bioRxiv Science⌕ Search

bioRxiv · 10.1101/098228

Patterns of polymorphism at the self-incompatibility locus in 1,083 Arabidopsis thaliana genomes

Abstract

Although the transition to selfing in the model plant Arabidopsis thaliana involved the loss of the self-incompatibility (SI) system, it clearly did not occur due to the fixation of a single inactivating mutation at the locus determining the specificities of SI (the S-locus). At least three groups of divergent haplotypes (haplogroups), corresponding to ancient functional S-alleles, have been maintained at this locus, and extensive functional studies have shown that all three carry distinct inactivating mutations. However, the historical process of loss of SI is not well understood, in particular its relation with the last glaciation. Here, we took advantage of recently published genomic re-sequencing data in 1,083 Arabidopsis thaliana accessions that we combined with BAC sequencing to obtain polymorphism information for the whole S-locus region at a species-wide scale. The accessions differed by several major rearrangements including large deletions and inter-haplogroup recombinations, forming a set of haplogroups that are widely distributed throughout the native range and largely overlap geographically. Relict A. thaliana accessions that directly derive from glacial refugia are polymorphic at the S-locus, suggesting that the three haplogroups were already present when glacial refugia from the last Ice Age became isolated. Inter-haplogroup recombinant haplotypes were highly frequent, and detailed analysis of recombination breakpoints suggested multiple independent origins. These findings suggest that the complete loss of SI in A. thaliana involved independent self-compatible mutants that arose prior to the last Ice Age, and experienced further rearrangements during post-glacial colonization.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Tsuchimatsu, T., Goubet, P., Gallina, S., Holl, A.-C., Fobis-Loisy, I., Berges, H., Marande, W., Prat, E., Meng, D., Long, Q., Platzer, A., Nordborg, M., Vekemans, X., Castric, V.. 2017-01-04. Patterns of polymorphism at the self-incompatibility locus in 1,083 Arabidopsis thaliana genomes. https://doi.org/10.1101/098228

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Efficient growth factor production stabilizes cooperation in a cellular public goods game

Eukaryotic cells secrete growth factors that facilitate the proliferation and survival of neighboring cells in a coordinated manner essential for tissue development, repair, and homeostasis. However, mutant cells that fail to produce these factors may exploit the benefits provided by neighboring producers, thereby gaining a proliferative advantage that could lead to the extinction of the producer clone. Evolutionary theory predicts that preventing this "tragedy of the commons" requires a fixed spatial structure or other mechanisms that enable cells to interact preferentially with copies of themselves. Contrary to this expectation, we found that, in competition experiments, cells producing the diffusible growth factor interleukin-3 (IL3) resist invasion by non-producing mutant cells even in well-mixed populations, and that non-producers are driven to extinction instead. Using evolutionary game theory, we show that this outcome arises when the cost-to-benefit ratio of growth factor production falls below a critical threshold. We derive this tipping point analytically across the full parameter space of benefit function shape and group size and confirm that IL3 production in our experimental system satisfies this condition with a production cost less than 0.1% of the benefit conferred. These results demonstrate that efficient public good production alone can resolve the tragedy of the commons in populations of cells, and potentially in other biological systems.

evolutionary biology↗

Repeated Transitions in Migratory Behavior Across a Songbird Radiation Are Not Driven by Selection on Shared Variation in Candidate Genes

Understanding the mechanisms facilitating the repeated evolution of traits is a core question in evolutionary biology. While repeated evolution has been observed across many systems, behavioral phenotypes have been less well studied than morphological traits. Migration is a behavioral adaptation to seasonality that has evolved independently in many animals, and repeated gains and losses of migratory behavior have been especially prevalent throughout the diversification of birds. While migratory traits are heritable in many taxa and candidate genes underlying intraspecific variation in migratory behavior have been identified, whether similar genetic changes are responsible for the repeated evolution of migration remains poorly understood. We used a phylogenomic approach to investigate the relationship between variation in candidate genes and migratory propensity across nearly all species in the parulid warbler radiation (n = 101), a group of songbirds in which migratory behavior has been lost and gained multiple times. Comparisons of candidate gene tree topologies to the parulid warbler species tree revealed cases of discordance, though these were explained by differences in the number of phylogenetically informative sites among genes rather than by elevated genetic similarity among species sharing migratory strategies. Testing models of coding sequence evolution identified sites with elevated dN/dS in five candidate genes, suggestive of positive selection; however, variation at these sites showed no clear association with migratory strategy, nor did we detect recurrent selection across lineages where transitions in migratory behavior most likely occurred. Together, these results contradict the hypothesis that selection on shared variation (ancestral polymorphisms or introgressed alleles) facilitated the repeated evolution of migration in this clade.

evolutionary biology↗

Why development time matters: temperature influences plasticity while nutritional stress reshapes selection and evolutionary potential

The time it takes organisms to reach adulthood is often considered a central life-history trait that influences fitness and is highly plastic across environments. Despite its importance, direct estimates of how selection on development time varies across combinations of environmental stressors remain rare, limiting our understanding of its role in population responses to environmental change. We reared 68 full-sibling families of the vinegar fly, Drosophila melanogaster, at two temperatures (14{degrees}C and 28{degrees}C) on two diets (standard and low-calorie), and measured development time, body size (mass and wing size), egg-to-adult viability and productivity (number of offspring). Temperature caused the largest plastic response, with development taking 4-5 times longer at 14{degrees}C, whereas the low-calorie diet extended development by 20-30%. Yet diet, not temperature, changed directional selection on development time. On the standard diet, faster development was associated with higher fitness at both temperatures. On the low-calorie diet, this advantage disappeared, and at 14{degrees}C slower-developing females tended to produce more offspring. Viability selection showed consistent patterns. The low-calorie diet also increased evolvability in development time c.10-16-fold at both temperatures, and genetic correlations between diets were close to zero, indicating strong genotype-by-environment interactions. Plasticity in development time was not associated with fitness in any treatment. Overall, we provide evidence that development time is a functional trait whose relationship with fitness depends on the environment. Nutritional stress induced a smaller plastic response in development time than temperature, but had a larger effect on directional selection and evolvability. The stressor causing the greatest plastic change in a functional trait is therefore not necessarily the one that shapes its selection and evolution.

evolutionary biology↗