberg, Carl-Philipp J}, journal = {Development}, number = {6}, pages = {1187 -- 1198}, publisher = {Company of Biologists}, title = {{Shield formation at the onset of zebrafish gastrulation}}, doi = {10.1242/dev.01667}, volume = {132}, year = {2005}, } @article{4249, abstract = {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 = {Jitka Polechova and Nicholas Barton}, journal = {Evolution; International Journal of Organic Evolution}, number = {6}, pages = {1194 -- 1210}, publisher = {Wiley-Blackwell}, title = {{Speciation through competition: A critical review}}, doi = {10.1111/j.0014-3820.2005.tb01771.x}, volume = {59}, year = {2005}, } @article{4251, abstract = {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 = {Nicholas Barton and Otto, Sarah P}, journal = {Genetics}, number = {4}, pages = {2353 -- 2370}, publisher = {Genetics Society of America}, title = {{Evolution of recombination due to random drift}}, doi = {10.1534/genetics.104.032821}, volume = {169}, year = {2005}, } @article{4252, abstract = {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 = {Johnson, Toby and Nicholas Barton}, journal = {Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences}, number = {1459}, pages = {1411 -- 1425}, publisher = {Royal Society, The}, title = {{Theoretical models of selection and mutationon quantitative traits}}, doi = {10.1098/rstb.2005.1667}, volume = {360}, year = {2005}, }