138 research outputs found
Analytical solution of a neutral model of biodiversity.
International audienceThe unified neutral model of biodiversity proposed by S. Hubbell is solved analytically: The distributions of species abundance in the metacommunity and in a local community are calculated exactly as a function of speciation and migration rates and of the size of the community. In the limit of large population sizes the densities of species of given relative abundance are found to be given by universal functions depending only on two parameters
When it Pays to Rush: Interpreting Morphogen Gradients Prior to Steady-State
During development, morphogen gradients precisely determine the position of
gene expression boundaries despite the inevitable presence of fluctuations.
Recent experiments suggest that some morphogen gradients may be interpreted
prior to reaching steady-state. Theoretical work has predicted that such
systems will be more robust to embryo-to-embryo fluctuations. By analysing two
experimentally motivated models of morphogen gradient formation, we investigate
the positional precision of gene expression boundaries determined by
pre-steady-state morphogen gradients in the presence of embryo-to-embryo
fluctuations, internal biochemical noise and variations in the timing of
morphogen measurement. Morphogens that are direct transcription factors are
found to be particularly sensitive to internal noise when interpreted prior to
steady-state, disadvantaging early measurement, even in the presence of large
embryo-to-embryo fluctuations. Morphogens interpreted by cell-surface receptors
can be measured prior to steady-state without significant decrease in
positional precision provided fluctuations in the timing of measurement are
small. Applying our results to experiment, we predict that Bicoid, a
transcription factor morphogen in Drosophila, is unlikely to be interpreted
prior to reaching steady-state. We also predict that Activin in Xenopus and
Nodal in zebrafish, morphogens interpreted by cell-surface receptors, can be
decoded in pre-steady-state.Comment: 18 pages, 3 figure
Morphogen Transport in Epithelia
We present a general theoretical framework to discuss mechanisms of morphogen
transport and gradient formation in a cell layer. Trafficking events on the
cellular scale lead to transport on larger scales. We discuss in particular the
case of transcytosis where morphogens undergo repeated rounds of
internalization into cells and recycling. Based on a description on the
cellular scale, we derive effective nonlinear transport equations in one and
two dimensions which are valid on larger scales. We derive analytic expressions
for the concentration dependence of the effective diffusion coefficient and the
effective degradation rate. We discuss the effects of a directional bias on
morphogen transport and those of the coupling of the morphogen and receptor
kinetics. Furthermore, we discuss general properties of cellular transport
processes such as the robustness of gradients and relate our results to recent
experiments on the morphogen Decapentaplegic (Dpp) that acts in the fruit fly
Drosophila
Embryonic Pattern Scaling Achieved by Oppositely Directed Morphogen Gradients
Morphogens are proteins, often produced in a localised region, whose
concentrations spatially demarcate regions of differing gene expression in
developing embryos. The boundaries of expression must be set accurately and in
proportion to the size of the one-dimensional developing field; this cannot be
accomplished by a single gradient. Here, we show how a pair of morphogens
produced at opposite ends of a developing field can solve the pattern-scaling
problem. In the most promising scenario, the morphogens effectively interact
according to the annihilation reaction and the switch occurs
according to the absolute concentration of or . In this case embryonic
markers across the entire developing field scale approximately with system
size; this cannot be achieved with a pair of non-interacting gradients that
combinatorially regulate downstream genes. This scaling occurs in a window of
developing-field sizes centred at a few times the morphogen decay length.Comment: 24 pages; 11 figures; uses iopar
Finding the center reliably: robust patterns of developmental gene expression
We investigate a mechanism for the robust identification of the center of a
developing biological system. We assume the existence of two morphogen
gradients, an activator emanating from the anterior, and a co-repressor from
the posterior. The co-repressor inhibits the action of the activator in
switching on target genes. We apply this system to Drosophila embryos, where we
predict the existence of a hitherto undetected posterior co-repressor. Using
mathematical modelling, we show that a symmetric activator-co-repressor model
can quantitatively explain the precise mid-embryo expression boundary of the
hunchback gene, and the scaling of this pattern with embryo size.Comment: 4 pages, 3 figure
Phase transitions and correlations in the bosonic pair contact process with diffusion: Exact results
The variance of the local density of the pair contact process with diffusion
(PCPD) is investigated in a bosonic description. At the critical point of the
absorbing phase transition (where the average particle number remains constant)
it is shown that for lattice dimension d>2 the variance exhibits a phase
transition: For high enough diffusion constants, it asymptotically approaches a
finite value, while for low diffusion constants the variance diverges
exponentially in time. This behavior appears also in the density correlation
function, implying that the correlation time is negative. Yet one has dynamical
scaling with a dynamical exponent calculated to be z=2.Comment: 20 pages, 5 figure
Equilibrium winding angle of a polymer around a bar
The winding angle probability distribution of a planar self-avoiding walk has
been known exactly since a long time: it has a gaussian shape with a variance
growing as . For the three-dimensional case of a walk
winding around a bar, the same scaling is suggested, based on a first-order
epsilon-expansion. We tested this three-dimensional case by means of Monte
Carlo simulations up to length and using exact enumeration
data for sizes . We find that the variance of the winding angle scales
as , with . The ratio is incompatible with the gaussian value
, but consistent with the observation that the tail of the
probability distribution function is found to decrease slower than
a gaussian function. These findings are at odds with the existing first-order
-expansion results.Comment: 18 pages, 12 figures, 1 tabl
A mechanism for morphogen-controlled domain growth
Many developmental systems are organised via the action of graded distributions of morphogens. In the Drosophila wing disc, for example, recent experimental evidence has shown that graded expression of the morphogen Dpp controls cell proliferation and hence disc growth. Our goal is to explore a simple model for regulation of wing growth via the Dpp gradient: we use a system of reaction-diffusion equations to model the dynamics of Dpp and its receptor Tkv, with advection arising as a result of the flow generated by cell proliferation. We analyse the model both numerically and analytically, showing that uniform domain growth across the disc produces an exponentially growing wing disc
Analysis of a spatial Lotka-Volterra model with a finite range predator-prey interaction
We perform an analysis of a recent spatial version of the classical
Lotka-Volterra model, where a finite scale controls individuals' interaction.
We study the behavior of the predator-prey dynamics in physical spaces higher
than one, showing how spatial patterns can emerge for some values of the
interaction range and of the diffusion parameter.Comment: 7 pages, 7 figure
The Evolution of Robust Development and Homeostasis in Artificial Organisms
During embryogenesis, multicellular animals are shaped via cell proliferation, cell rearrangement, and apoptosis. At the end of development, tissue architecture is then maintained through balanced rates of cell proliferation and loss. Here, we take an in silico approach to look for generic systems features of morphogenesis in multicellular animals that arise as a consequence of the evolution of development. Using artificial evolution, we evolved cellular automata-based digital organisms that have distinct embryonic and homeostatic phases of development. Although these evolved organisms use a variety of strategies to maintain their form over time, organisms of different types were all found to rapidly recover from environmental damage in the form of wounds. This regenerative response was most robust in an organism with a stratified tissue-like architecture. An evolutionary analysis revealed that evolution itself contributed to the ability of this organism to maintain its form in the face of genetic and environmental perturbation, confirming the results of previous studies. In addition, the exceptional robustness of this organism to surface injury was found to result from an upward flux of cells, driven in part by cell divisions with a stable niche at the tissue base. Given the general nature of the model, our results lead us to suggest that many of the robust systems properties observed in real organisms, including scar-free wound-healing in well-protected embryos and the layered tissue architecture of regenerating epithelial tissues, may be by-products of the evolution of morphogenesis, rather than the direct result of selection
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