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Traulsen, A.

Publications and source records attributed to Traulsen, A..

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Stochastic population dynamics driven by mutant interactors

Spontaneous random mutations are an important source of variation in populations. Many evolutionary models consider mutants with a fixed fitness chosen from a certain fitness distribution without considering any interactions among the residents and mutants. Here, we go beyond this and consider \"mutant interactors\", which lead to new interactions between the residents and invading mutants that can affect the carrying capacity and the extinction risk of populations. We model microscopic interactions between individuals by using a dynamical payoff matrix and analyze the stochastic dynamics of such populations. New interactions drawn from invading mutants can drive the population away from the previous equilibrium, and lead to changes in the population size -- the population size is an evolving property rather than a fixed number or externally controlled variable. We present analytical results for the average population size over time and quantify the extinction risk of the population by the mean time to extinction.

evolutionary biology

The Neutral Metaorganism

Almost all animals and plants are inhabited by diverse communities of microorganisms, the microbiota. The hosts often pose highly selective environments, which only a subset of the environmentally available microbes are able to colonize. From the hosts perspective it seems useful to shape the community composition of these allowed microbes to promote a beneficial host-microbe symbiosis. In contrast to this, neutral models assume that the structure of the microbiota is entirely shaped by random population dynamics and dispersal. We here show that microbiota community structure from a wide range of host organisms, in particular including previously understudied invertebrates, is in almost all cases consistent with neutral expectations. Moreover, we demonstrate that apparent discrepancies with the neutral model can be due to transient community states rather than host selection. In conclusion, even though hosts are often assumed to control microbiota composition to ensure beneficial interactions, our broad-scale analysis highlights that following colonization, it could rather be neutral processes that determine microbial community structure.

ecology

Reproduction costs can drive the evolution of groups

A fascinating wealth of life cycles is observed in biology, from unicellularity to the concerted fragmentation of multi-cellular units. However, the understanding of factors driving the evolution of life cycles is still limited. We investigate how reproduction costs influence this process. We consider a basic model of a group structured population of undifferentiated cells, where groups reproduce by fragmentation. Fragmentation events are associated with a cost expressed by either a fragmentation delay, a fragmentation risk, or a fragmentation loss. The introduction of such fragmentation costs vastly increases the set of potentially optimal life cycles. Based on these findings, we suggest that the evolution of life cycles and the splitting into multiple offspring can be directly associated with the fragmentation cost. Moreover, the impact of this cost alone is strong enough to drive the emergence of multicellular groups, even under scenarios that strongly disfavour groups compared to solitary individuals.

evolutionary biology

Replicative cellular age distributions in compartmentalised tissues

The cellular age distribution of hierarchically organized tissues can reveal important insights into the dynamics of cell differentiation and self-renewal and associated cancer risks. Here, we examine theoretically the effect of progenitor compartments with varying differentiation and self-renewal capacities on the resulting observable distributions of replicative cellular ages. We find that strongly amplifying progenitor compartments, i.e. compartments with high self-renewal capacities, substantially broaden the age distributions which become skewed towards younger cells with a long tail of few old cells. However, since mutations predominantly accumulate during cell division, a few old cells may considerably increase cancer risk. In contrast, if tissues are organised into many downstream compartments with low self-renewal capacity, the shape of the replicative cell distributions in more differentiated compartments are dominated by stem cell dynamics with little added variation. In the limiting case of a strict binary differentiation tree without self-renewal, the shape of the output distribution becomes indistinguishable from the shape of the input distribution. Our results suggest that a comparison of cellular age distributions between healthy and cancerous tissues may inform about dynamical changes within the hierarchical tissue structure, i.e. an acquired increased self-renewal capacity in certain tumours.

evolutionary biology

Temperate phages as frequency-dependent weapons in bacterial competition

Microbial communities are accompanied by a diverse array of viruses. Through infections of abundant microbes, these viruses have the potential to mediate competition within the community, effectively weakening competitive interactions and promoting coexistence. This is of particular relevance for host-associated microbial communities, since the diversity of the microbiota has been linked to host health and functioning. Here, we study the interaction between two key members of the microbiota of the freshwater metazoan Hydra vulgaris. The two commensal bacteria Curvibacter sp. and Duganella sp. protect their host from fungal infections, but only if both of them are present. Coexistence of the two bacteria is thus beneficial for Hydra. Intriguingly, Duganella sp. appears to be the superior competitor in vitro due to its higher growth rate when both bacteria are grown seperately, but in coculture the outcome of competition depends on the relative initial abundances of the two species. The presence of an inducible prophage in the Curvibacter sp. genome which is able to lytically infect Duganella sp., led us to hypothesise that the phage modulates the interaction between these two key members of the Hydra microbiota. Using a mathematical model we show that the interplay of the lysogenic life-cycle of the Curvibacter phage and the lytic life-cycle on Duganella sp. can explain the observed complex competitive interaction between the two bacteria. Our results highlight the importance of taking lysogeny into account for understanding microbe-virus interactions and show the complex role phages can play in promoting coexistence of their bacterial hosts.

microbiology

Social Dilemma In The External Immune System Of The Red Flour Beetle? It Is A Matter Of Time

Sociobiology has revolutionized our understanding of interactions between organisms. Interactions may present a social dilemma where the interests of individual actors do not align with those of the group as a whole. Viewed through a sociobiological lens, nearly all interactions can be described in terms of their costs and benefits and a number of them then resemble a social dilemma. Numerous experimental systems, from bacteria to mammals, have been proposed as models for studying such dilemmas. Here we make use of the external immune system of the red flour beetle, Tribolium castaneum, to investigate how the experimental duration can affect whether the external secretion comprises a social dilemma or not. Some beetles (secretors) produce a costly quinone-rich external secretion that inhibits microbial growth in the surrounding environment, providing the secretors with direct personal benefits. However, since the antimicrobial secretion acts in the environment of the beetle it is potentially also advantageous to other beetles (non-secretors), who avoid the cost of producing the secretion. We test experimentally if the secretion qualifies as a public good. We find that in the short term, costly quinone secretion can be interpreted as a public good presenting a social dilemma where the presence of secretors increases the fitness of the group. In the long run, the benefit to the group of having more secretors vanishes and actually becomes detrimental to the group. Therefore, in such semi-natural environmental conditions, it turns out that qualifying a trait as social can be a matter of timing.

evolutionary biology

Fragmentation Modes And The Evolution Of Life Cycles

Reproduction is a defining feature of living systems. To reproduce, aggregates of biological units (e.g., multicellular organisms or colonial bacteria) must fragment into smaller parts. Fragmentation modes in nature range from binary fission in bacteria to collective-level fragmentation and the production of unicellular propagules in multicellular organisms. Despite this apparent ubiquity, the adaptive significance of fragmentation modes has received little attention. Here, we develop a model in which groups arise from the division of single cells that do not separate but stay together until the moment of group fragmentation. We allow for all possible fragmentation patterns and calculate the population growth rate of each associated life cycle. Fragmentation modes that maximise growth rate comprise a restrictive set of patterns that include production of unicellular propagules and division into two similar size groups. Life cycles marked by single-cell bottlenecks maximise population growth rate under a wide range of conditions. This surprising result offers a new evolutionary explanation for the widespread occurrence of this mode of reproduction. All in all, our model provides a framework for exploring the adaptive significance of fragmentation modes and their associated life cycles.\n\nAuthor SummaryMode of reproduction is a defining trait of all organisms, including colonial bacteria and multicellular organisms. To produce offspring, aggregates must fragment by splitting into two or more groups. The particular way that a given group fragments defines the life cycle of the organism. For instance, insect colonies can reproduce by splitting or by producing individuals that found new colonies. Similarly, some colonial bacteria propagate by fission or by releasing single cells, while others split in highly sophisticated ways; in multicellular organisms reproduction typically proceeds via a single cell bottleneck phase. The space of possibilities for fragmentation is so vast that an exhaustive analysis seems daunting. Focusing on fragmentation modes of a simple kind we parametrise all possible modes of group fragmentation and identify those modes leading to the fastest population growth rate. Two kinds of life cycle dominate: one involving division into two equal size groups, and the other involving production of a unicellular propagule. The prevalence of these life cycles in nature is consistent with our null model and suggests that benefits accruing from population growth rate alone may have shaped the evolution of fragmentation mode.

evolutionary biology

Discovering Complete Quasispecies In Bacterial Genomes

Mobile genetic elements can be found in almost all genomes. Possibly the most common non-autonomous mobile genetic elements in bacteria are REPINs that can occur hundreds of times within a genome. The sum of all REPINs within a genome are an evolving populations because they replicate and mutate. We know the exact composition of this population and the sequence of each member of a REPIN population, in contrast to most other biological populations. Here, we model the evolution of REPINs as quasispecies. We fit our quasispecies model to ten different REPIN populations from ten different bacterial strains and estimate duplication rates. We find that our estimated duplication rates range from about 5 x 10-9 to 37 x 10-9 duplications per generation per genome. The small range and the low level of the REPIN duplication rates suggest a universal trade-off between the survival of the REPIN population and the reduction of the mutational load for the host genome. The REPIN populations we investigated also possess features typical of other natural populations. One population shows hallmarks of a population that is going extinct, another population seems to be growing in size and we also see an example of competition between two REPIN populations.

evolutionary biology

Ribosome reinitiation can explain length-dependent translation of messenger RNA

Models of mRNA translation usually presume that transcripts are linear; upon reaching the end of a transcript each terminating ribosome returns to the cytoplasmic pool before initiating anew on a different transcript. A consequence of linear models is that faster translation of a given mRNA is unlikely to generate more of the encoded protein, particularly at low ribosome availability. Recent evidence indicates that eukaryotic mRNAs are circularized, potentially allowing terminating ribosomes to preferentially reinitiate on the same transcript. Here we model the effect of ribosome reinitiation on translation and show that, at high levels of reinitiation, protein synthesis rates are dominated by the time required to translate a given transcript. Our model provides a simple mechanistic explanation for many previously enigmatic features of eukaryotic translation, including the negative correlation of both ribosome densities and protein abundance on transcript length, the importance of codon usage in determining protein synthesis rates, and the negative correlation between transcript length and both codon adaptation and 5' mRNA folding energies. In contrast to linear models where translation is largely limited by initiation rates, our model reveals that all three stages of translation - initiation, elongation, and termination/reinitiation - determine protein synthesis rates even at low ribosome availability.

molecular biology