An organism’s adaptation to changing environments is fueled by its genetic variability, which is established by mechanisms ranging from single-nucleotide polymorphisms to large-scale structural variations, all of which affect chromosomal shape, organization, and gene content . These processes are particularly relevant for pathogens that must respond to continual selection pressure arising from host immune systems that evolved to detect the presence or activity of potential microbial pathogens through a variety of invasion patterns . In their adaptive response, pathogens evolve strategies, often involving secreted effector molecules, to overcome host immunity and support host colonization . Thus, it can be anticipated that this coevolutionary arms race leads to highly specific interactions between adapted pathogens and their specific hosts. Paradoxically, particular pathogens successfully colonize a broad range of hosts, yet how such pathogens cope in arms races with such a diversity of hosts remains unknown.
A structured genome drives adaptive evolution. It has been proposed that filamentous fungal and oomycete plant pathogens often evolved structured genomes with two distinct types of genomic regions: (1) gene-rich regions containing slowly evolving genes that mediate general physiology and (2) gene-poor regions that are dynamic and enriched for repetitive DNA such as transposable elements (TEs) and virulence-related genes that often display signs of accelerated evolution [4,5]. Extensive structural variation often occurs in these fast-evolving regions, leading to translocation, duplication, or loss of genetic material [1,4,5]. The highly dynamic regions can either be embedded within the core chromosomes or be located on separate chromosomes that often display presence/absence variations within a population, known as conditionally dispensable or accessory chromosomes [4,6]. The common occurrence of these bipartite genomes led to the “two-speed” model for pathogen genome evolution , suggesting that specific regions form sites of rapid genomic diversification to facilitate coevolution during host interactions [1,4,5].
Transposable elements shape “two-speed” genomes. It is generally observed that the dynamic regions of two-speed genomes are enriched in TEs, yet it remains undemonstrated how they mechanistically contribute to genome variability [1,4,5]. Recently, the contribution of TEs towards the evolution of the two-speed genome in the vascular wilt pathogen Verticillium dahliae was reported . Extensive genome rearrangements are generated by double-strand repair pathways that erroneously utilize stretches of homologous sequence at an unlinked locus, the majority of which occur around TEs simply as a consequence of their abundance and sequence similarity (Fig 1A) . Genomic rearrangements often occur at dynamic regions that are enriched for recent segmental duplications, generating genetic material subject to evolutionary diversification, e.g., by reciprocal gene loss (Fig 1A) [7,8]. Furthermore, these dynamic regions are enriched in in planta induced effectors  and evolutionary young and “active” TEs (Fig 1B). These TEs likely contribute to accelerated genomic diversification of dynamic effector regions .