Spectral stability of pattern-forming fronts in the complex Ginzburg–Landau equation with a quenching mechanism

We consider pattern-forming fronts in the complex Ginzburg–Landau equation with a traveling spatial heterogeneity which destabilises, or quenches, the trivial ground state while progressing through the domain. We consider the regime where the heterogeneity propagates with speed c just below the linear invasion speed of the pattern-forming front in the associated homogeneous system. In this situation, the front locks to the interface of the heterogeneity leaving a long intermediate state lying near the unstable ground state, possibly allowing for growth of perturbations. This manifests itself in the spectrum of the linearisation about the front through the accumulation of eigenvalues onto the absolute spectrum associated with the unstable ground state. As the quench speed c increases towards the linear invasion speed, the absolute spectrum stabilises with the same rate at which eigenvalues accumulate onto it allowing us to rigorously establish spectral stability of the front in L 2 ( R ) . The presence of unstable absolute spectrum poses a technical challenge as spatial eigenvalues along the intermediate state no longer admit a hyperbolic splitting and standard tools such as exponential dichotomies are unavailable. Instead, we projectivise the linear flow, and use Riemann surface unfolding in combination with a superposition principle to study the evolution of subspaces as solutions to the associated matrix Riccati differential equation on the Grassmannian manifold. Eigenvalues can then be identified as the roots of the meromorphic Riccati–Evans function, and can be located using winding number and parity arguments.

Anomalous invasion dynamics due to dispersal polymorphism and dispersal–reproduction trade-offs

Dispersal polymorphism and mutation play significant roles during biological invasions, potentially leading to evolution and complex behaviour such as accelerating or decelerating invasion fronts. However, life-history theory predicts that reproductive fitness—another key determinant of invasion dynamics—may be lower for more dispersive strains. Here, we use a mathematical model to show that unexpected invasion dynamics emerge from the combination of heritable dispersal polymorphism, dispersal-fitness trade-offs, and mutation between strains. We show that the invasion dynamics are determined by the trade-off relationship between dispersal and population growth rates of the constituent strains. We find that invasion dynamics can be ‘anomalous’ (i.e. faster than any of the strains in isolation), but that the ultimate invasion speed is determined by the traits of, at most, two strains. The model is simple but generic, so we expect the predictions to apply to a wide range of ecological, evolutionary, or epidemiological invasions.

Anomalous invasion dynamics due to dispersal polymorphism and dispersal-reproduction trade-offs

Dispersal polymorphism and mutation play significant roles during biological invasions, potentially leading to evolution and complex behaviour such as accelerating or decelerating invasion fronts. However, life history theory predicts that reproductive fitness — another key determinant of invasion dynamics – may be lower for more dispersive strains. Here, we use a mathematical model to show that unexpected invasion dynamics emerge from the combination of heritable dispersal polymorphism, dispersal-fitness trade-offs, and mutation between strains. We show that the invasion dynamics are determined by the trade-off relationship between dispersal and population growth rates of the constituent strains. We find that invasion dynamics can be “anomalous” (i.e. faster than any of the strains in isolation), but that the ultimate invasion speed is determined by the traits of at most two strains. The model is simple but generic, so we expect the predictions to apply to a wide range of ecological, evolutionary or epidemiological invasions.

ASSESSING THE INVASION SPEED OF TRIATOMINE POPULATIONS, CHAGAS DISEASE VECTORS

Spraying insecticides to control triatomine populations, the vectors of Chagas disease, does not prevent the disease’s reemergence in infested areas. Mathematical models try to explain this reemergence in terms of the factors underlying sylvatic transmission of the parasite Trypanosoma cruzi. The presence of reservoir hosts such as woodrats is essential to the infection’s geographical spread. This study models a vector-host system using integrodifference equations to incorporate dispersal as well as hostvector interactions. These equations capture, simultaneously, the three processes taking place between successive generations: demography, infection and spatial dispersal. Travelling waves, the solutions of the integrodifference equations thus derived, allow one to calculate numerically the invasion speed of the disease. Neubert-Caswell’s theorem can then be applied to calculate the analytical invasion speed.

Matrix metalloproteinase 1 modulates invasive behavior of tracheal branches during entry into Drosophila flight muscles

Tubular networks like the vasculature extend branches throughout animal bodies, but how developing vessels interact with and invade tissues is not well understood. We investigated the underlying mechanisms using the developing tracheal tube network of Drosophila indirect flight muscles (IFMs) as a model. Live imaging revealed that tracheal sprouts invade IFMs directionally with growth-cone-like structures at branch tips. Ramification inside IFMs proceeds until tracheal branches fill the myotube. However, individual tracheal cells occupy largely separate territories, possibly mediated by cell-cell repulsion. Matrix metalloproteinase 1 (MMP1) is required in tracheal cells for normal invasion speed and for the dynamic organization of growth-cone-like branch tips. MMP1 remodels the CollagenIV-containing matrix around branch tips, which show differential matrix composition with low CollagenIV levels, while Laminin is present along tracheal branches. Thus, tracheal-derived MMP1 sustains branch invasion by modulating the dynamic behavior of sprouting branches as well as properties of the surrounding matrix.

Individual Variability in Dispersal and Invasion Speed

We model the growth, dispersal and mutation of two phenotypes of a species using reaction–diffusion equations, focusing on the biologically realistic case of small mutation rates. Having verified that the addition of a small linear mutation term to a Lotka–Volterra system limits it to only two steady states in the case of weak competition, an unstable extinction state and a stable coexistence state, we exploit the fact that the spreading speed of the system is known to be linearly determinate to show that the spreading speed is a nonincreasing function of the mutation rate, so that greater mixing between phenotypes leads to slower propagation. We also find the ratio at which the phenotypes occur at the leading edge in the limit of vanishing mutation.