Abstract: How was the eukaryotic cell assembled? How did complex multicellularity emerge? How do our tissues produce tens of billions of cells each day and yet keep somatic evolution in check?
These questions can be answered by reconstructing phylogenetic trees.
With the advent of genome-scale sequencing, however, molecular phylogeny, which reconstructs phylogenetic trees from related gene sequences, has reached an impasse. Instead of answering open questions, new genomes have reignited old debates. The problem is clear, the phylogenetic trees of genes (i.e., gene trees) are not the phylogenetic trees of species (i.e. the species tree). Instead, each gene tree is the unique result of a series of evolutionary events. If, however, we model these differences in the context of a common species tree, we can access a wealth of information on genome evolution and the diversification of species that is not available to traditional methods. For example, as horizontal gene transfer (HGT) can only occur between coexisting species, HGTs provide information on the order of speciations.
I describe progress on developing probabilistic models of genome evolution that can be used to systematically extract information on the pattern and timing of genomic evolution by explaining differences between gene trees. I discuss some of our recent results and future plans for applying these methods to open problems, such as resolving the timing of microbial evolution and its relationship to Earth history, where the extreme paucity of fossils limits the use of molecular dating methods.
Finally, I briefly introduce probabilistic models of another type of tree: the tree of a single life, traced by cell divisions that start from a single cell and produce and maintain our tissues. It is along this cell lineage tree that somatic evolution, including ageing and the development of cancer, occurs. I describe our theoretical results derived using these models on how hierarchically differentiating tissues can limit somatic evolution and maintain low cancer incidence by balancing mutation accumulation and the cells' commitment to differentiation.

us02web.zoom.us/j/4082603129