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Redundant representations in evolutionary computation.

This paper discusses how the use of redundant representations influences the performance of genetic and evolutionary algorithms. Representations are redundant if the number of genotypes exceeds the number of phenotypes. A distinction is made between synonymously and non-synonymously redundant representations. Representations are synonymously redundant if the genotypes that represent the same phenotype are very similar to each other. Non-synonymously redundant representations do not allow genetic operators to work properly and result in a lower performance of evolutionary search. When using synonymously redundant representations, the performance of selectorecombinative genetic algorithms (GAs) depends on the modification of the initial supply. We have developed theoretical models for synonymously redundant representations that show the necessary population size to solve a problem and the number of generations goes with O(2(kr)/r), where kr is the order of redundancy and r is the number of genotypic building blocks (BB) that represent the optimal phenotypic BB. As a result, uniformly redundant representations do not change the behavior of GAs. Only by increasing r, which means overrepresenting the optimal solution, does GA performance increase. Therefore, non-uniformly redundant representations can only be used advantageously if a-priori information exists regarding the optimal solution. The validity of the proposed theoretical concepts is illustrated for the binary trivial voting mapping and the real-valued link-biased encoding. Our empirical investigations show that the developed population sizing and time to convergence models allow an accurate prediction of the empirical results.

Algorithms↗

Constructing large-scale genetic maps using an evolutionary strategy algorithm.

This article is devoted to the problem of ordering in linkage groups with many dozens or even hundreds of markers. The ordering problem belongs to the field of discrete optimization on a set of all possible orders, amounting to n!/2 for n loci; hence it is considered an NP-hard problem. Several authors attempted to employ the methods developed in the well-known traveling salesman problem (TSP) for multilocus ordering, using the assumption that for a set of linked loci the true order will be the one that minimizes the total length of the linkage group. A novel, fast, and reliable algorithm developed for the TSP and based on evolution-strategy discrete optimization was applied in this study for multilocus ordering on the basis of pairwise recombination frequencies. The quality of derived maps under various complications (dominant vs. codominant markers, marker misclassification, negative and positive interference, and missing data) was analyzed using simulated data with approximately 50-400 markers. High performance of the employed algorithm allows systematic treatment of the problem of verification of the obtained multilocus orders on the basis of computing-intensive bootstrap and/or jackknife approaches for detecting and removing questionable marker scores, thereby stabilizing the resulting maps. Parallel calculation technology can easily be adopted for further acceleration of the proposed algorithm. Real data analysis (on maize chromosome 1 with 230 markers) is provided to illustrate the proposed methodology.

Algorithms↗

Evolutionary conservation of a genetic pathway of programmed cell death.

Genetic analysis of programmed cell death in Caenorhabditis elegans has led to the identification of 13 genes that constitute a developmental pathway of programmed cell death. Two of the three key genes in this pathway, ced-9, a cell death suppressor, and ced-3, a cell death inducer, were found to encode proteins that share structural and functional similarities with the mammalian proto-oncogene product Bcl-2 and interleukin-1 beta converting enzyme, respectively. These results suggest that the genetic pathway of programmed cell death may be evolutionarily conserved from worms to mammals.

Animals↗

An evolutionary model for identifying genetic adaptation to high altitude.

Coordinated maternal/fetal responses to pregnancy are required to ensure continuous O2 delivery to the developing organism. Mammals employ distinctive reproductive strategies that afford their young an improved chance of survival through the completion or the reproductive period. Thus, mortality prior to the end of the reproductive period is concentrated in the earliest phases of the lifecycle. At high altitude, fetal growth restriction reduces birth weight and likely compromises survival during the early postnatal period. Population variation in the frequency of the altitude-associated increase in intrauterine growth restriction (IUGR) demonstrates that multigenerational Tibetan and Andean high-altitude populations are protected compared with shorter duration, European or Han (Chinese) residents. This experiment of nature permits testing the hypothesis that genetic factors (a) influence susceptibility to altitude-associated IUGR, (b) act on maternal vascular adjustments to pregnancy determining uteroplacental blood flow, and (c) involve genes which regulate and/or are regulated by hypoxia-inducible factors (HIFs). Serial, studies during pregnancy as well as postpartum in Andean and European residents of high (3600 m) and low (300 m) altitude will permit evaluation of whether uteroplacental O2 delivery is lower in the European than Andean women and, if so, the physiological factors responsible. Comparisons of HIF-targeted vasoactive substances and SNPs in or near HIF-regulatory or targeted genes will permit determination of whether these regions are distinctive in the Andean population. Studies coupling genetic and genomic approaches with more traditional physiological measures may be productively employed for determining the genetic mechanisms influencing physiological adaptation to high altitude.

Adolescent↗

The evolutionary change of the genetic code as restricted by the anticodon and identity of transfer RNA.

The discovery of non-universal genetic codes in several mitochondria and nuclear systems during the part ten years has necessitated a reconsideration of the concept that the genetic code is universal and frozen, as was once believed. Here, the flexibility of the relationship between codons and amino acids is discussed on the basis of the distribution of non-universal genetic codes in various organisms insofar as has been observed to date. Judging from the result of recent investigations into tRNA identity, it would appear that the non-participation of the anticodon in recognition by aminoacyl-tRNA synthetase has significantly influenced the variability of codons.

Animals↗

Aflatoxigenicity in Aspergillus: molecular genetics, phylogenetic relationships and evolutionary implications.

Aflatoxins (AFs) are toxic and carcinogenic secondary metabolites produced by isolates of Aspergillus section Flavi as well as a number of Aspergillus isolates that are classified outside of section Flavi. Characterization of the AF and sterigmatocystin (ST) gene clusters and analysis of factors governing regulation of their biosynthesis has resulted in these two mycotoxins being the most extensively studied of fungal secondary metabolites. This wealth of information has allowed the determination of the molecular basis for non-production of AF in natural isolates of A. flavus and domesticated strains of A. oryzae. This review provides an overview of the molecular analysis of the AF and ST gene clusters as well as new information on an AF gene cluster identified in the non-section Flavi isolate, Aspergillus ochraceoroseus. Additionally, molecular phylogenetic analysis using AF biosynthetic gene sequences as well as ribosomal DNA internal transcribed spacer (ITS) sequences between various section Flavi and non-section Flavi species has enabled determination of the probable evolutionary history of the AF and ST gene clusters. A model for the evolution of the AF and ST gene clusters as well as possible biological roles for AF are discussed.

Aflatoxins↗

Molecular genetic evidence for early evolutionary origin of budding peptidoglycan-less eubacteria.

Recent studies on the cell wall composition of budding, non-prosthecate bacteria have shown that representatives of the genera Planctomyces and Pasteuria (sensu Staley, 1973) lack the peptidoglycan moiety, which is the characteristic feature of eubacterial cell walls, but possess an as yet unidentified protein sheet instead; in this respect Planctomyces and Pasteuria strains resemble certain archaebacteria more than eubacteria. To determine their phylogenetic positions, the 16S ribosomal RNAs of three budding, peptidoglycan-less strains with and without stalks were subjected to partial sequence analyses. As we report here, the comparison of data with those obtained from about 320 eubacterial and 40 archaebacterial strains revealed that the strains investigated are not members of the archaebacterial kingdom but represent an ancient line of descent of the eubacterial kingdom. Furthermore the diphtheria toxin reaction of Planctomyces and Pasteuria shows that they behave like eubacteria.

Bacteria↗

An evolutionary reduction principle for genetic modifiers.

The joint evolution of major genes under viability selection and a modifier locus that controls recombination between the major genes, mutation at the major gene, or migration between two demes is studied. The modifying locus is selectively neutral and may have an arbitrary number of alleles. For each case a class of polymorphic equilibria exists in which the frequencies of the modifying alleles are those computed by assuming that the recombination, mutation, or migration rates were viabilities and in which the major and modifier loci are not statistically associated. These are called viability-analogous Hardy-Weinberg (VAHW) equilibria. A new allele introduced near these equilibria will enter the population if its marginal average rate of recombination, mutation, or migration (whichever applies) is less than the population average prior to its introduction. Stability properties of these VAHW equilibria are also reported.

Biological Evolution↗

Evolutionary divergence of the genetic architecture underlying photoperiodism in the pitcher-plant mosquito, Wyeomyia smithii.

We determine the contribution of composite additive, dominance, and epistatic effects to the genetic divergence of photoperiodic response along latitudinal, altitudinal, and longitudinal gradients in the pitcher-plant mosquito, Wyeomyia smithii. Joint scaling tests of crosses between populations showed widespread epistasis as well as additive and dominance differences among populations. There were differences due to epistasis between an alpine population in North Carolina and populations in Florida, lowland North Carolina, and Maine. Longitudinal displacement resulted in differences due to epistasis between Florida and Alabama populations separated by 300 km but not between Maine and Wisconsin populations separated by 2000 km. Genetic differences between New Jersey and Ontario did not involve either dominance or epistasis and we estimated the minimum number of effective factors contributing to a difference in mean critical photoperiod of 5 SD between them as nE = 5. We propose that the genetic similarity of populations within a broad northern region is due to their more recent origin since recession of the Laurentide Ice Sheet and that the unique genetic architecture of each population is the result of both mutation and repeated migration-founder-flush episodes during the dispersal of W. smithii in North America. Our results suggest that differences in composite additive and dominance effects arise early in the genetic divergence of populations while differences due to epistasis accumulate after more prolonged isolation.

Animals↗

The cyanobacterial tRNA(Leu) (UAA) intron: evolutionary patterns in a genetic marker.

Cyanobacterial tRNA(Leu) (UAA) intron sequences from natural populations of Nostoc and other cyanobacteria were compared. Variation between the different introns was not randomly distributed but strongly restricted by the secondary and tertiary structure of the intron. Although all Nostoc sequences examined shared high similarity, differences were observed in one stem-loop. This stem-loop could be divided into two classes, both built up from two base pairing heptanucleotide repeats. Size variation was primarily caused by different numbers of repeats, but some strains also contained additional sequences in this stem-loop not following the heptanucleotide repeat motif. Several sequences showing similarity with these additional sequences were identified in the Nostoc punctiforme genome. Furthermore, the regions flanking these sequences contained the same, or similar, heptanucleotide repeats as those flanking the corresponding sequences in the intron. It is proposed that both slipped strand mispairing during replication and homologous recombination among different loci in the genome are important processes causing variation between introns.

Cyanobacteria↗

The evolution of genetic architecture. I. Diversification of genetic backgrounds by genetic drift.

The genetic architecture of a phenotype plays a critical role in determining phenotypic evolution through its effects on patterns of genetic variation. Genetic architecture is often considered to be constant in evolutionary quantitative genetic models. However, genetic architecture may be variable and itself evolve when there are dominance and epistatic interactions among alleles at the same and different loci, respectively. The evolution of genetic architecture by genetic drift is examined here by testing the breeding value of four standard inbred mouse strains mated across a set of 26 related recombinant quasi-inbred (RqI) lines generated from the intercross of the Large (LG/J) and Small (SM/J) inbred mouse strains. Phenotypes of interest include age-specific body weights, growth, and adult body composition. If the genetic architecture of these traits has differentiated by genetic drift during the production of the RqI strains, we should observe interactions between tester strain and RqI strain. The breeding values of the tester strains will change relative to one another depending on which RqI strain they are crossed to. The study included an average of 15.1 offspring per cross, over a total of 100 different crosses. Multivariate and univariate analyses of variance indicate that there is strongly significant interaction for all traits. Interaction is more pronounced in males than in females and accounted for an average of about 40% of the explained variation in males and 30% in females. These results indicate that the genetic architecture of these traits has differentiated by genetic drift in the RqI strains since their isolation from a common founder population. Further analysis indicates that this differentiation results in changes in the order of tester strain effects so that common patterns of selection in these differentiated populations could result in the fixation of different alleles.

Animals↗

Mutational origin of new mating type specificities in flowering plants.

Many hermaphroditic plants avoid self-fertilization by rejecting pollen that express genetically-determined specificities in common with the pistil. Self-incompatibility systems typically show extremely high genetic diversity, some maintaining hundreds of specificities. This article addresses the genetic and evolutionary mechanisms through which new mating specificities arise. Recent investigations of the genetic and physiological basis of self-incompatibility are reviewed. Two evolutionary pathways are considered: one which requires full expression of self-incompatibility in all intermediates and one in which new mating specificities arise through episodes of partial breakdown and restoration of self-incompatibility.

Biological Evolution↗

Modification point depth and genome growth in genetic programming.

The evolutionary computation community has shown increasing interest in arbitrary-length representations, particularly in the field of genetic programming. A serious stumbling block to the scalability of such representations has been bloat: uncontrolled genome growth during an evolutionary run. Bloat appears across the evolutionary computation spectrum, but genetic programming has given it by far the most attention. Most genetic programming models explain this phenomenon as a result of the growth of introns, areas in an individual which serve no functional purpose. This paper presents evidence which directly contradicts intron theories as applied to tree-based genetic programming. The paper then uses data drawn from this evidence to propose a new model of genome growth. In this model, bloat in genetic programming is a function of the mean depth of the modification (crossover or mutation) point. Points far from the root are correspondingly less likely to hurt the child's survivability in the next generation. The modification point is in turn strongly correlated to average parent tree size and to removed subtree size, both of which are directly linked to the size of the resulting child.

Algorithms↗

From complex traits to complex alleles.

Several recent studies using natural populations of Drosophila show that one must be very careful when sorting among the large number of molecular polymorphisms found at most loci to identify the nucleotide changes responsible for phenotypic variation in complex traits. Indeed, several mutations within a single allele can interact to generate the overall observed effect. The results are instructive both for those interested in the genetics of evolutionary change and for those attempting to ferret out the genetic basis of complex human diseases.

Alleles↗