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In Search of Microbe Number One Masatoshi Nei Lecture (July 9, 9:00−10:00) Masatoshi Nei Lecture In search of microbe number one William Martin1 1University of Dusseldorf (United States) Life is a chemical reaction. More specifically, life is an exergonic chemical reaction. What was the chemical reaction from which the first cells arose, and what was the chemical reaction that fuelled the first free-living cells? These are questions about chemistry and physiology, but molecular evolution can contribute. The last universal common ancestor (LUCA) is the assemblage of cells from which all life evolved roughly four billion years ago. Genomes and phylogeny have yielded new avenues to understanding early evolution and LUCA. We know LUCA had the universal genetic code shared by all descendant life forms. But how did LUCA harness energy? The chemical reactions that help cells harness energy from their environments today seem almost as diverse as life itself. Which forms of energy harnessing are ancient? We looked at that question using data from sequenced microbial genomes. We found that LUCA lived from gases ? H2, CO2, H2S, CO, N2 ? in a setting that looked very much like a modern submarine hydrothermal vent. The classical approach to investigate LUCA using genomes is to identify genes that are present in all modern cells hence present present in LUCA. We asked which genes trace to LUCA by phylogenetic criteria. The results indicate that the first forms of life were anaerobic chemoautotrophs that evolved from preexisting geochemical processes involving exergonic reactions of H2, metals, and CO2. Plenary Session 1 (July 10, 9:00−10:00) Plenary-1 Evolution of sequence-specific anti-silencing systems in Arabidopsis Tetsuji Kakutani1, 2 1The University of Tokyo (Japan), 2National Institute of Genetics (Japan) The arms race between parasitic sequences and hosts is a major driving force for evolution of gene control systems. Since transposable elements (TEs) are potentially deleterious, eukaryotes silence them by epigenetic mechanisms such as DNA methylation. Little is known about how TEs counteract the silencing to propagate during evolution. Here we report behavior of sequence-specific anti-silencing proteins used by Arabidopsis TEs and coevolution of those proteins and their target sequences. Through this coevolution, these TEs propagate with minimum host damage. Our findings provide insight into the evolutionary dynamics of these apparently "selfish" sequences. They also provide potential tools to edit epigenomes in a sequence-specific manner. Plenary Session 2 (July 12, 16:00−17:00) Plenary-2 Tracking a killer: using ancient DNA to understand the evolutionary history of tuberculosis Anne C. Stone1 1Arizona State University (United States) Ancient DNA has become a powerful tool to investigate human population history, plant and animal domestication, as well as the pathogens that have impacted us through time. In this talk, I will discuss how ancient DNA allows us to examine the history of Mycobacterium tuberculosis and related strains in the Mycobacterium tuberculosiscomplex (MTBC) which cause tuberculosis (TB). Long a scourge of humans, as well as other animals, TB has now surpassed HIV as the leading cause of death from infectious disease. Here, I will focus on patterns of pathogen exchange before and after the •gAge of Exploration•h in the Americas and discuss ways that TB may have adapted to humans and other animals. Previous research from our group led to the recovery of MTBC genomes from three 1000-year old skeletal TB cases from coastal Peru and showed that these strains are closely related to strains adapted to sea mammals (specifically Southern Hemisphere pinnipeds). However, it is unclear whether these strains spread to inland South America and to North America by human-to-human transmission or whether different strains spread into North America via another route. Also, after contact, European strains were introduced, ultimately replacing pre-contact strains, but the timing and extent of this is unknown. Our present work focuses on skeletal TB cases from pre-contact and historic sites from the Americas and shows evidence for spread of pinniped-derived MTBC strains to people in non-coastal areas and the presence of European M. tuberculosis strains post-contact. This work was supported by funding from the National Science Foundation (BCS- 1063939 and BCS- 1515163), the Wenner Gren Foundation, and the Max Planck Institute. Walter Fitch Symposium (July 10, 10:00−12:00) O-02-WF01 Re-thinking a classic clinal trait: Pleiotropic consequences of thermally adaptive dopamine on pigmentation clines in Drosophila Ana Marija Jaksic1, 2, Viola Nolte1, Neda Barghi1, Francois Mallard1, Kathrin Anna Otte1, Lidija Svecnjak3, Kirsten-Andre Senti1, Christian Schlotterer1 1Vetmeduni Vienna (Austria), 2Vetmeduni Vienna (Austria), 3University of Zagreb (Austria) Clinal variation is widely regarded as strong evidence for adaptation in natural populations. One of the best-studied clinal phenotypes is the latitudinal melanism cline in ectotherms. Owing to the repeatability of clinal pigmentation across species and continents, this trait is frequently considered as a classic example for an adaptive trait. Nevertheless, how selection operates on this trait is still debated. The thermal budget hypothesis, one popular explanation, suggests that pigmentation intensity modulates the use of sunlight for thermoregulation. Here, we challenge this hypothesis and show how misleading the evolutionary interpretation of phenotypic variation can be. Using highly replicated experimental evolution setup, we exposed natural Drosophila simulans populations to novel thermal environments. After more than 100 generations of adaptation to hot temperature, the key components of melanin metabolism evolved in the same direction as in natural clines. Because temperature adaptation was not mediated by exposure to sun, we searched for alternative explanations. Melanin, the key ingredient for pigmentation, is synthesized from dopamine, a highly pleiotropic neurotransmitter. Using RNA-seq, metabolomics, and transgenic and pharmacologic modulation of dopamine, we uncovered the adaptive role of dopamine levels. Temperature strongly modulates signaling activity and in our experiment and natural populations, evolution modulates dopaminergic signaling to maintain synaptic homeostasis. We demonstrate that the evolutionary modulation of dopaminergic signaling helps to maintain normal locomotion even at high temperatures. We conclude that the pigmentation cline in Drosophila is a pleiotropic read-out of adaptive changes in dopamine metabolism, rather than an adaptive phenotype. Our results demonstrate that pleiotropy is a major challenge for the interpretation of phenotypic variation in a causative evolutionary framework. Walter Fitch Symposium (July 10, 10:00−12:00) O-02-WF02 Antagonistic pleiotropy is rare among new mutations Mrudula Sunil Sane1, Deepa Agashe1 1National Centre for Biological Sciences, Tata Institute of Fundamental Research (India) Pleiotropic effects of mutations may lead to tradeoffs, which are thought to constrain adaptation and play an important role in diverse biological phenomena. Specifically, antagonistic pleiotropic effects are thought to be frequent, especially in large-effect mutations. Theory and experiments have typically focused on pleiotropic effects of beneficial mutations arising under strong selection. This is a problem because most mutations are deleterious or neutral, and are rarely observed under strong selection. Additionally, strong selection on a few traits allows deleterious mutations to accumulate in other traits, causing apparent tradeoffs and confounding estimates of true pleiotropy. Here, we characterize the incidence, nature and effect size of pleiotropy for carbon utilization among single evolved mutations in Escherichia coli populations from a mutation accumulation experiment. While synergistic pleiotropy was fairly common (SP, ~28% of mutations), very few mutations showed antagonistic pleiotropy (AP, ~10% of mutations). Thus, true tradeoffs, measured as AP, are rare. Comparing with null expectations generated from the independent distributions of effect sizes for each resource, we found that AP is significantly rarer than expected. Similarly, compared to null expectation, we find that large-effect mutations are more likely to show AP. Thus, AP may be more important during the early stages of adaptive evolution when large- effect beneficial mutations dominate. Our unbiased quantification of pleiotropy provides the first empirical support for long-standing evolutionary hypotheses. Contrary to current thought, our results suggest that at the mechanistic level, tradeoffs may only rarely constrain adaptation, largely when it proceeds through large-effect mutations. Walter Fitch Symposium (July 10, 10:00−12:00) O-02-WF03 The mechanistic basis of epistatic variety in a metabolic pathway uncovered by high-resolution fitness interaction mapping Harry Kemble1, Catherine Eisenhauer1, Audrey Chapron1, Melanie Magnan1, Herve Le Nagard1, Philippe Nghe2, Olivier Tenaillon1 1INSERM (France), 2ESPCI (France) Fitness epistasis, the interdependence of mutations in their fitness impacts, can play a significant role in shaping evolutionary dynamics and determining evolutionarily accessible paths. It results from both direct interactions on the genotype-phenotype scale and non-linearity in the phenotype-fitness map. Empirical measurements of fitness epistasis can therefore provide information
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