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Emergence of evolutionary driving forces in pattern-forming microbial populations.

ABSTRACT: Evolutionary dynamics are controlled by a number of driving forces, such as natural selection, random genetic drift and dispersal. In this perspective article, we aim to emphasize that these forces act at the population level, and that it is a challenge to understand how they emerge from the stochastic and deterministic behaviour of individual cells. Even the most basic steric interactions between neighbouring cells can couple evolutionary outcomes of otherwise unrelated individuals, thereby weakening natural selection and enhancing random genetic drift. Using microbial examples of varying degrees of complexity, we demonstrate how strongly cell-cell interactions influence evolutionary dynamics, especially in pattern-forming systems. As pattern formation itself is subject to evolution, we propose to study the feedback between pattern formation and evolutionary dynamics, which could be key to predicting and potentially steering evolutionary processes. Such an effort requires extending the systems biology approach from the cellular to the population scale.This article is part of the theme issue 'Self-organization in cell biology'.

SUBMITTER: Kayser J

PROVIDER: S-EPMC5904294 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature

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Emergence of evolutionary driving forces in pattern-forming microbial populations.

Kayser Jona J Schreck Carl F CF Yu QinQin Q Gralka Matti M Hallatschek Oskar O

Philosophical transactions of the Royal Society of London. Series B, Biological sciences 20180501 1747

Evolutionary dynamics are controlled by a number of driving forces, such as natural selection, random genetic drift and dispersal. In this perspective article, we aim to emphasize that these forces act at the population level, and that it is a challenge to understand how they emerge from the stochastic and deterministic behaviour of individual cells. Even the most basic steric interactions between neighbouring cells can couple evolutionary outcomes of otherwise unrelated individuals, thereby wea ...[more]

PMID: 29632260

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Project description:BACKGROUND: Nuclear genome size varies 300 000-fold, whereas transcriptome size varies merely 17-fold. In the largest genomes nearly all DNA is non-genic secondary DNA, mostly intergenic but also within introns. There is now compelling evidence that secondary DNA is functional, i.e. positively selected by organismal selection, not the purely neutral or 'selfish' outcome of mutation pressure. The skeletal DNA theory argued that nuclear volumes are genetically determined primarily by nuclear DNA amounts, modulated somewhat by genes affecting the degree of DNA packing or unfolding; the huge spread of nuclear genome sizes is the necessary consequence of the origin of the nuclear envelope and the nucleation of its assembly by DNA, plus the adaptively significant 300 000-fold range of cell volumes and selection for balanced growth by optimizing karyoplasmic volume ratios (essentially invariant with cell volume in growing/multiplying cells). This simple explanation of the C-value paradox is refined here in the light of new insights into the nature of heterochromatin and the nuclear lamina, the genetic control of cell volume, and large-scale eukaryote phylogeny, placing special emphasis on protist test cases of the basic principles of nuclear genome size evolution. GENOME MINIATURIZATION: and Expansion Intracellular parasites (e.g. Plasmodium, microsporidia) dwarfed their genomes by gene loss and eliminating virtually all secondary DNA. The primary driving forces for genome reduction are metabolic and spatial economy and cell multiplication speed. Most extreme nuclear shrinkage yielded genomes as tiny as 0.38 Mb (making the nuclear genome size range effectively 1.8 million-fold!) in some minute enslaved nuclei (nucleomorphs) of cryptomonads and chlorarachneans, chimaeric cells that also retain a separate normal large nucleus. The latter shows typical correlation between genome size and cell volume, but nucleomorphs do not despite co-existing in the same cell for >500 My. Thus mutation pressure does not inexorably increase genome size; selection can eliminate essentially all non-coding DNA if need be. Nucleomorphs and microsporidia even reduced gene size. Expansion of secondary DNA in the main nucleus, and in large-celled eukaryotes generally, must be positively selected for function. Ciliate nuclear dimorphism provides a key test that refutes the selfish DNA and strongly supports the skeletal DNA/karyoplasmic ratio interpretation of genome size evolution. GENETIC CONTROL OF CELL VOLUME IS MULTIGENIC: The quantitatively proportional correlation between genome size and cell size cannot be explained by purely mutational theories, as eukaryote cell volumes are causally determined by cell cycle control genes, not by DNA amounts.

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Emergence of evolutionary driving forces in pattern-forming microbial populations.

Publications

Emergence of evolutionary driving forces in pattern-forming microbial populations.

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