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Register a new userFrom genotypes to organisms: State-of-the-art and perspectives of a cornerstone in evolutionary dynamics
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Understanding how genotypes map onto phenotypes, fitness, and eventually organisms is arguably the next major missing piece in a fully predictive theory of evolution. We refer to this generally as the problem of the genotype-phenotype map. Though we are still far from achieving a complete picture of these relationships, our current understanding of simpler questions, such as the structure induced in the space of genotypes by sequences mapped to molecular structures, has revealed important facts that deeply affect the dynamical description of evolutionary processes. Empirical evidence supporting the fundamental relevance of features such as phenotypic bias is mounting as well, while the synthesis of conceptual and experimental progress leads to questioning current assumptions on the nature of evolutionary dynamics-cancer progression models or synthetic biology approaches being notable examples. This work delves into a critical and constructive attitude in our current knowledge of how genotypes map onto molecular phenotypes and organismal functions, and discusses theoretical and empirical avenues to broaden and improve this comprehension. As a final goal, this community should aim at deriving an updated picture of evolutionary processes soundly relying on the structural properties of genotype spaces, as revealed by modern techniques of molecular and functional analysis.
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Since the sequencing of large genomes, many statistical features of their sequences have been found. One intriguing feature is that certain subsequences are much more abundant than others. In fact, abundances of subsequences of a given length are distributed with a scale-free power-law tail, resembling properties of human texts, such as the Zipfs law. Despite recent efforts, the understanding of this phenomenon is still lacking. Here we find that selfish DNA elements, such as those belonging to the Alu family of repeats, dominate the power-law tail. Interestingly, for the Alu elements the power-law exponent increases with the length of the considered subsequences. Motivated by these observations, we develop a model of selfish DNA expansion. The predictions of this model qualitatively and quantitatively agree with the empirical observations. This allows us to estimate parameters for the process of selfish DNA spreading in a genome during its evolution. The obtained results shed light on how evolution of selfish DNA elements shapes non-trivial statistical properties of genomes.
There is a deep connection between the ground states of transverse-field spin systems and the late-time distributions of evolving viral populations -- within simple models, both are obtained from the principal eigenvector of the same matrix. However, that vector is the wavefunction amplitude in the quantum spin model, whereas it is the probability itself in the population model. We show that this seemingly minor difference has significant consequences: phase transitions which are discontinuous in the spin system become continuous when viewed through the population perspective, and transitions which are continuous become governed by new critical exponents. We introduce a more general class of models which encompasses both cases, and that can be solved exactly in a mean-field limit. Numerical results are also presented for a number of one-dimensional chains with power-law interactions. We see that well-worn spin models of quantum statistical mechanics can contain unexpected new physics and insights when treated as population-dynamical models and beyond, motivating further studies.
Our understanding of the evolutionary process has gone a long way since the publication, 150 years ago, of On the origin of species by Charles R. Darwin. The XXth Century witnessed great efforts to embrace replication, mutation, and selection within the framework of a formal theory, able eventually to predict the dynamics and fate of evolving populations. However, a large body of empirical evidence collected over the last decades strongly suggests that some of the assumptions of those classical models necessitate a deep revision. The viability of organisms is not dependent on a unique and optimal genotype. The discovery of huge sets of genotypes (or neutral networks) yielding the same phenotype --in the last term the same organism--, reveals that, most likely, very different functional solutions can be found, accessed and fixed in a population through a low-cost exploration of the space of genomes. The evolution behind the curtain may be the answer to some of the current puzzles that evolutionary theory faces, like the fast speciation process that is observed in the fossil record after very long stasis periods.
The incubation period of a disease is the time between an initiating pathologic event and the onset of symptoms. For typhoid fever, polio, measles, leukemia and many other diseases, the incubation period is highly variable. Some affected people take much longer than average to show symptoms, leading to a distribution of incubation periods that is right skewed and often approximately lognormal. Although this statistical pattern was discovered more than sixty years ago, it remains an open question to explain its ubiquity. Here we propose an explanation based on evolutionary dynamics on graphs. For simple models of a mutant or pathogen invading a network-structured population of healthy cells, we show that skewed distributions of incubation periods emerge for a wide range of assumptions about invader fitness, competition dynamics, and network structure. The skewness stems from stochastic mechanisms associated with two classic problems in probability theory: the coupon collector and the random walk. Unlike previous explanations that rely crucially on heterogeneity, our results hold even for homogeneous populations. Thus, we predict that two equally healthy individuals subjected to equal doses of equally pathogenic agents may, by chance alone, show remarkably different time courses of disease.
Started in Wuhan, China, the COVID-19 has been spreading all over the world. We calibrate the logistic growth model, the generalized logistic growth model, the generalized Richards model and the generalized growth model to the reported number of infected cases for the whole of China, 29 provinces in China, and 33 countries and regions that have been or are undergoing major outbreaks. We dissect the development of the epidemics in China and the impact of the drastic control measures both at the aggregate level and within each province. We quantitatively document four phases of the outbreak in China with a detailed analysis on the heterogeneous situations across provinces. The extreme containment measures implemented by China were very effective with some instructive variations across provinces. Borrowing from the experience of China, we made scenario projections on the development of the outbreak in other countries. We identified that outbreaks in 14 countries (mostly in western Europe) have ended, while resurgences of cases have been identified in several among them. The modeling results clearly show longer after-peak trajectories in western countries, in contrast to most provinces in China where the after-peak trajectory is characterized by a much faster decay. We identified three groups of countries in different level of outbreak progress, and provide informative implications for the current global pandemic.
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