No Arabic abstract
The two classic theories for the existence of sexual replication are that sex purges deleterious mutations from a population, and that sex allows a population to adapt more rapidly to changing environments. These two theories have often been presented as opposing explanations for the existence of sex. Here, we develop and analyze evolutionary models based on the asexual and sexual replication pathways in Saccharomyces cerevisiae (Bakers yeast), and show that sexual replication can both purge deleterious mutations in a static environment, as well as lead to faster adaptation in a dynamic environment. This implies that sex can serve a dual role, which is in sharp contrast to previous theories.
We discovered a dynamic phase transition induced by sexual reproduction. The dynamics is a pure Darwinian rule with both fundamental ingredients to drive evolution: 1) random mutations and crossings which act in the sense of increasing the entropy (or diversity); and 2) selection which acts in the opposite sense by limiting the entropy explosion. Selection wins this competition if mutations performed at birth are few enough. By slowly increasing the average number m of mutations, however, the population suddenly undergoes a mutational degradation precisely at a transition point mc. Above this point, the bad alleles spread over the genetic pool of the population, overcoming the selection pressure. Individuals become selectively alike, and evolution stops. Only below this point, m < mc, evolutionary life is possible. The finite-size-scaling behaviour of this transition is exhibited for large enough chromosome lengths L. One important and surprising observation is the L-independence of the transition curves, for large L. They are also independent on the population size. Another is that mc is near unity, i.e. life cannot be stable with much more than one mutation per diploid genome, independent of the chromosome length, in agreement with reality. One possible consequence is that an eventual evolutionary jump towards larger L enabling the storage of more genetic information would demand an improved DNA copying machinery in order to keep the same total number of mutations per offspring.
Growing mixtures of annual arable crop species or genotypes is a promising way to improve crop production without increasing agricultural inputs. To design optimal crop mixtures, choices of species, genotypes, sowing proportion, plant arrangement, and sowing date need to be made but field experiments alone are not sufficient to explore such a large range of factors. Crop modeling allows to study, understand and ultimately design cropping systems and is an established method for sole crops. Recently, modeling started to be applied to annual crop mixtures as well. Here, we review to what extent crop simulation models and individual-based models are suitable to capture and predict the specificities of annual crop mixtures. We argued that: 1) The crop mixture spatio-temporal heterogeneity (influencing the occurrence of ecological processes) determines the choice of the modeling approach (plant or crop centered). 2) Only few crop models (adapted from sole crop models) and individual-based models currently exist to simulate annual crop mixtures. 3) Crop models are mainly used to address issues related to crop mixtures management and to the integration of crop mixtures into larger scales such as the rotation, whereas individual-based models are mainly used to identify plant traits involved in crop mixture performance and to quantify the relative contribution of the different ecological processes (niche complementarity, facilitation, competition, plasticity) to crop mixture functioning. This review highlights that modeling of annual crop mixtures is in its infancy and gives to model users some important keys to choose the model based on the questions they want to answer, with awareness of the strengths and weaknesses of each of the modeling approaches.
The Robinson-Foulds (RF) distance is by far the most widely used measure of dissimilarity between trees. Although the distribution of these distances has been investigated for twenty years, an algorithm that is explicitly polynomial time has yet to be described for computing this distribution (which is also the distribution of trees around a given tree under the popular Robinson-Foulds metric). In this paper we derive a polynomial-time algorithm for this distribution. We show how the distribution can be approximated by a Poisson distribution determined by the proportion of leaves that lie in `cherries of the given tree. We also describe how our results can be used to derive normalization constants that are required in a recently-proposed maximum likelihood approach to supertree construction.
This technical report addresses a pressing issue in the trajectory of the coronavirus outbreak; namely, the rate at which effective immunity is lost following the first wave of the pandemic. This is a crucial epidemiological parameter that speaks to both the consequences of relaxing lockdown and the propensity for a second wave of infections. Using a dynamic causal model of reported cases and deaths from multiple countries, we evaluated the evidence models of progressively longer periods of immunity. The results speak to an effective population immunity of about three months that, under the model, defers any second wave for approximately six months in most countries. This may have implications for the window of opportunity for tracking and tracing, as well as for developing vaccination programmes, and other therapeutic interventions.
Interlocus gene conversion (IGC) homogenizes paralogs. Little is known regarding the mutation events that cause IGC and even less is known about the IGC mutations that experience fixation. To disentangle the rates of fixed IGC mutations from the tract lengths of these fixed mutations, we employ a composite likelihood procedure. We characterize the procedure with simulations. We apply the procedure to duplicated primate introns and to protein-coding paralogs from both yeast and primates. Our estimates from protein-coding data concerning the mean length of fixed IGC tracts were unexpectedly low and are associated with high degrees of uncertainty. In contrast, our estimates from the primate intron data had lengths in the general range expected from IGC mutation studies. While it is challenging to separate the rate at which fixed IGC mutations initiate from the average number of nucleotide positions that these IGC events affect, all of our analyses indicate that IGC is responsible for a substantial proportion of evolutionary change in duplicated regions. Our results suggest that IGC should be considered whenever the evolution of multigene families is examined.