Computational universality of fungal sandpile automata

Hyphae within the mycelia of the ascomycetous fungi are compartmentalised by septa. Each septum has a pore that allows for inter-compartmental and inter-hyphal streaming of cytosol and even organelles. The compartments, however, have special organelles, Woronin bodies, that can plug the pores. When the pores are blocked, no flow of cytoplasm takes place. Inspired by the controllable compartmentalisation within the mycelium of the ascomycetous fungi we designed two-dimensional fungal automata. A fungal automaton is a cellular automaton where communication between neighbouring cells can be blocked on demand. We demonstrate computational universality of the fungal automata by implementing sandpile cellular automata circuits there. We reduce the Monotone Circuit Value Problem to the Fungal Automaton Prediction Problem. We construct families of wires, cross-overs and gates to prove that the fungal automata are P-complete

Fungal Automata

We study a cellular automaton (CA) model of information dynamics on a single hypha of a fungal mycelium. Such a filament is divided in compartments (here also called cells) by septa. These septa are invaginations of the cell wall and their pores allow for flow of cytoplasm between compartments and hyphae. The septal pores of the fungal phylum of the Ascomycota can be closed by organelles called Woronin bodies. Septal closure is increased when the septa become older and when exposed to stress conditions. Thus, Woronin bodies act as informational flow valves. The one dimensional fungal automata is a binary state ternary neighbourhood CA, where every compartment follows one of the elementary cellular automata (ECA) rules if its pores are open and either remains in state `0' (first species of fungal automata) or its previous state (second species of fungal automata) if its pores are closed. The Woronin bodies closing the pores are also governed by ECA rules. We analyse a structure of the composition space of cell-state transition and pore-state transitions rules, complexity of fungal automata with just few Woronin bodies, and exemplify several important local events in the automaton dynamics

Exploring the Dynamics of Fungal Cellular Automata

Cells in a fungal hyphae are separated by internal walls (septa). The septa have tiny pores that allow cytoplasm flowing between cells. Cells can close their septa blocking the flow if they are injured, preventing fluid loss from the rest of filament. This action is achieved by special organelles called Woronin bodies. Using the controllable pores as an inspiration we advance one and two-dimensional cellular automata into Elementary fungal cellular automata (EFCA) and Majority fungal automata (MFA) by adding a concept of Woronin bodies to the cell state transition rules. EFCA is a cellular automaton where the communications between neighboring cells can be blocked by the activation of the Woronin bodies (Wb), allowing or blocking the flow of information (represented by a cytoplasm and chemical elements it carries) between them. We explore a novel version of the fungal automata where the evolution of the system is only affected by the activation of the Wb. We explore two case studies: the Elementary Fungal Cellular Automata (EFCA), which is a direct application of this variant for elementary cellular automata rules, and the Majority Fungal Automata (MFA), which correspond to an application of the Wb to two dimensional automaton with majority rule with Von Neumann neighborhood. By studying the EFCA model, we analyze how the 256 elementary cellular automata rules are affected by the activation of Wb in different modes, increasing the complexity on applied rule in some cases. Also we explore how a consensus over MFA is affected when the continuous flow of information is interrupted due to the activation of Woronin bodies.Comment: 31 pages, 30 figure

Network Automata: Coupling structure and function in real-world networks

We introduce Network Automata, a framework which couples the topological evolution of a network to its structure. It is useful for dealing with networks in which the topology evolves according to some specified microscopic rules and, simultaneously, there is a dynamic process taking place on the network that both depends on its structure but is also capable of modifying it. It is a generic framework for modeling systems in which network structure, dynamics, and function are interrelated. At the practical level, this framework allows for easy implementation of the microscopic rules involved in such systems. To demonstrate the approach, we develop a class of simple biologically inspired models of fungal growth.Comment: 7 pages, 5 figures, 1 tables. Revised content - surplus text and figures remove

A new paradigm for SpeckNets:inspiration from fungal colonies

In this position paper, we propose the development of a new biologically inspired paradigm based on fungal colonies, for the application to pervasive adaptive systems. Fungal colonies have a number of properties that make them an excellent candidate for inspiration for engineered systems. Here we propose the application of such inspiration to a speckled computing platform. We argue that properties from fungal colonies map well to properties and requirements for controlling SpeckNets and suggest that an existing mathematical model of a fungal colony can developed into a new computational paradigm

Mathematical modelling of angiogenesis and vascular adaptation

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Applications of percolation theory to fungal spread with synergy

There is increasing interest in the use of the percolation paradigm to analyze and predict the progress of disease spreading in spatially-structured populations of animals and plants. The wider utility of the approach has been limited, however, by several restrictive assumptions, foremost of which is a strict requirement for simple nearest-neighbour transmission, in which the disease history of an individual is in uenced only by that of its neighbours. In a recent paper the percolation paradigm has been generalised to incorporate synergistic interactions in host infectivity and susceptibility and the impact of these interactions on the invasive dynamics of an epidemic has been demonstrated. In the current paper we elicit evidence that such synergistic interactions may underlie transmission dynamics in real-world systems by rst formulating a model for the spread of a ubiquitous parasitic and saprotrophic fungus through replicated populations of nutrient sites and subsequently tting and testing the model using data from experimental microcosms. Using Bayesian computational methods for model tting, we demonstrate that synergistic interactions are necessary to explain the dynamics observed in the replicate experiments. The broader implications of this work in identifying disease control strategies that de ect epidemics from invasive to non-invasive regimes are discussed