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R E Michod

Publications and source records attributed to R E Michod.

At least 19 recordsLinked to original sources
PubMed2001

Cooperation and conflict in the evolution of multicellularity.

Multicellular organisms probably originated as groups of cells formed in several ways, including cell proliferation from a group of founder cells and aggregation. Cooperation among cells benefits the group, but may be costly (altruistic) or beneficial (synergistic) to individual cooperating cells. In this paper, we study conflict mediation, the process by which genetic modifiers evolve that enhance cooperation by altering the parameters of development or rules of formation of cell groups. We are particularly interested in the conditions under which these modifiers lead to a new higher-level unit of selection with increased cooperation among group members and heritable variation in fitness at the group level. By sculpting the fitness variation and opportunity for selection at the two levels, conflict modifiers create new functions at the organism level. An organism is more than a group of cooperating cells related by common descent; organisms require adaptations that regulate conflict within. Otherwise their continued evolution is frustrated by the creation of within-organism variation and conflict between levels of selection. The evolution of conflict modifiers is a necessary prerequisite to the emergence of individuality and the continued well being of the organism. Conflict leads--through the evolution of adaptations that reduce i--to greater individuality and harmony for the organism.

Animals↗
PubMed1998

Origin of sex for error repair. III. Selfish sex.

According to the repair hypothesis, sex originated as a cooperative interaction-the benefit being damage repair. As with all cooperative strategies, cooperative sex may be vulnerable to selfish mutants. The purpose of the present paper is to understand what implications such selfish mutants may have both for the origin of sex, especially in competition with asexual diploidy, and for the elaboration of the sexual cycle, especially in facultatively sexual organisms. Asexual diploids are assumed to effectively and instantaneously repair all damages without expression of deleterious recessive mutations. Costs to asexual diploidy are considered in terms of its birth rate and mortality rate. The main results of the present paper are as follows. (i) Asexual diploidy wins when the costs of diploidy are small, mortality rates low, and damage rates high. (ii) Beginning with an ancestral state in which cells are asexual haploids, the sexual life cycle would emerge before asexual diploidy as a response to increasing DNA damage. (iii) Selfish sex is a far more robust repair strategy than cooperative sex, especially in competition with asexual diploidy. (iv) Although cooperative sex is more adaptive in extreme environments characterized by high damage and high mortality, selfish sex can still invade in these regions and take the entire system to extinction. (v) Once it is present, selfish sex is stable to asexual diploidy over a wide range of parameter values and can persist in regions of parameter space forbidded to the asexual diploid. These results help to address a concern of the gene repair theory of sex, which is that efficient repair in an asexual diploid is a better strategy than sex. Data from microbes bearing on the results are discussed as is the relationship between facultative sex in multicellular organisms and selfish sex in microbes.

Bacterial Physiological Phenomena↗
PubMed1997

Transitions in individuality.

The evolution of multicellular organisms is the premier example of the integration of lower levels into a single, higher-level individual. Explaining the evolutionary transition from single cells to multicellular organisms is a major challenge for evolutionary theory. We provide an explicit two locus genetic framework for understanding this transition in terms of the increase of cooperation among cells and the regulation of conflict within the emerging organism. Heritability of fitness and individuality at the new level emerge as a result of the evolution of organismal functions that restrict the opportunity for conflict within and ensure cooperation among cells. Conflict leads, through the evolution of adaptations that reduce it, to greater individuality and harmony for the organism.

Adaptation, Physiological↗
PubMed1996

Cooperation and conflict in the evolution of individuality. II. Conflict mediation.

Evolutionary transitions in the units of selection require the promotion of cooperation and the regulation of conflict among the lower level units. For multicellular organisms to emerge as a new unit of selection, the selfish tendencies of their component cells had to be controlled. Theoretical results indicate organisms may regulate this internal conflict and competition in several ways: by reducing the somatic mutation rate, by sequestering cells in a germ line and by directly reducing the benefits to cell of defecting.

Animals↗
PubMed1995

Invading wave of cooperation in a spatial iterated prisoner's dilemma.

Explaining the emergence of cooperative behaviours in a selfish world remains a major challenge for sociobiology. The iterated prisoner's dilemma offers a well-studied metaphor with which to explore theoretically the evolution of cooperation by reciprocation. Our current understanding is that 'tit-for-tat' should be the very first step (if not the aim) of evolution towards cooperation, but that mobility of the players in space seems to raise a devastating obstacle to the spread of tit-for-tat, by allowing egoists to exploit cooperation and escape retaliation. The second point is based on models that represent mobility only implicitly (in terms of travelling costs) and assume random interactions. Here we develop a more explicit theory of spatial iterated games: individual mobility is represented in terms of a diffusion process and interactions--defined locally--are inherently non-random. Our model reveals the existence of critical levels of individual mobility allowing for the evolution of cooperation. In fact, tit-for-tat can spread and take over among mobile players even when originating from extreme rarity. The dynamics of invasion of tit-for-tat develop as a travelling wave which propagates the cooperative strategy through space. Significant mobility is required to make the pioneering moves of cooperators towards the front of invasion less hazardous; it also contributes to neutralizing those defectors who may intrude the core of a cluster of cooperative players.

Game Theory↗
PubMed1995

Origin of sex for error repair. I. Sex, diploidy, and haploidy.

Genetic damage is a fundamental problem for living systems. Recombination can repair a damaged gene, so long as there is an undamaged copy of the gene available in the cell. This requires that the cell be diploid for the damaged locus. During sex, outcrossing generates the diploid state by temporarily fusing two haploid cells (as in the case of meiosis) or by bringing DNA into the cell from outside (as in the case of bacterial transformation). But why should cells alternate between the haploid and diploid states in the first place? Why not just remain diploid, if damage repair is the only problem for a cell? The goal of our work is to understand if the problem of genetic damage would select for diploidy or for the alternation between diploid and haploid states--that is, sex--early in the history of life. Using mathematical models we study competition between asexual haploids (termed "haploids"), sexuals (termed "sexuals"), and asexual diploids (termed "diploids"). Haploid cells are efficient replicators, while diploid cells are resistant to damage. A sexual may combine the advantages of both: spending much of its life cycle in the haploid state, then temporarily fusing to become diploid, followed by splitting to the haploid state. During the diploid state DNA damage can be repaired, since there are two copies of the gene in the cell and one copy is presumed to be undamaged. We describe the competition in terms of mathematical models, employing five rate parameters which represent the life processes of cells most probably active at the time that sexuality arose: birth and death; genomic damage (for the haploids alone); and, for the sexual cell, fusion and splitting. Parameter space bifurcation diagrams for the equilibria are drawn in the three-dimensional space of damage, splitting, and fusion, and solutions of the equations (i.e., the outcomes of the competition) are described in terms of them. It turns out that those three parameters suffice to give an essentially complete description of the qualitative behavior possible, since one parameter can be scaled out of the equations we ultimately consider, and the other permits generic analysis, for the range of parameter values of interest, at a fixed value of that parameter. Each type of cell has a region of the parameter space that it occupies exclusively (given its initial presence in the competition). The haploid can win only in environments characterized by low damage (relative to mortality), while the diploid can win only in environments characterized by high damage (relative to mortality).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Origin of sex for error repair. II. Rarity and extreme environments.

In a previous paper we studied the simultaneous, and at times conflicting, needs of coping with DNA damage, efficient cell replication, and the avoidance of cell mortality. These selective factors operated on sexual and asexual haploid and diploid populations that were reproductively isolated from one another. We concluded, in part, that a sexual type of cell could not expand from extreme rarity in populations dominated by asexual haploid and diploid cells. In the present paper we show that it is relatively easy for a rare sexual mutant to expand in a population dominated by asexual haploid cells if some matings occur between sexual and asexual cell types. We also study the persistence of sex in high mortality, high damage environments, in which neither the asexual diploid nor haploid can survive. The diploid cannot survive because its lower birth rate cannot overcome mortality and the haploid cannot survive because its birth rate cannot overcome gene damage. Sex can persist in these punishing environments by tuning the parameters of the sexual cycle, and the fusion and splitting rates, into a specified region, thereby reaping both benefits of damage repair and efficient replication.

Animals↗
PubMed1991

DNA repair and the evolution of transformation in Bacillus subtilis. III. Sex with damaged DNA.

Natural genetic transformation in the bacterium Bacillus subtilis provides an experimental system for studying the evolutionary function of sexual recombination. The repair hypothesis proposes that during transformation the exogenous DNA taken up by cells is used as template for recombinational repair of damages in the recipient cell's genome. Earlier results demonstrated that the population density of transformed cells (i.e., sexual cells) increases, relative to nontransformed cells (primarily asexual cells), with increasing dosage of ultraviolet irradiation, provided that the cells are transformed with undamaged homologous DNA after they have become damaged. In nature, however, donor DNA for transformation is likely to come from cells that are as damaged as the recipient cells. In order to better simulate the effects of transformation in natural populations we conducted similar experiments as those just described using damaged donor DNA. We document in this report that transformants continue to increase in relative density even if they are transformed with damaged donor DNA. These results suggest that sites of transformation are often damaged sites in the recipient cell's genome.

Bacillus subtilis↗
PubMed1989

DNA repair and the evolution of transformation in Bacillus subtilis. II. Role of inducible repair.

In Bacillus subtilis, DNA repair and recombination are intimately associated with competence, the physiological state in which the bacterium can bind, take up and recombine exogenous DNA. Previously, we have shown that the homologous DNA transformation rate (ratio of transformants to total cells) increases with increasing UV dosage if cells are transformed after exposure to UV radiation (UV-DNA), whereas the transformation rate decreases if cells are transformed before exposure to UV (DNA-UV). In this report, by using different DNA repair-deficient mutants, we show that the greater increase in transformation rate in UV-DNA experiments than in DNA-UV experiments does not depend upon excision repair or inducible SOS-like repair, although certain quantitative aspects of the response do depend upon these repair systems. We also show that there is no increase in the transformation rate in a UV-DNA experiment when repair and recombination proficient cells are transformed with nonhomologous plasmid DNA, although the results in a DNA-UV experiment are essentially unchanged by using plasmid DNA. We have used din operon fusions as a sensitive means of assaying for the expression of genes under the control of the SOS-like regulon in both competent and noncompetent cell subpopulations as a consequence of competence development and our subsequent experimental treatments. Results indicate that the SOS-like system is induced in both competent and noncompetent subpopulations in our treatments and so should not be a major factor in the differential response in transformation rate observed in UV-DNA and DNA-UV treatments. These results provide further support to the hypothesis that the evolutionary function of competence is to bring DNA into the cell for use as template in the repair of DNA damage.

Bacillus subtilis↗
PubMed1988

The effect of the reproductive system on mutation load.

J. B. S. Haldane (Amer. Nat. 71, 337-349, 1937) argued that, in equilibrium populations, the effect of deleterious mutation on average fitness depends primarily on the mutation rate and is independent of the severity of the mutations. Specifically, the equilibrium population fitness is e-microH, where microH is the haploid genomic mutation rate. Here we extend Haldane's result to a variety of reproductive systems. Using an analysis based on the frequency of classes of individuals with a specified number of mutations, we show that Haldane's principle holds exactly for haploid sex, haploid apomixis, and facultative haploid sex. In the cases of diploid automixis with terminal fusion, diploid automixis with central fusion, and diploid selfing, Haldane's principle holds exactly for recessive mutations and approximately for mutations with some heterozygous effect. In the cases of K-ploid apomixis, diploid endomitosis, and haplodiploidy, we show that Haldane's principle holds exactly for recessive lethal mutations. In addition we extend Haldane's result to various mixtures of the above-mentioned reproductive systems. In the case of diploid out-crossing sexuals, we do not obtain an exact analytic result, but present arguments and computer simulations which show that Haldane's result extends to this case as well in the limit as the number of loci becomes large. Although diverse reproductive systems are equally fit at equilibrium, different reproductive systems harbor vastly different numbers of recessive genes at equilibrium and we provide estimates of these numbers. These different numbers of mutations may create transient selective pressures on individuals with reproductive systems different from that of the equilibrium population.

Animals↗
PubMed1988

DNA repair and the evolution of transformation in the bacterium Bacillus subtilis.

The purpose of the work reported here is to test the hypothesis that natural genetic transformation in the bacterium Bacillus subtilis has evolved as a DNA repair system. Specifically, tests were made to determine whether transformation functions to provide DNA template for the bacteria] cell to use in recombinational repair. The survivorship and the homologous transformation rate as a function of dose of ultraviolet irradiation (UV) was studied in two experimental treatments, in which cells were either transformed before (DNA-UV), or after (UV-DNA), treatment with UV. The results show that there is a qualitative difference in the relationship between the survival of transformed cells (sexual cells) and total cells (primarily asexual cells) in the two treatments. As predicted by the repair hypothesis, in the UV-DNA treatment, transformed cells had greater average survivorship than total cells, while in the DNA-UV treatment this relationship was reversed. There was also a consistent and qualitative difference between the UV-DNA and DNA-UV treatments in the relationship between the homologous transformation rate (transformed cells/total cells) and UV dosage. As predicted by the repair hypothesis, the homologous transformation rate increases with UV dose in the UV-DNA experiments but decreases with UV dose in the DNA-UV treatments. However, the transformation rate for plasmid DNA does not increase in a UV-DNA treatment. These results support the DNA repair hypothesis for the evolution of transformation in particular, and sex generally.

Bacillus subtilis↗
PubMed1987

The molecular basis of the evolution of sex.

Traditionally, sexual reproduction has been explained as an adaptation for producing genetic variation through allelic recombination. Serious difficulties with this explanation have led many workers to conclude that the benefit of sex is a major unsolved problem in evolutionary biology. A recent informational approach to this problem has led to the view that the two fundamental aspects of sex, recombination and outcrossing, are adaptive responses to the two major sources of noise in transmitting genetic information, DNA damage and replication errors. We refer to this view as the repair hypothesis, to distinguish it from the traditional variation hypothesis. On the repair hypothesis, recombination is a process for repairing damaged DNA. In dealing with damage, recombination produces a form of informational noise, allelic recombination, as a by-product. Recombinational repair is the only repair process known which can overcome double-strand damages in DNA, and such damages are common in nature. Recombinational repair is prevalent from the simplest to the most complex organisms. It is effective against many different types of DNA-damaging agents, and, in particular, is highly efficient in overcoming double-strand damages. Current understanding of the mechanisms of recombination during meiosis suggests that meiosis is designed for repairing DNA. These considerations form the basis for the first part of the repair hypothesis, that recombination is an adaptation for dealing with DNA damage. The evolution of sex can be viewed as a continuum on the repair hypothesis. Sex is presumed to have arisen in primitive RNA-containing protocells whose sexual process was similar to that of recombinational repair in extent segmented, single-stranded RNA viruses, which are among the simplest known organisms. Although this early form of repair occurred by nonenzymatic reassortment of replicas of undamaged RNA segments, it evolved into enzyme-mediated breakage and exchange between long DNA molecules. As some lines of descent became more complex, their genome information increased, leading to increased vulnerability to mutation. The diploid stage of the sexual cycle, which was at first transient, became the predominant stage in some lines of descent because it allowed complementation, the masking of deleterious recessive mutations. Out-crossing, the second fundamental aspect of sex, is also maintained by the advantage of masking mutations. However, outcrossing can be abandoned in favor of parthenogenesis or selfing under conditions in which the costs of mating are very high.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Sex and the emergence of species.

We argue that the existence of species as distinct and relatively homogeneous groupings of individuals is a consequence of the nonlinear dynamics inherent in sexual reproduction. This approach provides an answer to two interrelated problems which Darwin posed and tried to solve. Why are there missing links (i.e. gaps) between species in habitat space, and why are there missing links between species in time as evidenced in the fossil record? A crucial difference between outcrossing sexual organisms (i.e. organisms in which mating is between different individuals) and obligate selfers or parthenogens lies in the dynamic of the underlying replication process. Replication is a linear function of density for obligate selfers or parthenogens but nonlinear for outcrossing sexuals. The non-linearity stems from the simple fact that with outcrossing, two individuals must come together to mate. We argue that this fact leads to density dependent fitness (per capita rate of increase) with an intrinsic disadvantage of low population density. This cost of rarity results in a distribution of distinct species. By establishing the causal connections in evolution between outcrossing sex and the very existence of species as distinct collections of organisms, our account lends theoretical support to a unitary concept of species with interbreeding as the fundamental defining property.

Adaptation, Physiological↗
PubMed1985

Genetic damage, mutation, and the evolution of sex.

The two fundamental aspects of sexual reproduction, recombination and outcrossing, appear to be maintained respectively by the advantages of recombinational repair and genetic complementation. Genetic variation is produced as a by-product of recombinational repair, but it may not be the function of sexual reproduction.

Animals↗
PubMed1985

The evolutionary role of recombinational repair and sex.

We have argued that sexual reproduction arose very early in the evolution of life as a way of overcoming informational damage or loss through recombinational repair. As organisms became more complex and genome information content expanded, diploidy, at first transient, became the predominant way of coping with increased vulnerability to mutation. This allowed further genome expansion. Once such expansion had occurred, however, diploidy became essentially irreversible, since reversion to haploidy would lead to expression of accumulated deleterious recessive alleles. This expression of recessive alleles also imposes a stiff penalty on organisms that experiment with close inbreeding forms of recombinational repair. A consequence of sex is that fitness (defined as per capita rate of increase) is density dependent. At low population density, fitness declines due to increased costs of finding a mate. This fundamental constraint on population increase can inhibit evolutionary success of the best adapted species if it is small in numbers. Sexual reproduction also tends to eliminate new coadapted genotypes within a species by breaking up their coadapted gene complexes; this also contributes to the cohesion of species. In general, we think the existence of species and their characteristic cohesion and stability over time are direct consequences of sex; and sex in turn is a consequence of the need to overcome gene damage through recombinational repair while at the same time masking the deleterious effects of mutation.

Animals↗
PubMed1984

Origin of sex.

The competitive advantage of sex consists in being able to use redundancy to recover lost genetic information while minimizing the cost of redundancy. We show that the major selective forces acting early in evolution lead to RNA protocells in which each protocell contains one genome, since this maximizes the growth rate. However, damages to the RNA which block replication and failure of segregation make it advantageous to fuse periodically with another protocell to restore reproductive ability. This early, simple form of genetic recovery is similar to that occurring in extant segmented single stranded RNA viruses. As duplex DNA became the predominant form of the genetic material, the mechanism of genetic recovery evolved into the more complex process of recombinational repair, found today in a range of species. We thus conclude that sexual reproduction arose early in the evolution of life and has had a continuous evolutionary history. We cite reasons to reject arguments for gaps in the evolutionary sequence of sexual reproduction based on the presumed absence of sex in the cyanobacteria. Concerning the maintenance of the sexual cycle among current organisms, we take care to distinguish between the recombinational and outbreeding aspects of the sexual cycle. We argue that recombination, whether it be in outbreeding organisms, self-fertilizing organisms or automictic parthenogens, is maintained by the advantages of recombinational repair. We also discuss the role of DNA repair in maintaining the outbreeding aspects of the sexual cycle.

Biological Evolution↗