Phylogenetics is concerned with uncovering the relationships among organisms (the “Tree of Life”), and statistical computational research has made many important contributions to achieving this goal. In this talk I discuss a major overall challenge facing the field as DNA sequencing efforts have become central to this work: many individual genes have tree topologies that do not match the tree describing relationships among species. Such gene-tree discordance poses many new difficulties for inferring the Tree of Life. Here, I present three approaches for dealing with discordance: 1) an ILS-aware method for counting gene duplications and losses; 2) a quartet summary approach that combines many different gene-tree topologies to construct an accurate species tree, even in the presence of duplication and loss; and 3) a probabilistic approach to reconstructing the history of different traits on a species tree in the presence of discordance. These three problems (and their solutions) represent just a fraction of the challenges now facing the field of phylogenetics.

The nucleosome is a complex of histones and ~150 bp of DNA. It is a major constituent of chromatin in eukaryotes, covering 75–90% of genomes. Our team has developed a physical model based on the elastic properties of the DNA sequence (Vaillant et al. 2007). This model predicts Nucleosome Inhibitory Energy Barriers (NIEBs), at the border of which nucleosomes are positionned through statistical positioning (Kornberg & Stryer 1988). Here, we report that NIEBs can be predicted across eukaryotes and are functional, i.e they position nucleosomes in every eukaryotic species tested (from human to Trypanosoma brucei). We report that NIEBs affect local sequence evolution in a strikingly similar manner across eukaryotes. Their evolution is also affected by microsatellites and transposable elements (SINE and LINEs). Finally, some level of association with TSS and TTS is reported, hinting at one possible biological function, even though a lot of work remain to be done on this subject.

HLA (Human Leukocyte Antigen) immune genes are pivotal in mediating immune responses and maintaining the delicate balance between immune recognition and tolerance. Their high variability is assumed to be shaped by evolutionary pressures, such as infectious diseases, leading to complex patterns of selection and adaptation. Understanding the mechanisms underlying HLA gene variability is crucial for insights into immune function and susceptibility to both infectious and autoimmune diseases. Here I will share some recent insights into the evolutionary dynamics of HLA genes, highlighting factors that contribute to their diversity and adaptation over time. A better comprehension of the intricate workings of the adaptive immune system will improve our ability to develop personalized medicine, vaccines, and therapies targeting immune-related disorders. This research thus underscores the benefit of taking an evolutionary medicine perspective in human health and disease.

The evolutionary arms race between parasites and hosts can culminate into complex extended phenotypes that benefit disease progression and transmission. The fungus-adaptive changes in behaviour as seen in Ophiocordyceps-infected carpenter ants are a prime example. These “zombie ants” demonstrate behaviours that are thought to circumvent the social immune responses of the colony. Subsequently, the hijacked ant attaches itself at an elevated position that benefits fungal spore development and dispersal. The precise mechanisms involved are unknown. To unravel them, we have developed “zombie ants” into an integrative model system. By combining fungal culturing and lab infections with behavioural assays and multi-omics, we propose several hypotheses about the fungal proteins and ant receptors involved. To determine the function of presumed fungal “manipulation” effectors, the host behaviours they elicit, and the host pathways that underly those phenotypes, we are currently, for the first time, integrating functional genetics. Our results are providing some of the first insights into parasitic hijacking of animal behaviour.

Marine invertebrates are continuously exposed to highly diverse microbial communities, making them powerful models for studying host–microbe interactions. In my talk, I will present our work on the sea anemone Nematostella vectensis to uncover mechanisms that govern bacterial recognition, microbiome establishment, and host adaptation. We show that host colonization is not a passive process but is controlled by selective innate immune responses mediated by specialized phagocytic cell clusters, the nematosomes. These immune structures preferentially eliminate foreign bacteria while permitting colonization by native strains, thereby shaping microbiome composition. Using genetic and functional approaches, we identify the transcription factor cJUN as a key regulator of this selective phagocytosis and microbiome homeostasis. Beyond host control of bacterial membership, we explore how microbial colonizers contribute to host acclimation and adaptation to environmental stress. Given the rapid pace of climate change, genetic adaptation alone may be insufficient for long-lived organisms. Our results support the concept that the microbiota provides a mechanism for rapid, flexible adaptation, highlighting the holobiont as a critical unit of resilience in changing marine environments.