Biology subjects

De Monte, S.

Publications and source records attributed to De Monte, S..

7 recordsLinked to original sources

bioRxiv2024

Interplay of structured and random interactions in many-species ecological dynamics

Minimal models for complex ecosystems often assume random interactions, whose statistics suffice to predict dynamical and macroecological patterns. However, ecological networks commonly possess a variety of properties, such as hierarchies or functional groups, that structure species interactions. Here, we ask how conclusions from random interaction models are altered by the presence of such community-level network structures. We consider a Lotka-Volterra model where pairwise species interactions combine structure and randomness, and study macroscopic community-level observables, abundance distributions and dynamical regimes. Randomness and structure combine in a surprisingly yet deceptively straightforward way: contributions from each component to community patterns are largely independent. Yet, their interplay has non-trivial consequences, notably out of equilibrium. We conclude that whether interaction structure matters depends on the pattern: when breaking species equivalence, static patterns of species presence and abundance predicted from random interaction models are less robust than the qualitative nature of dynamical regimes. Author summaryEcological communities with many species are a challenge for theoretical ecology, since they harbour many and very diverse interactions. A common approach is to focus on aggregated quantities, such as the abundance of broad taxonomic or functional groups, thus neglecting all the diversity at finer scales. We develop a theoretical framework that combines both ecological structure and fine-grained heterogeneity, which we represent with randomness. We find that structure and randomness contribute to ecosystem properties with effects that can be largely disentangled, allowing a continuous transition between two simple effective descriptions of the community dynamics. Still, they interact in unexpected ways. For instance, we show that species heterogeneity can simplify the dynamics of functional groups, countering the idea that complexity should always destabilize large ecosystems. Data availability statement: The source code used to produce the results and analyses presented in this manuscript is freely available at the GitHub repository: https://github.com/juanelogiral/interplay-structure-randomness.git

ecology↗

bioRxiv2022

Single-cell phenotypic plasticity modulates social behaviour in Dictyostelium discoideum.

In Dictyostelium chimeras, strains social behaviour is defined based on their relative representation in the spores - the reproductive cells resulting from development - referred to as spore bias. Some strains, called cheaters, display systematically positive spore bias in chimeras and are considered a threat to the evolutionary stability of multicellular organization. The selective advantage gained by cheaters is indeed predicted to undermine collective functions whenever social behaviours are genetically determined. However, genotypes are not the only determinant of spore bias, and the relative role of genetic and plastic phenotypic differences in strains evolutionary success is unclear. Here, we control phenotypic heterogeneity by harvesting cells in different growth phases, and study the effects of plastic variation on spore bias in chimeras composed of isogenic or genetically different populations. Spore bias is shown to depend both on growth phase and on population composition, and to be negatively correlated to the fraction of loners, i.e. cells that do not join aggregates. We examined several single-cell mechanical properties that are expected to affect aggregation efficiency, and found that variations in the fraction of slowly moving cells with growth phase may explain why earlier cultures appear to be underrepresented in the spores. The involvement of a go-or-grow mechanism during cell aggregation is also consistent with known variations of cell-cycle phase distribution during population growth. We confirm the expected ubiquity of growth-phase induced spore bias variation by showing that it is not negligible in genetic chimeras, and can even reverse the classification of a strains social behaviour. These results suggest that aggregation can provide an efficient lottery system to harness the evolutionary spread of cheaters.

evolutionary biology↗

bioRxiv2021

Evolving social behaviour through selection of single-cell adhesion in Dictyostelium discoideum

The social amoeba Dictyostelium discoideum commonly forms chimeric fruiting bodies. Genetic variants that produce a higher proportion of spores are predicted to undercut multicellular organization unless cooperators assort positively. Cell adhesion is considered a primary factor driving such assortment, but evolution of adhesion has not been experimentally connected to changes in social performance. We modified by experimental evolution the efficiency of individual cells in attaching to a surface. Surprisingly, evolution appears to have produced social cooperators irrespective of whether stronger or weaker adhesion was selected. Quantification of reproductive success, cell-cell adhesion and developmental patterns, however, revealed two distinct social behaviours, as captured when the classical metric for social success is generalized by considering clonal spore production. Our work shows that cell mechanical interactions can constrain evolution of development and sociality in chimeras, and that elucidation of proximate mechanisms is necessary in order to understand the ultimate emergence of multicellular organization.

evolutionary biology↗

bioRxiv2019

Eco-evolutionary dynamics of nested Darwinian populations and the emergence of community-level heredity

Interactions among microbial cells can generate new chemistries and functions, but exploitation requires establishment of communities that reliably recapitulate community-level phenotypes. Using mechanistic mathematical models, we show how simple manipulations to population structure can exogenously impose Darwinian-like properties on communities. Such scaffolding causes communities to participate directly in the process of evolution by natural selection and drives the evolution of cell-level interactions to the point where, despite underlying stochasticity, derived communities give rise to offspring communities that faithfully re-establish parental phenotype. The mechanism is akin to a developmental process (developmental correction) that arises from density dependent interactions among cells. Knowledge of ecological factors affecting evolution of developmental correction has implications for understanding the evolutionary origin of major egalitarian transitions, symbioses, and for top-down engineering of microbial communities.

evolutionary biology↗

bioRxiv2019

Intracellular AIEC LF82 relies on SOS and stringent responses to survive, multiply and tolerate antibiotics.

Adherent Invasive Escherichia coli (AIEC) strains recovered from Crohn's disease lesions survive and multiply within macrophages. A reference strain for this pathovar, AIEC LF82, forms microcolonies within phagolysosomes, an environment that prevents commensal E. coli multiplication. Little is known about the LF82 intracellular growth status, and signals leading to macrophage intra-vacuolar multiplication. We used single-cell analysis, genetic dissection and mathematical models to monitor the growth status and cell cycle regulation of intracellular LF82. We found that within macrophages, bacteria may replicate or undergo non-growing phenotypic switches. This switch results from stringent response firing immediately after uptake by macrophages or at later stages, following genotoxic damage and SOS induction during intracellular replication. Importantly, non-growers resist treatment with various antibiotics. Thus, intracellular challenges induce AIEC LF82 phenotypic heterogeneity and non-growing bacteria that could provide a reservoir for antibiotic-tolerant bacteria responsible for relapsing infections.

microbiology↗

bioRxiv2018

Ubiquitous abundance distribution of non-dominant plankton across the world’s ocean

Species Abundance Distributions (SADs) bear the imprint of ecological processes that shape biological communities, and are therefore used to discriminate among different scenarios of community assembly. Even though empirical distributions appear to follow a handful of qualitative laws, it is still unclear if and how quantitative variation in SADs reflects peculiar features of the communities and their environmental context. Here, we use the extensive dataset generated by the Tara Oceans expedition for marine microbial eukaryotes (protists) and an adaptive algorithm to explore how SADs vary across plankton communities in the global ocean. We show that the decay in abundance of non-dominant OTUs, comprising over 99% of local richness, is commonly governed by a power-law. The power-law exponent varies by less than 10% across locations and shows no biogeographical signature, but is weakly modulated by cell size. Our findings suggest that large-scale ubiquitous ecological processes govern the assembly of non-dominant plankton throughout the global ocean.

ecology↗

bioRxiv2018

Pyrimidine starvation activates a bistable phenotypic switch leading to ribosome provisioning and rapid exit from stationary phase

Observations of bacteria at the single-cell level have revealed many instances of phenotypic heterogeneity within otherwise clonal populations, but the selective causes, molecular bases and broader ecological relevance remain poorly understood. In an earlier experiment in which the bacterium Pseudomonas fluorescens SBW25 was propagated under a selective regime that mimicked the host immune response, a genotype evolved that stochastically switched between capsulation states. The genetic cause was a mutation in carB that decreased the pyrimidine pool (and growth rate), lowering the activation threshold of a pre-existing but hitherto unrecognised phenotypic switch. Genetic components surrounding bifurcation of UTP flux towards DNA/RNA or UDP-glucose (a precursor of colanic acid forming the capsules) were implicated as key components. Extending these molecular analyses - and based on a combination of genetics, transcriptomics, biochemistry and mathematical modelling - we show that pyrimidine limitation triggers an increase in ribosome biosynthesis and that switching is caused by competition between ribosomes and CsrA/RsmA proteins for the mRNA transcript of a feed-forward regulator of colanic acid biosynthesis. We additionally show that in the ancestral bacterium the switch is part of a programme that determines stochastic entry into the semi-quiescent capsulated state, ensures that such cells are provisioned with excess ribosomes, and enables provisioned cells to exit rapidly from stationary phase under permissive conditions.

microbiology↗