The effect of landscape fragmentation on Turing-pattern formation

<abstract><p>Diffusion-driven instability and Turing pattern formation are a well-known mechanism by which the local interaction of species, combined with random spatial movement, can generate stable patterns of population densities in the absence of spatial heterogeneity of the underlying medium. Some examples of such patterns exist in ecological interactions between predator and prey, but the conditions required for these patterns are not easily satisfied in ecological systems. At the same time, most ecological systems exist in heterogeneous landscapes, and landscape heterogeneity can affect species interactions and individual movement behavior. In this work, we explore whether and how landscape heterogeneity might facilitate Turing pattern formation in predator–prey interactions. We formulate reaction-diffusion equations for two interacting species on an infinite patchy landscape, consisting of two types of periodically alternating patches. Population dynamics and movement behavior differ between patch types, and individuals may have a preference for one of the two habitat types. We apply homogenization theory to derive an appropriately averaged model, to which we apply stability analysis for Turing patterns. We then study three scenarios in detail and find mechanisms by which diffusion-driven instabilities may arise even if the local interaction and movement rates do not indicate it.</p></abstract>

Spatio-Temporal Patterns of Predator–Prey Model with Allee Effect and Constant Stocking Rate for Predator

A diffusive predator–prey model with Allee effect and constant stocking rate for predator is investigated and it is shown that Allee effect is the decisive factor driving the formation of Turing pattern. Furthermore, it is observed that Turing pattern appears only when the diffusion rate of the prey is faster than that of the predator, which is just opposite to the condition of Turing pattern in the classical predator–prey system. Some sufficient conditions are obtained to ensure the asymptotical stability of a spatially homogeneous steady-state solution. The existence and nonexistence of positive nonconstant steady-state solutions are investigated to understand the mechanisms of generating spatiotemporal patterns. Furthermore, Hopf and steady-state bifurcations are analyzed in detail by using Lyapunov–Schmidt reduction.

Delay-Induced Self-Organization Dynamics in a Prey-Predator Network with Diffusion

Time delays can induce the loss of stability and degradation of performance. In this paper, the pattern dynamics of a prey-predator network with diffusion and delay are investigated, where the inhomogeneous distribution of species in space can be viewed as a random network, and delay can affect the stability of the network system. Our results show that time delay can induce the emergence of Hopf and Turing bifurcations, which are independent of the network, and the conditions of bifurcation are derived by linear stability analysis. Moreover, we find that the Turing pattern can be related to the network connection probability. The Turing instability region involving delay and network connection probability is obtained. Finally, the numerical simulation verifies our results.

Studies of Turing pattern formation in zebrafish skin

Skin patterns are the first example of the existence of Turing patterns in living organisms. Extensive research on zebrafish, a model organism with stripes on its skin, has revealed the principles of pattern formation at the molecular and cellular levels. Surprisingly, although the networks of cell–cell interactions have been observed to satisfy the ‘short-range activation and long-range inhibition’ prerequisites for Turing pattern formation, numerous individual reactions were not envisioned based on the classical reaction–diffusion model. For example, in real skin, it is not an alteration in concentrations of chemicals, but autonomous migration and proliferation of pigment cells that establish patterns, and cell–cell interactions are mediated via direct contact through cell protrusions. Therefore, the classical reaction–diffusion mechanism cannot be used as it is for modelling skin pattern formation. Various studies are underway to adapt mathematical models to the experimental findings on research into skin patterns, and the purpose of this review is to organize and present them. These novel theoretical methods could be applied to autonomous pattern formation phenomena other than skin patterns. This article is part of the theme issue ‘Recent progress and open frontiers in Turing's theory of morphogenesis’.

Turing pattern design principles and their robustness

Turing patterns have morphed from mathematical curiosities into highly desirable targets for synthetic biology. For a long time, their biological significance was sometimes disputed but there is now ample evidence for their involvement in processes ranging from skin pigmentation to digit and limb formation. While their role in developmental biology is now firmly established, their synthetic design has so far proved challenging. Here, we review recent large-scale mathematical analyses that have attempted to narrow down potential design principles. We consider different aspects of robustness of these models and outline why this perspective will be helpful in the search for synthetic Turing-patterning systems. We conclude by considering robustness in the context of developmental modelling more generally. This article is part of the theme issue ‘Recent progress and open frontiers in Turing’s theory of morphogenesis’.

A model of octopus epidermis pattern mimicry mechanisms using inverse operation of the Turing reaction model

Many cephalopods such as octopi and squid can purposefully and rapidly change their skin color. Furthermore, it is widely known that some octopi have the ability to rapidly change the color and unevenness of their skin to mimic their surroundings. However, there has been little research published on the mechanisms by which an octopus recognizes its surrounding landscape and changes its skin pattern. We are unaware of any hypothetical model that explains this mimicry mechanism to date. In this study, the mechanism of octopus skin pattern change was assumed to be based on the Turing pattern model. Here, pattern formation using the Turing model was realized using an equivalent filter calculation model and a cellular automaton instead of directly solving the differential equations. It was shown that this model can create various patterns using two feature parameters. Furthermore, for visual recognition where two features are extracted from the Turing pattern image, a method that requires minimal calculation using the characteristics of the cellular Turing pattern model is proposed. These two calculations can be expressed in the same mathematical frame based on the cellular automaton model using a convolution filter. As a result, a model that is capable of extracting features from patterns and reconstructing those patterns rapidly can be created. This represents a basic model of the mimicry mechanism of octopi. Further, this study demonstrates the potential for creating a model with minimal learning calculation for application to machine learning.

Correspondences between parameters in a reaction-diffusion model and connexin functions during zebrafish stripe formation

Different diffusivities among interacting substances actualize the potential instability of a system. When these elicited instabilities manifested as forms of spatial periodicity, they are called Turing patterns. Simulations using general reaction-diffusion (RD) models have demonstrated that pigment patterns on the body trunk of growing fish follow a Turing pattern. Laser ablation experiments performed on zebrafish revealed apparent interactions among pigment cells, which allowed for a three-components RD model to be derived. However, the underlying molecular mechanisms responsible for Turing pattern formation in this system had been remained unknown. A zebrafish mutant with a spotted pattern was found to have a defect in Connexin41.8 (Cx41.8) which, together with Cx39.4, exists in pigment cells and controls pattern formations. Here, molecular-level evidence derived from connexin analyses was linked to the interactions among pigment cells described in previous RD modeling. Channels on pigment cells were generalized as “gates,” and the effects of respective gates were deduced. The model used partial differential equations (PDEs) to enable numerical and mathematical analyses of characteristics observed in the experiments. Furthermore, the improved PDE model included nonlinear reaction terms, enabled the consideration of the behavior of components.