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Register a new userEvolution of adaptation mechanisms: adaptation energy, stress, and oscillating death
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In 1938, H. Selye proposed the notion of adaptation energy and published Experimental evidence supporting the conception of adaptation energy. Adaptation of an animal to different factors appears as the spending of one resource. Adaptation energy is a hypothetical extensive quantity spent for adaptation. This term causes much debate when one takes it literally, as a physical quantity, i.e. a sort of energy. The controversial points of view impede the systematic use of the notion of adaptation energy despite experimental evidence. Nevertheless, the response to many harmful factors often has general non-specific form and we suggest that the mechanisms of physiological adaptation admit a very general and nonspecific description. We aim to demonstrate that Selyes adaptation energy is the cornerstone of the top-down approach to modelling of non-specific adaptation processes. We analyse Selyes axioms of adaptation energy together with Goldstones modifications and propose a series of models for interpretation of these axioms. {em Adaptation energy is considered as an internal coordinate on the `dominant path in the model of adaptation}. The phenomena of `oscillating death and `oscillating remission are predicted on the base of the dynamical models of adaptation. Natural selection plays a key role in the evolution of mechanisms of physiological adaptation. We use the fitness optimization approach to study of the distribution of resources for neutralization of harmful factors, during adaptation to a multifactor environment, and analyse the optimal strategies for different systems of factors.
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The purpose of this roadmap article is to draw attention to a paradigm shift in our understanding of evolution towards a perspective of ecological-evolutionary feedback, highlighted through two recent highly simplified examples of rapid evolution. The first example focuses primarily on population dynamics: anomalies in population cycles can reflect the influence of strong selection and the interplay with mutations. The second focuses primarily on the way in which ecological structure can potentially be influenced by what is arguably the most powerful source of genetic novelty: horizontal gene transfer. We review the status of rapid evolution and also enumerate the current and future challenges of achieving a full understanding of rapid evolution in all its manifestations.
Our models for detecting the effect of adaptation on population genomic diversity are often predicated on a single newly arisen mutation sweeping rapidly to fixation. However, a population can also adapt to a new situation by multiple mutations of similar phenotypic effect that arise in parallel. These mutations can each quickly reach intermediate frequency, preventing any single one from rapidly sweeping to fixation globally (a soft sweep). Here we study models of parallel mutation in a geographically spread population adapting to a global selection pressure. The slow geographic spread of a selected allele can allow other selected alleles to arise and spread elsewhere in the species range. When these different selected alleles meet, their spread can slow dramatically, and so form a geographic patchwork which could be mistaken for a signal of local adaptation. This random spatial tessellation will dissipate over time due to mixing by migration, leaving a set of partial sweeps within the global population. We show that the spatial tessellation initially formed by mutational types is closely connected to Poisson process models of crystallization, which we extend. We find that the probability of parallel mutation and the spatial scale on which parallel mutation occurs is captured by a single characteristic length that reflects the expected distance a spreading allele travels before it encounters a different spreading allele. This characteristic length depends on the mutation rate, the dispersal parameter, the effective local density of individuals, and to a much lesser extent the strength of selection. We argue that even in widely dispersing species, such parallel geographic sweeps may be surprisingly common. Thus, we predict, as more data becomes available, many more examples of intra-species parallel adaptation will be uncovered.
Interactions among individuals in natural populations often occur in a dynamically changing environment. Understanding the role of environmental variation in population dynamics has long been a central topic in theoretical ecology and population biology. However, the key question of how individuals, in the middle of challenging social dilemmas (e.g., the tragedy of the commons), modulate their behaviors to adapt to the fluctuation of the environment has not yet been addressed satisfactorily. Utilizing evolutionary game theory and stochastic games, we develop a game-theoretical framework that incorporates the adaptive mechanism of reinforcement learning to investigate whether cooperative behaviors can evolve in the ever-changing group interaction environment. When the action choices of players are just slightly influenced by past reinforcements, we construct an analytical condition to determine whether cooperation can be favored over defection. Intuitively, this condition reveals why and how the environment can mediate cooperative dilemmas. Under our model architecture, we also compare this learning mechanism with two non-learning decision rules, and we find that learning significantly improves the propensity for cooperation in weak social dilemmas, and, in sharp contrast, hinders cooperation in strong social dilemmas. Our results suggest that in complex social-ecological dilemmas, learning enables the adaptation of individuals to varying environments.
Existing Unsupervised Domain Adaptation (UDA) literature adopts the covariate shift and conditional shift assumptions, which essentially encourage models to learn common features across domains. However, due to the lack of supervision in the target domain, they suffer from the semantic loss: the feature will inevitably lose non-discriminative semantics in source domain, which is however discriminative in target domain. We use a causal view -- transportability theory -- to identify that such loss is in fact a confounding effect, which can only be removed by causal intervention. However, the theoretical solution provided by transportability is far from practical for UDA, because it requires the stratification and representation of the unobserved confounder that is the cause of the domain gap. To this end, we propose a practical solution: Transporting Causal Mechanisms (TCM), to identify the confounder stratum and representations by using the domain-invariant disentangled causal mechanisms, which are discovered in an unsupervised fashion. Our TCM is both theoretically and empirically grounded. Extensive experiments show that TCM achieves state-of-the-art performance on three challenging UDA benchmarks: ImageCLEF-DA, Office-Home, and VisDA-2017. Codes are available in Appendix.
During the last decade, network approaches became a powerful tool to describe protein structure and dynamics. Here, we describe first the protein structure networks of molecular chaperones, then characterize chaperone containing sub-networks of interactomes called as chaperone-networks or chaperomes. We review the role of molecular chaperones in short-term adaptation of cellular networks in response to stress, and in long-term adaptation discussing their putative functions in the regulation of evolvability. We provide a general overview of possible network mechanisms of adaptation, learning and memory formation. We propose that changes of network rigidity play a key role in learning and memory formation processes. Flexible network topology provides learning competent state. Here, networks may have much less modular boundaries than locally rigid, highly modular networks, where the learnt information has already been consolidated in a memory formation process. Since modular boundaries are efficient filters of information, in the learning competent state information filtering may be much smaller, than after memory formation. This mechanism restricts high information transfer to the learning competent state. After memory formation, modular boundary-induced segregation and information filtering protect the stored information. The flexible networks of young organisms are generally in a learning competent state. On the contrary, locally rigid networks of old organisms have lost their learning competent state, but store and protect their learnt information efficiently. We anticipate that the above mechanism may operate at the level of both protein-protein interaction and neuronal networks.
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