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De Monte, S.

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

2 recordsLinked to original sources

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

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