Early blight of potato is caused by the fungal pathogen Alternaria solani and is an increasing problem</p><p>worldwide. The primary strategy to control the disease is applying fungicides such as succinate</p><p>dehydrogenase inhibitors (SDHI). SDHI-resistant strains, showing reduced sensitivity to treatments,</p><p>appeared in Germany in 2013, five years after the introduction of SDHIs. Two primary mutations in the SDH</p><p>complex (SdhB-H278Y and SdhC-H134R) have been frequently found throughout Europe. How these</p><p>resistances arose and spread, and whether they are linked to other genomic features, remains unknown.</p><p>We performed whole-genome sequencing for A. solani isolates from potato fields across Europe (Germany,</p><p>Sweden, Belgium, and Serbia) to better understand the pathogen's genetic diversity in general and</p><p>understand the development and spread of the genetic mutations that lead to SDHI resistance. We used</p><p>ancestry analysis and phylogenetics to determine the genetic background of 48 isolates. The isolates can be</p><p>grouped into 7 genotypes. These genotypes do not show a geographical pattern but appear spread</p><p>throughout Europe. The Sdh mutations appear in different genetic backgrounds, suggesting they arose</p><p>independently, and the observed admixtures might indicate a higher adaptive potential in the fungus than</p><p>previously thought.</p><p>Our research gives insights into the genetic diversity of A. solani on a genome level. The mixed occurrence</p><p>of different genotypes and apparent admixture in the populations indicate higher genomic complexity than</p><p>anticipated. The conclusion that SDHI tolerance arose multiple times independently has important</p><p>implications for future fungicide resistance management strategies. These should not solely focus on</p><p>preventing the spread of isolates between locations but also on limiting population size and the selective</p><p>pressure posed by fungicides in a given field to avoid the rise of new mutations in other genetic</p><p>backgrounds.