How biological codes break causal chains to enable autonomy for organisms.

Autonomy, meaning freedom from exogenous control, requires independence of both constitution and cybernetic regulation. Here, the necessity of biological codes to achieve both is explained, assuming that Aristotelian efficient cause is 'formal cause empowered by physical force'. Constitutive independence requires closure to efficient causation (in the Rosen sense); cybernetic independence requires transformation of cause-effect into signal-response relations at the organism boundary; the combination of both kinds of independence enables adaptation and evolution. Codes and cyphers translate information from one form of physical embodiment (domain) to another. Because information can only contribute as formal cause to efficient cause within the domain of its embodiment, translation can extend or restrict the range over which information is effective. Closure to efficient causation requires internalised information to be isolated from the cycle of efficient causes that it informs: e.g. Von Neumann self-replicator requires a (template) source of information that is causally isolated from the physical replication system. Life operationalises this isolation with the genetic code translating from the (isolated) domain of codons to that of protein interactions. Separately, cybernetic freedom is achieved at the cell boundary because transducers, which embody molecular coding, translate exogenous information into a domain where it no longer has the power of efficient cause. Information, not efficient cause, passes through the boundary to serve as stimulus for an internally generated response. Coding further extends freedom by enabling historically accumulated information to be selectively transformed into efficient cause under internal control, leaving it otherwise stored inactive. Code-based translation thus enables selective causal isolation, controlling the flow from cause to effect. Genetic code, cell-signalling codes and, in eukaryotes, the histone code, signal sequence based protein sorting and other code-dependent processes all regulate and separate causal chains. The existence of life can be seen as an expression of the power of molecular codes to selectively isolate and thereby organise causal relations among molecular interactions to form an organism.

Why it hurts: with freedom comes the biological need for pain.

We argue that pain is not needed to protect the body from damage unless the organism is able to make free choices in action selection. Then pain (including its affective and evaluative aspects) provides a necessary prioritising motivation to select actions expected to avoid it, whilst leaving the possibility of alternative actions to serve potentially higher priorities. Thus, on adaptive grounds, only organisms having free choice over action selection should experience pain. Free choice implies actions must be selected following appraisal of their effects, requiring a predictive model generating estimates of action outcomes. These features give organisms anticipatory behavioural autonomy (ABA), for which we propose a plausible system using an internal predictive model, integrated into a system able to produce the qualitative and affective aspects of pain. Our hypothesis can be tested using behavioural experiments designed to elicit trade-off responses to novel experiences for which algorithmic (automaton) responses might be inappropriate. We discuss the empirical evidence for our hypothesis among taxonomic groups, showing how testing for ABA guides thinking on which groups might experience pain. It is likely that all vertebrates do and plausible that some invertebrates do (decapods, cephalopods and at least some insects).

How an information perspective helps overcome the challenge of biology to physics.

Living systems have long been a puzzle to physics, leading some to claim that new laws of physics are needed to explain them. Separating physical reality into the general (laws) and the particular (location of particles in space and time), it is possible to see that the combination of these amounts to efficient causation, whereby forces are constrained by patterns that constitute embodied information which acts as formal cause. Embodied information can only be produced by correlation with existing patterns, but sets of patterns can be arranged to form reflexive relations in which constraints on force are themselves formed by the pattern that results from action of those same constrained forces. This inevitably produces a higher level of pattern which reflexively reinforces itself. From this, multi-level hierarchies and downward causation by information are seen to be patterns of patterns that constrain forces. Such patterns, when causally cyclical, are closed to efficient causation. But to be autonomous, a system must also have its formative information accumulated by repeated cycles of selection until sufficient is obtained to represent the information content of the whole (which is the essential purpose of information oligomers such as DNA). Living systems are the result of that process and therefore cannot exist unless they are both closed to efficient causation and capable of embodying an independent supply of information sufficient to constitute their causal structure. Understanding this is not beyond the scope of standard physics, but it does recognise the far greater importance of information accumulation in living than in non-living systems and, as a corollary, emphasises the dependence of biological systems on the whole history of life, leading up to the present state of any and all organisms.

Model of two competing populations in two habitats with migration: Application to optimal marine protected area size.

The standard model of a single population fragmented into two patches connected by migration, was first introduced in the 1970s by Freedman and Waltman, since generating long-term research interest, though its full analysis for arbitrary values of migration rate has only been completed relatively recently. Here, we present a model of two competing species in a two-patch habitat with migrations between patches. We derive equilibrium solutions of this model for three cases of migration rate resulting in isolated, well-mixed and semi-isolated habitats. We evaluate the full range of effects of habitat, life-history and migration parameters on population sizes. Finally, we add harvesting mortality and define conditions under which introduction of a no-harvesting (protected) area may lead to increased maximum sustainable yield. The results have applications in mixed fishery management and the design of wildlife protection zones, including marine protected areas (MPAs).

An organisational systems-biology view of viruses explains why they are not alive.

Whether or not viruses are alive remains unsettled. Discoveries of giant viruses with translational genes and large genomes have kept the debate active. Here, a fresh approach is introduced, based on the organisational definition of life from within systems biology. It views living as a circular process of self-organisation and self-construction which is 'closed to efficient causation'. How information combines with force to fabricate and organise environmentally obtained materials, given an energy source, is here explained as a physical embodiment of informational constraint. Comparing a general virus replication cycle with Rosen's (M,R)-system shows it to be linear, rather than closed. Some viruses contribute considerable organisational information, but so far none is known to supply all required, nor the material nor energy necessary to complete their replication cycle. As a result, no known virus replication cycle is closed to efficient causation: unlike cellular obligate parasites, viruses do not match the causal structure of an (M,R)-system. Analysis based in identifying a Markov blanket in causal structure proved inconclusive, but using Integrated Information Theory on a Boolean representation, it was possible to show that the causal structure of a virocell is not different from that of the host cell.

Microbial lag phase can be indicative of, or independent from, cellular stress.

Measures of microbial growth, used as indicators of cellular stress, are sometimes quantified at a single time-point. In reality, these measurements are compound representations of length of lag, exponential growth-rate, and other factors. Here, we investigate whether length of lag phase can act as a proxy for stress, using  a number of model systems (Aspergillus penicillioides; Bacillus subtilis; Escherichia coli; Eurotium amstelodami, E. echinulatum, E. halophilicum, and E. repens; Mrakia frigida; Saccharomyces cerevisiae; Xerochrysium xerophilum; Xeromyces bisporus) exposed to mechanistically distinct types of cellular stress including low water activity, other solute-induced stresses, and dehydration-rehydration cycles. Lag phase was neither proportional to germination rate for X. bisporus (FRR3443) in glycerol-supplemented media (r2 = 0.012), nor to exponential growth-rates for other microbes. In some cases, growth-rates varied greatly with stressor concentration even when lag remained constant. By contrast, there were strong correlations for B. subtilis in media supplemented with polyethylene-glycol 6000 or 600 (r2 = 0.925 and 0.961), and for other microbial species. We also  analysed data from independent studies of food-spoilage fungi under glycerol stress (Aspergillus aculeatinus and A. sclerotiicarbonarius); mesophilic/psychrotolerant bacteria under diverse, solute-induced stresses (Brochothrix thermosphacta, Enterococcus faecalis, Pseudomonas fluorescens, Salmonella typhimurium, Staphylococcus aureus); and fungal enzymes under acid-stress (Terfezia claveryi lipoxygenase and Agaricus bisporus tyrosinase). These datasets also exhibited diversity, with some strong- and moderate correlations between length of lag and exponential growth-rates; and sometimes none. In conclusion, lag phase is not  a reliable measure of stress because length of lag and growth-rate inhibition are sometimes highly correlated, and sometimes not at all.

Impact of biodiversity loss on production in complex marine food webs mitigated by prey-release.

Public concern over biodiversity loss is often rationalized as a threat to ecosystem functioning, but biodiversity-ecosystem functioning (BEF) relations are hard to empirically quantify at large scales. We use a realistic marine food-web model, resolving species over five trophic levels, to study how total fish production changes with species richness. This complex model predicts that BEF relations, on average, follow simple Michaelis-Menten curves when species are randomly deleted. These are shaped mainly by release of fish from predation, rather than the release from competition expected from simpler communities. Ordering species deletions by decreasing body mass or trophic level, representing 'fishing down the food web', accentuates prey-release effects and results in unimodal relationships. In contrast, simultaneous unselective harvesting diminishes these effects and produces an almost linear BEF relation, with maximum multispecies fisheries yield at ≈40% of initial species richness. These findings have important implications for the valuation of marine biodiversity.

Living is information processing: from molecules to global systems.

We extend the concept that life is an informational phenomenon, at every level of organisation, from molecules to the global ecological system. According to this thesis: (a) living is information processing, in which memory is maintained by both molecular states and ecological states as well as the more obvious nucleic acid coding; (b) this information processing has one overall function-to perpetuate itself; and (c) the processing method is filtration (cognition) of, and synthesis of, information at lower levels to appear at higher levels in complex systems (emergence). We show how information patterns, are united by the creation of mutual context, generating persistent consequences, to result in 'functional information'. This constructive process forms arbitrarily large complexes of information, the combined effects of which include the functions of life. Molecules and simple organisms have already been measured in terms of functional information content; we show how quantification may be extended to each level of organisation up to the ecological. In terms of a computer analogy, life is both the data and the program and its biochemical structure is the way the information is embodied. This idea supports the seamless integration of life at all scales with the physical universe. The innovation reported here is essentially to integrate these ideas, basing information on the 'general definition' of information, rather than simply the statistics of information, thereby explaining how functional information operates throughout life.

Universal power-law diet partitioning by marine fish and squid with surprising stability-diversity implications.

A central question in community ecology is how the number of trophic links relates to community species richness. For simple dynamical food-web models, link density (the ratio of links to species) is bounded from above as the number of species increases; but empirical data suggest that it increases without bounds. We found a new empirical upper bound on link density in large marine communities with emphasis on fish and squid, using novel methods that avoid known sources of bias in traditional approaches. Bounds are expressed in terms of the diet-partitioning function (DPF): the average number of resources contributing more than a fraction f to a consumer's diet, as a function of f. All observed DPF follow a functional form closely related to a power law, with power-law exponents independent of species richness at the measurement accuracy. Results imply universal upper bounds on link density across the oceans. However, the inherently scale-free nature of power-law diet partitioning suggests that the DPF itself is a better defined characterization of network structure than link density.

Parasitism may enhance rather than reduce the predatory impact of an invader.

Invasive species can have profound impacts on communities and it is increasingly recognized that such effects may be mediated by parasitism. The 'enemy release' hypothesis posits that invaders may be successful and have high impacts owing to escape from parasitism. Alternatively, we hypothesize that parasites may increase host feeding rates and hence parasitized invaders may have increased community impacts. Here, we investigate the influence of parasitism on the predatory impact of the invasive freshwater amphipod Gammarus pulex. Up to 70 per cent of individuals are infected with the acanthocephalan parasite Echinorhynchus truttae, but parasitized individuals were no different in body condition to those unparasitized. Parasitized individuals consumed significantly more prey (Asellus aquaticus; Isopoda) than did unparasitized individuals. Both parasitized and unparasitized individuals displayed Type-II functional responses (FRs), with the FR for parasitized individuals rising more steeply, with a higher asymptote, compared with unparasitized individuals. While the parasite reduced the fitness of individual females, we predict a minor effect on population recruitment because of low parasite prevalence in the peak reproductive period. The parasite thus has a large per capita effect on predatory rate but a low population fitness effect, and thus may enhance rather than reduce the impact of this invader.

Comparison of the functional responses of invasive and native amphipods.

While we can usually understand the impacts of invasive species on recipient communities, invasion biology lacks methodologies that are potentially more predictive. Such tools should ideally be straightforward and widely applicable. Here, we explore an approach that compares the functional responses (FRs) of invader and native amphipod crustaceans. Dikerogammarus villosus is a Ponto-Caspian amphipod currently invading Europe and poised to invade North America. Compared with other amphipods that it actively replaces in freshwaters, D. villosus exhibited significantly greater predation, consuming significantly more prey with a higher type II FR. This corroborates the known dramatic field impacts of D. villosus on invaded communities. In another species, FRs were nearly identical in invasive and native ranges. We thus propose that if FRs of other taxa and trophic groups follow such general patterns, this methodology has potential in predicting future invasive species impacts.

How optimal life history changes with the community size-spectrum.

This paper derives optimal life histories for fishes or other animals in relation to the size spectrum of the ecological community in which they are both predators and prey. Assuming log-linear size-spectra and well known scaling laws for feeding and mortality, we first construct the energetics of the individual. From these we find, using dynamic programming, the optimal allocation of energy between growth and reproduction as well as the trade-off between offspring size and numbers. Optimal strategies were found to be strongly dependent on size spectrum slope. For steep size spectra (numbers declining rapidly with size), determinate growth was optimal and allocation to somatic growth increased rapidly with increasing slope. However, restricting reproduction to a fixed mating season changed optimal allocations to give indeterminate growth approximating a von Bertalanffy trajectory. The optimal offspring size was as small as possible given other restrictions such as newborn starvation mortality. For shallow size spectra, finite optimal maturity size required a decline in fitness for large size or age. All the results are compared with observed size spectra of fish communities to show their consistency and relevance.