Biology subjects

van Dijk, B.

Publications and source records attributed to van Dijk, B..

10 recordsLinked to original sources

bioRxiv2026

Spatial structure drives the evolution of parasites into host defense systems

Host defense systems in prokaryotes and eukaryotes often appear to be derived from the very parasites they now defend against, yet the evolutionary route for such a transition remains poorly understood. Based on the biology of integrating viruses such as temperate bacteriophages and retroviruses, we develop a multilevel eco-evolutionary framework in which within-host viral replication is treated as a public goods game over a costly, shared replication product. In well-mixed host populations, we predict convergence on a single viral strategy of intermediate replicative investment. However, when we impose spatial structure by restricting host reproduction and virus transmission to local events, the virus population diversifies into two lineages: a horizontally transmitted lineage that parasitises hosts, and a vertically transmitted hyperparasitic lineage that parasitises the horizontally transmitting viruses. The latter "hyperparasite" is a viral cheat that suppresses the replication and propagation of the parasitic virus, thereby acting as a defense system to the hosts. Local interactions concentrate the benefits of this suppression among neighbouring hosts that carry related proviruses, allowing selection on the proviral cheat as a host-level defense. Our results show that evolutionary cheating within parasite populations can drive the evolution of parasites into defense systems in spatially structured host populations.

evolutionary biology↗

bioRxiv2025

Spatial structure and differential gene dispersal explains the evolutionary association of accessory genes with prophages

Genes encoding for virulence factors are frequently found on prophages, yet the evolutionary forces driving this association remain unclear. The evolutionary association of mobile genetic elements (MGEs) with host-beneficial genes is known to be hindered by the stability of chromosomal loci and competition with MGEs lacking accessory genes. Using a mathematical model that incorporates these constraints, we identify two key mechanisms that help overcome them, resulting in the evolutionary linkage of accessory genes, like virulence genes, to prophages. First, we show that migration across bacterial populations favours the association of genes with prophages when the gene is beneficial in certain environments (e.g. virulence genes in the gut) that also trigger higher rates of prophage induction. Second, we show that within-population spatial dynamics also promotes the association of weakly selected genes and phages. Here, virion dispersal allows phage-encoded genes to spread into patches of bacteria lacking the gene, giving them a selective advantage over immobile chromosomal genes. We argue that these mechanisms are less applicable for plasmids and other MGEs, highlighting a potentially unique role for phages in shaping bacterial adaptation. By demonstrating how phage lifecycle dynamics and spatial heterogeneity drive MGE-gene associations, our work provides new insights into the evolution of phage-encoded virulence.

evolutionary biology↗

bioRxiv2024

REPORTH: Determining orthologous locations of repetitive sequences between genomes

Repetitive sequences are a common feature of bacterial genomes. Some repetitive sequences such as REPINs are mobile within the genome but inherited only vertically from mother to daughter across bacterial genomes. Selfish elements in contrast are mobile within the genome but also travel horizontally from genome to genome. Yet, no matter the nature of the association between the repetitive elements and the host, it is difficult to study the evolutionary dynamics of repetitive sequences across genomes. If it is unclear whether two sequences in two different genomes are in orthologous positions, it is difficult to infer parameters like the replication rate, horizontal transfer rate and rate of loss. Here we present a tool to facilitate these analyses called REPORTH. REPORTH determines whether repetitive sequences in different but closely related bacterial genomes occur in orthologous genomic positions. Whether a position is orthologous or not depends on the orthology of flanking sequences. Flanking sequences are deemed orthologous if they are bidirectional best hits. All repetitive sequences that are found in orthologous positions across different genomes are grouped together. Analyses of these groups can be used to study the evolutionary dynamics of selfish repetitive elements such as insertion sequences, but also for mutualistic repetitive elements such as REPINs.

bioinformatics↗

bioRxiv2024

Interaction range of common goods shapes Black Queen dynamics beyond the cheater-cooperator narrative

Dependencies among microorganisms often appear mutualistic in the lab, as microbes grow faster together than alone. However, according to the Black Queen (BQ) hypothesis, these dependencies are underpinned by the evolutionary benefits from loss-of-function mutations when others in the community can supply the necessary common goods. BQ dynamics often describe a cheater-cooperator scenario, where some ecotypes, the "cheaters," produce no common goods and rely on others, the "cooperators", for survival. We have previously proposed that in systems with multiple common goods, an alternative endpoint for BQ dynamics can emerge. This endpoint describes an ecosystem of interdependent ecotypes engaging in "mutual cheating", i.e. where common good production is distributed. However, even with multiple goods the common good production can be centralized, i.e. with one ecotype providing all common goods for the ecosystem. Here, we present an eco-evolutionary model that reveals that BQ dynamics can result in both distributed- or centralized common good production. The interaction range, i.e. the number of beneficiaries a producer can support, distinguishes between these two endpoints. While many ecosystems evolve to be maximally distributed or maximally centralized, we also find intermediate ecosystems, where ecotypes that appear redundant are coexisting for long periods of time. Due to the limited interaction range, these redundant ecotypes are unable to distribute the production of common goods fully due to the presence of non-producing types. Despite non-producers thus stalling the division of labor, we observe that sudden structural shifts can occur that purge the non-producers from the ecosystem. Overall, our findings broaden the understanding of BQ dynamics, unveiling complex interactions beyond the simple cheater-cooperator narrative.

evolutionary biology↗

bioRxiv2024

Factors that influence the caste ratio in a bacterial division of labour

Colonies of the bacteria Streptomyces coelicolor divide labour between cells that specialize on growth and sporulation and cells that specialize on antibiotic production. This division of labour arises due to costly chromosome deletions in the antibiotic overproducers. However, little is known about when and where these mutations occur or whether their frequency - which we liken to the caste ratio in social insects - is phenotypically plastic. To elucidate changes in the proportions of specialized cells (measured as the mutation frequency), we sampled S. coelicolor colonies grown under different conditions. Temporally, mutation frequency increased linearly with colony age and size. Spatially, mutations accumulated disproportionately in the colony center, despite greater growth and sporulation at the periphery. Exposing colonies to sub-inhibitory concentrations of some antibiotics, a competitive cue in Streptomyces, increased mutation frequencies. Finally, direct competition with other Streptomyces that naturally produce antibiotics increased mutation frequencies, while also increasing spore production. Our findings provide insights into the intrinsic and environmental factors driving division of labor in Streptomyces colonies by showing that mutation frequencies are dynamic and responsive to the competitive environment. These results show that chromosome deletions are phenotypically plastic and suggest that Streptomyces can flexibly adjust their caste ratio.

evolutionary biology↗

bioRxiv2021

Evolution of genome fragility enables microbial division of labor

Division of labor can evolve when social groups benefit from the functional specialization of its members. Recently, a novel means of coordinating division of labor was found in the antibiotic-producing bacterium Streptomyces coelicolor, where functionally specialized cells are generated through large-scale genomic re-organization. Here, we investigate how the evolution of a genome architecture enables such mutation-driven division of labor, using a multi-scale mathematical model of bacterial evolution. We let bacteria compete on the basis of their antibiotic production and growth rate in a spatially structured environment. Bacterial behavior is determined by the structure and composition of their genome, which encodes antibiotics, growth-promoting genes and fragile genomic loci that can induce chromosomal deletions. We find that a genomic organization evolves that partitions growth-promoting genes and antibiotic-coding genes to distinct parts of the genome, separated by fragile genomic loci. Mutations caused by these fragile sites mostly delete growth-promoting genes, generating antibiotic-producing mutants from non-producing (and weakly-producing) progenitors, in agreement with experimental observations. Mutants protect their colony from competitors but are themselves unable to replicate. We further show that this division of labor enhances the local competition between colonies by promoting antibiotic diversity. These results show that genomic organization can co-evolve with genomic instabilities to enable reproductive division of labor. Motivation of current workDivision of labor can evolve if trade-offs are present between different traits. To organize a division of labor, the genome architecture must evolve to enable differentiated cellular phenotypes. Cell differentiation may be coordinated through gene regulation, as occurs during embryonic development. Alternatively, when mutation rates are high, mutations themselves can guide cell and functional differentiation; however, how this evolves and is organized at the genome level remains unclear. Here, using a model of antibiotic-producing bacteria based on multicellular Streptomyces, we show that if antibiotic production trades off with replication, genome architecture can evolve to support a mutation-driven division of labor. These results are consistent with recent experimental observations and may underlie division of labor in many bacterial groups.

evolutionary biology↗

bioRxiv2021

Transposable elements drive the evolution of genome streamlining

Eukaryotes and prokaryotes have distinct genome architectures, with marked differences in genome size, the ratio of coding/non-coding DNA, and the abundance of transposable elements (TEs). As TEs replicate independently of their hosts, the proliferation of TEs is thought to have driven genome expansion in eukaryotes. However, prokaryotes also have TEs in intergenic spaces, so why do prokaryotes have small, streamlined genomes? Using an in silico model describing the genomes of single-celled asexual organisms that co-evolve with TEs, we show that TEs acquired from the environment by horizontal gene transfer can drive the evolution of genome streamlining. The process depends on local interactions and is underpinned by rock-paper-scissor dynamics in which populations of cells with streamlined genomes beat TEs, which beat non-streamlined genomes, in continuous and repeating cycles. Streamlining is maladaptive to individual cells, but delivers lineage-level benefits. Streamlining does not evolve in sexually reproducing populations because recombination partially frees TEs from the deleterious effects they cause.

evolutionary biology↗

bioRxiv2021

Human monoclonal antibodies against Staphylococcus aureus surface antigens recognize in vitro biofilm and in vivo implant infections

Implant-associated Staphylococcus aureus infections are difficult to treat because of biofilm formation. Bacteria in a biofilm are often insensitive to antibiotics and host immunity. Monoclonal antibodies (mAbs) could provide an alternative approach to improve the diagnosis and/or treatment of biofilm-related infections. Here we show that mAbs targeting common surface components of S. aureus can recognize clinically relevant biofilm types. We identify two groups of antibodies: one group that uniquely binds S. aureus in biofilm state and one that recognizes S. aureus in both biofilm and planktonic state. In a mouse model, we show that mAb 4497 (recognizing wall teichoic acid (WTA)) specifically localizes to biofilm-infected implants. In conclusion, we demonstrate the capacity of several human mAbs to detect S. aureus biofilms in vitro and in vivo. This is an important first step to develop mAbs for imaging or treating S. aureus biofilms.

microbiology↗

bioRxiv2020

Nutrition or nature: disentangling the complex forces shaping prokaryote pan-genomes

Microbial pan-genomes are shaped by a complex combination of stochastic and deterministic forces. Even closely related genomes often exhibit extensive variation in their gene content. Understanding what drives this variation requires exploring the interactions of genes with each other and with their external environments. However, to date, conceptual models of pan-genome dynamics often represent genes as independent units and provide limited information about their mechanistic interactions. Here, we use pan-reactomes as proxies for pan-genomes since they can explicitly represent the interactions between the genes that code for metabolic reactions and simulate complex phenotypes that interact with the metabolic environment. We interpreted pan-reactomes as dynamic pools of metabolic reactions that are potentially gained or lost and simulated the routes along which different lineages lose reactions in alternative environments. We performed these simulations on the pan-reactomes of 46 bacterial and archaeal families covering a broad taxonomic range. These simulations allowed us to disentangle metabolic reactions whose presence does, and does not depend on the metabolite composition of the external environment, allowing us to identify reactions constrained "by nutrition" and "by nature", respectively. By comparing the frequency of reactions from the first group with their observed frequencies in bacterial and archaeal families, we predicted the metabolic niches that shaped the genomic composition of these lineages in their evolutionary past. Moreover, we found that the lineages that were shaped by a more diverse metabolic niche also occur in more diverse biomes as assessed by global environmental sequencing datasets. Together, we introduce a computational framework for analyzing and interpreting pan-reactomes that provides new insights into the ecological and evolutionary drivers of pan-genome composition.

evolutionary biology↗

bioRxiv2019

Anticipation of a serial transfer protocol through the evolution of fine-tuned growth dynamics

BackgroundExperimental evolution of microbes often involves a serial transfer protocol, where microbes are repeatedly diluted by transfer to a fresh medium, starting a new growth cycle. This protocol has revealed that evolution can be remarkably reproducible, where microbes show parallel adaptations both on the level of the phenotype as well as the genotype. However, these studies also reveal a strong potential for divergent evolution, leading to diversity both between and within replicate populations. We here study how in silico evolved Virtual Microbe "wild types" (WTs) adapt to a serial transfer protocol to investigate both the generic evolutionary adaptation to such an environment which are independent of prior evolution, and the variety of ways in which the adaptation is implemented at the individual and ecosystem level. ResultsWe show that all pre-evolved WTs evolve to anticipate the regularity of the serial transfer protocol by adopting a fine-tuned balance of growth and survival. We find that this anticipation can be done in a variety of ways, either by a single lineage or by several lineages in consort. Interestingly, replicate populations of the same WT initially show similar trajectories, but may subsequently diverge along a growth rate versus yield trade-off. ConclusionsWe find that all our in silico WTs show the same anticipation effects -- fitting the periodicity of a serial transfer protocol -- but do so by a variety of mechanisms. Our results reveal new insights into the dynamics and relevant selection pressures in experimental evolution, but also highlight how, in an eco-evolutionary context, numerous mechanisms can evolve to the same end.

evolutionary biology↗