Evolution of Robustness and Plasticity under Environmental Fluctuation: Formulation in terms of Phenotypic Variances

The characterization of plasticity, robustness, and evolvability, an important issue in biology, is studied in terms of phenotypic fluctuations. By numerically evolving gene regulatory networks, the proportionality between the phenotypic variances of epigenetic and genetic origins is confirmed. The former is given by the variance of the phenotypic fluctuation due to noise in the developmental process; and the latter, by the variance of the phenotypic fluctuation due to genetic mutation. The relationship suggests a link between robustness to noise and to mutation, since robustness can be defined by the sharpness of the distribution of the phenotype. Next, the proportionality between the variances is demonstrated to also hold over expressions of different genes (phenotypic traits) when the system acquires robustness through the evolution. Then, evolution under environmental variation is numerically investigated and it is found that both the adaptability to a novel environment and the robustness are made compatible when a certain degree of phenotypic fluctuations exists due to noise. The highest adaptability is achieved at a certain noise level at which the gene expression dynamics are near the critical state to lose the robustness. Based on our results, we revisit Waddington's canalization and genetic assimilation with regard to the two types of phenotypic fluctuations.Comment: 23 pages 11 figure

Why don't the modules dominate - Investigating the Structure of a Well-Known Modularity-Inducing Problem Domain

Wagner's modularity inducing problem domain is a key contribution to the study of the evolution of modularity, including both evolutionary theory and evolutionary computation. We study its behavior under classical genetic algorithms. Unlike what we seem to observe in nature, the emergence of modularity is highly conditional and dependent, for example, on the eagerness of search. In nature, modular solutions generally dominate populations, whereas in this domain, modularity, when it emerges, is a relatively rare variant. Emergence of modularity depends heavily on random fluctuations in the fitness function, with a randomly varied but unchanging fitness function, modularity evolved far more rarely. Interestingly, high-fitness non-modular solutions could frequently be converted into even-higher-fitness modular solutions by manually removing all inter-module edges. Despite careful exploration, we do not yet have a full explanation of why the genetic algorithm was unable to find these better solutions

Specialization Can Drive the Evolution of Modularity

Organismal development and many cell biological processes are organized in a modular fashion, where regulatory molecules form groups with many interactions within a group and few interactions between groups. Thus, the activity of elements within a module depends little on elements outside of it. Modularity facilitates the production of heritable variation and of evolutionary innovations. There is no consensus on how modularity might evolve, especially for modules in development. We show that modularity can increase in gene regulatory networks as a byproduct of specialization in gene activity. Such specialization occurs after gene regulatory networks are selected to produce new gene activity patterns that appear in a specific body structure or under a specific environmental condition. Modules that arise after specialization in gene activity comprise genes that show concerted changes in gene activities. This and other observations suggest that modularity evolves because it decreases interference between different groups of genes. Our work can explain the appearance and maintenance of modularity through a mechanism that is not contingent on environmental change. We also show how modularity can facilitate co-option, the utilization of existing gene activity to build new gene activity patterns, a frequent feature of evolutionary innovations

A microbial inspired routing protocol for VANETs

We present a bio-inspired unicast routing protocol for vehicular Ad Hoc Networks which uses the cellular attractor selection mechanism to select next hops. The proposed unicast routing protocol based on attractor selecting (URAS) is an opportunistic routing protocol, which is able to change itself adaptively to the complex and dynamic environment by routing feedback packets. We further employ a multi-attribute decision-making strategy, the Technique for Order Preference by Similarity to an Ideal Solution (TOPSIS), to reduce the number of redundant candidates for next-hop selection, so as to enhance the performance of attractor selection mechanism. Once the routing path is found, URAS maintains the current path or finds another better path adaptively based on the performance of current path, that is, it can self-evolution until the best routing path is found. Our simulation study compares the proposed solution with the state-of-the-art schemes, and shows the robustness and effectiveness of the proposed routing protocol and the significant performance improvement, in terms of packet delivery, end-to-end delay, and congestion, over the conventional method

A Publish-Subscribe Model of Genetic Networks

We present a simple model of genetic regulatory networks in which regulatory connections among genes are mediated by a limited number of signaling molecules. Each gene in our model produces (publishes) a single gene product, which regulates the expression of other genes by binding to regulatory regions that correspond (subscribe) to that product. We explore the consequences of this publish-subscribe model of regulation for the properties of single networks and for the evolution of populations of networks. Degree distributions of randomly constructed networks, particularly multimodal in-degree distributions, which depend on the length of the regulatory sequences and the number of possible gene products, differed from simpler Boolean NK models. In simulated evolution of populations of networks, single mutations in regulatory or coding regions resulted in multiple changes in regulatory connections among genes, or alternatively in neutral change that had no effect on phenotype. This resulted in remarkable evolvability in both number and length of attractors, leading to evolved networks far beyond the expectation of these measures based on random distributions. Surprisingly, this rapid evolution was not accompanied by changes in degree distribution; degree distribution in the evolved networks was not substantially different from that of randomly generated networks. The publish-subscribe model also allows exogenous gene products to create an environment, which may be noisy or stable, in which dynamic behavior occurs. In simulations, networks were able to evolve moderate levels of both mutational and environmental robustness