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Tree pathogens cause some of the most devastating forest epidemics. In spite of their importance, we know relatively little about their origin and sources. We used a population genomics approach to study these questions in the poplar canker pathogen, <i>Mycosphaerella populorum</i> (anamorph: <i>Septoria musiva </i>syn. <i>Sphaerulina musiva</i>). This pathogen is presumed to have co-evolved with the eastern cottonwood, <i>Populus deltoides</i>, but has recently been expanding to new hosts such as <i>P. trichocarpa</i> and <i>P. balsamifera</i>. Genome comparisons between <i>M. populorum</i>, which causes both leaf spots and cankers, and <i>M. populicola</i>, a close relative that also attacks poplar but does not cause cankers, indicate that <i>M. populorum</i> has acquired a unique set of genes via horizontal gene transfer (HGT) that are important to its ability to attack woody hosts. Population genomic analyses of 89 <i>M. populorum</i> samples from across its distribution range yielded over 1M SNPs and highlight an unusually high and uneven level of diversity even in recently introduced populations. The patterns suggest both extensive migration and possibly additional unsampled ghost populations. We discovered that a jump to <i>P. balsamifera</i> could be driving speciation by imposing selection at the MAT locus, causing a shift from sexual to asexual reproduction, followed by isolation and drift. These results highlight very dynamic mechanisms leading to host colonization and incipient speciation and specialization in this tree pathogen.