Complex ecosystems generally consist of a large number of different species utilizing a large number of different resources. Several of their features cannot be captured by models comprising just a few species and resources. Recently, Tikhonov and Monasson have shown that a high-dimensional version of MacArthur's resource competition model exhibits a phase transition from a 'vulnerable' to a 'shielded' phase in which the species collectively protect themselves against an inhomogeneous resource influx from the outside. Here we point out that this transition is more general and may be traced back to the existence of non-negative solutions to large systems of random linear equations. Employing Farkas' Lemma we map this problem to the properties of a fractional volume in high dimensions which we determine using methods from the statistical mechanics of disordered systems.

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Systems of random linear equations may or may not have solutions with all components being non-negative. The question is, e.g., of relevance when the unknowns are concentrations or population sizes. In the present paper we show that if such systems are large the transition between these two possibilities occurs at a sharp value of the ratio between the number of unknowns and the number of equations. We analytically determine this threshold as a function of the statistical properties of the random parameters and show its agreement with numerical simulations. We also make contact with two special cases that have been studied before: the storage problem of a perceptron and the resource competition model of MacArthur.

We consider self-tolerance and its failure-autoimmunity-in a minimal mathematical model of the idiotypic network. A node in the network represents a clone of B-lymphocytes and its antibodies of the same idiotype which is encoded by a bitstring. The links between nodes represent possible interactions between clones of almost complementary idiotype. A clone survives only if the number of populated neighbored nodes is neither too small nor too large. The dynamics is driven by the influx of lymphocytes with randomly generated idiotype from the bone marrow. Previous work has revealed that the network evolves toward a highly organized modular architecture, characterized by groups of nodes which share statistical properties. The structural properties of the architecture can be described analytically, the statistical properties determined from simulations are confirmed by a modular mean-field theory. To model the presence of self we permanently occupy one or several nodes. These nodes influence their linked neighbors, the autoreactive clones, but are themselves not affected by idiotypic interactions. The architecture is very similar to the case without self, but organized such that the neighbors of self are only weakly occupied, thus providing self-tolerance. This supports the perspective that self-reactive clones, which regularly occur in healthy organisms, are controlled by anti-idiotypic clones. We discuss how perturbations, like an infection with foreign antigen, a change in the influx of new idiotypes, or the random removal of idiotypes, may lead to autoreactivity and devise protocols which cause a reconstitution of the self-tolerant state. The results could be helpful to understand network and probabilistic aspects of autoimmune disorders.

Bacteria live in environments that are continuously fluctuating and changing. Exploiting any predictability of such fluctuations can lead to an increased fitness. On longer timescales, bacteria can ‘learn’ the structure of these fluctuations through evolution. However, on shorter timescales, inferring the statistics of the environment and acting upon this information would need to be accomplished by physiological mechanisms. Here, we use a model of metabolism to show that a simple generalization of a common regulatory motif (end-product inhibition) is sufficient both for learning continuous-valued features of the statistical structure of the environment and for translating this information into predictive behavior; moreover, it accomplishes these tasks near-optimally. We discuss plausible genetic circuits that could instantiate the mechanism we describe, including one similar to the architecture of two-component signaling, and argue that the key ingredients required for such predictive behavior are readily accessible to bacteria.