Dynamics of collective cooperation under personalised strategy updates.

Collective cooperation is essential for many social and biological systems, yet understanding how it evolves remains a challenge. Previous investigations report that the ubiquitous heterogeneous individual connections hinder cooperation by assuming individuals update strategies at identical rates. Here we develop a general framework by allowing individuals to update strategies at personalised rates, and provide the precise mathematical condition under which universal cooperation is favoured. Combining analytical and numerical calculations on synthetic and empirical networks, we find that when individuals' update rates vary inversely with their number of connections, heterogeneous connections actually outperform homogeneous ones in promoting cooperation. This surprising property undercuts the conventional wisdom that heterogeneous structure is generally antagonistic to cooperation and, further helps develop an efficient algorithm OptUpRat to optimise collective cooperation by designing individuals' update rates in any population structure. Our findings provide a unifying framework to understand the interplay between structural heterogeneity, behavioural rhythms, and cooperation.

Fragmentation of outage clusters during the recovery of power distribution grids.

The understanding of recovery processes in power distribution grids is limited by the lack of realistic outage data, especially large-scale blackout datasets. By analyzing data from three electrical companies across the United States, we find that the recovery duration of an outage is connected with the downtime of its nearby outages and blackout intensity (defined as the peak number of outages during a blackout), but is independent of the number of customers affected. We present a cluster-based recovery framework to analytically characterize the dependence between outages, and interpret the dominant role blackout intensity plays in recovery. The recovery of blackouts is not random and has a universal pattern that is independent of the disruption cause, the post-disaster network structure, and the detailed repair strategy. Our study reveals that suppressing blackout intensity is a promising way to speed up restoration.

Evolution of cooperation on temporal networks.

Population structure is a key determinant in fostering cooperation among naturally self-interested individuals in microbial populations, social insect groups, and human societies. Traditional research has focused on static structures, and yet most real interactions are finite in duration and changing in time, forming a temporal network. This raises the question of whether cooperation can emerge and persist despite an intrinsically fragmented population structure. Here we develop a framework to study the evolution of cooperation on temporal networks. Surprisingly, we find that network temporality actually enhances the evolution of cooperation relative to comparable static networks, despite the fact that bursty interaction patterns generally impede cooperation. We resolve this tension by proposing a measure to quantify the amount of temporality in a network, revealing an intermediate level that maximally boosts cooperation. Our results open a new avenue for investigating the evolution of cooperation and other emergent behaviours in more realistic structured populations.

Controllability of multiplex, multi-time-scale networks.

The paradigm of layered networks is used to describe many real-world systems, from biological networks to social organizations and transportation systems. While recently there has been much progress in understanding the general properties of multilayer networks, our understanding of how to control such systems remains limited. One fundamental aspect that makes this endeavor challenging is that each layer can operate at a different time scale; thus, we cannot directly apply standard ideas from structural control theory of individual networks. Here we address the problem of controlling multilayer and multi-time-scale networks focusing on two-layer multiplex networks with one-to-one interlayer coupling. We investigate the practically relevant case when the control signal is applied to the nodes of one layer. We develop a theory based on disjoint path covers to determine the minimum number of inputs (N_{i}) necessary for full control. We show that if both layers operate on the same time scale, then the network structure of both layers equally affect controllability. In the presence of time-scale separation, controllability is enhanced if the controller interacts with the faster layer: N_{i} decreases as the time-scale difference increases up to a critical time-scale difference, above which N_{i} remains constant and is completely determined by the faster layer. We show that the critical time-scale difference is large if layer I is easy and layer II is hard to control in isolation. In contrast, control becomes increasingly difficult if the controller interacts with the layer operating on the slower time scale and increasing time-scale separation leads to increased N_{i}, again up to a critical value, above which N_{i} still depends on the structure of both layers. This critical value is largely determined by the longest path in the faster layer that does not involve cycles. By identifying the underlying mechanisms that connect time-scale difference and controllability for a simplified model, we provide crucial insight into disentangling how our ability to control real interacting complex systems is affected by a variety of sources of complexity.

Regularity underlies erratic population abundances in marine ecosystems.

The abundance of a species' population in an ecosystem is rarely stationary, often exhibiting large fluctuations over time. Using historical data on marine species, we show that the year-to-year fluctuations of population growth rate obey a well-defined double-exponential (Laplace) distribution. This striking regularity allows us to devise a stochastic model despite seemingly irregular variations in population abundances. The model identifies the effect of reduced growth at low population density as a key factor missed in current approaches of population variability analysis and without which extinction risks are severely underestimated. The model also allows us to separate the effect of demographic stochasticity and show that single-species growth rates are dominantly determined by stochasticity common to all species. This dominance-and the implications it has for interspecies correlations, including co-extinctions-emphasizes the need for ecosystem-level management approaches to reduce the extinction risk of the individual species themselves.

Realistic control of network dynamics.

The control of complex networks is of paramount importance in areas as diverse as ecosystem management, emergency response and cell reprogramming. A fundamental property of networks is that perturbations to one node can affect other nodes, potentially causing the entire system to change behaviour or fail. Here we show that it is possible to exploit the same principle to control network behaviour. Our approach accounts for the nonlinear dynamics inherent to real systems, and allows bringing the system to a desired target state even when this state is not directly accessible due to constraints that limit the allowed interventions. Applications show that this framework permits reprogramming a network to a desired task, as well as rescuing networks from the brink of failure-which we illustrate through the mitigation of cascading failures in a power-grid network and the identification of potential drug targets in a signalling network of human cancer.

Dispensability of Escherichia coli's latent pathways.

Gene-knockout experiments on single-cell organisms have established that expression of a substantial fraction of genes is not needed for optimal growth. This problem acquired a new dimension with the recent discovery that environmental and genetic perturbations of the bacterium Escherichia coli are followed by the temporary activation of a large number of latent metabolic pathways, which suggests the hypothesis that temporarily activated reactions impact growth and hence facilitate adaptation in the presence of perturbations. Here, we test this hypothesis computationally and find, surprisingly, that the availability of latent pathways consistently offers no growth advantage and tends, in fact, to inhibit growth after genetic perturbations. This is shown to be true even for latent pathways with a known function in alternate conditions, thus extending the significance of this adverse effect beyond apparently nonessential genes. These findings raise the possibility that latent pathway activation is in fact derivative of another, potentially suboptimal, adaptive response.