Highlights d Upon germination, cell divisions generate a PLT drop that forms the transition zone d A PLTs-ARR12 mutual antagonism restricts early root meristem expansion d ARR1 repression of cell division via KRP2 is key for meristem size stabilization

BackgroundChanging environmental conditions pose a challenge for the survival of species. To meet this challenge organisms adapt their phenotype by physiological regulation (phenotypic plasticity) or by evolving. Regulatory mechanisms that ensure a constant internal environment in the face of continuous external fluctuations (homeostasis) are ubiquitous and essential for survival. However, more drastic and enduring environmental change, often requires lineages to adapt by mutating. In vitro evolutionary experiments with microbes show that adaptive, large phenotypic changes occur remarkably quickly, requiring only a few mutations. It has been proposed that the high evolvability demonstrated by these microbes, is an evolved property. If both regulation (phenotypic plasticity) and evolvability can evolve as strategies to adapt to change, what are the conditions that favour the emergence of either of these strategy? Does evolution of one strategy hinder or facilitate evolution of the other strategy?ResultsHere we investigate this with computational evolutionary modelling in populations of Virtual Cells. During a preparatory evolutionary phase, Virtual Cells evolved homeostasis regulation for internal metabolite concentrations in a fluctuating environment. The resulting wild-type Virtual Cell strains (WT-VCS) were then exposed to periodic, drastic environmental changes, while maintaining selection on homeostasis regulation. In different sets of simulations the nature and frequencies of environmental change were varied. Pre-evolved WT-VCS were highly evolvable, showing rapid evolutionary adaptation after novel environmental change. Moreover, continued low frequency changes resulted in evolutionary restructuring of the genome that enables even faster adaptation with very few mutations. In contrast, when change frequency is high, lineages evolve phenotypic plasticity that allows them to be fit in different environments without mutations. Yet, evolving phenotypic plasticity is a comparatively slow process. Under intermediate change frequencies, both strategies occur.ConclusionsWe conclude that evolving a homeostasis mechanisms predisposes lineage to be evolvable to novel environmental conditions. Moreover, after continued evolution, evolvability can be a viable alternative with comparable fitness to regulated phenotypic plasticity in all but the most rapidly changing environments.Electronic supplementary materialThe online version of this article (doi:10.1186/s12862-017-0918-y) contains supplementary material, which is available to authorized users.

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Background Mutators are common in bacterial populations, both in natural isolates and in the lab. The fate of these lineages, which mutation rate is increased up to 100 ×, has long been studied using population genetics models, showing that they can spread in a population following an environmental change. However in stable conditions, they suffer from the increased mutational load, hence being overcome by non-mutators. However, these results don’t take into account the fact that an elevated mutation rate can impact the genetic structure, hence changing the sensitivity of the population to mutations. Here we used Aevol, an in silico experimental evolution platform in which genomic structures are free to evolve, in order to study the fate of mutator populations evolving for a long time in constant conditions. Results Starting from wild-types that were pre-evolved for 300,000 generations, we let 100 mutator populations (point mutation rate ×100) evolve for 100,000 further generations in constant conditions. As expected all populations initially undergo a fitness loss. However, after that the mutator populations started to recover. Most populations ultimately recovered their ancestors fitness, and a significant fraction became even fitter than the non-mutator control clones that evolved in parallel. By analyzing the genomes of the mutators, we show that the fitness recovery is due to two mechanisms: i. an increase in robustness through compaction of the coding part of the mutator genomes, ii. an increase of the selection coefficient that decreases the mean-fitness of the population. Strikingly the latter is due to the accumulation of non-coding sequences in the mutators genomes. Conclusion Our results show that the mutational burden that is classically thought to be associated with mutator phenotype is escapable. On the long run mutators adapted their genomes and reshaped the distribution of mutation effects. Therewith the lineage is able to recover fitness even though the population still suffers the elevated mutation rate. Overall these results change our view of mutator dynamics: by being able to reduce the deleterious effect of the elevated mutation rate, mutator populations may be able to last for a very long time; A situation commonly observed in nature.