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Einspanier, S.

Publications and source records attributed to Einspanier, S..

2 recordsLinked to original sources

High-resolution disease phenotyping reveals distinct resistance strategies of wild tomato crop wild relatives against Sclerotinia sclerotiorum

Besides the well-understood qualitative disease resistance, plants possess a more complex quantitative form of resistance: quantitative disease resistance (QDR). QDR is commonly defined as a partial but more durable form of resistance and, therefore, might display a valuable target for resistance breeding. The characterization of QDR phenotypes, especially of wild crop relatives, displays a major bottleneck in deciphering QDRs genomic and regulatory background. Moreover, the relationship between QDR parameters, such as infection frequency, lag phase duration, and lesion growth rate, remains elusive. High hurdles for applying modern phenotyping technology, such as the low availability of phenotyping facilities or complex data analysis, further dampen progress in understanding QDR. Here, we applied a low-cost phenotyping system to measure lesion growth dynamics of wild tomato species (e.g., S. pennellii or S. pimpinellifolium). We provide insight into QDR diversity of wild populations and derive specific QDR strategies and their crosstalk. We show how temporally continuous observations are required to dissect end-point severity into functional resistance strategies. The results of our study show how QDR can be maintained by facilitating different defense strategies during host-parasite interaction and that the capacity of the QDR toolbox highly depends on the hosts genetic context. We anticipate that the present findings display a valuable resource for more targeted functional characterization of the processes involved in QDR. Moreover, we show how modest phenotyping technology can be leveraged to help answer highly relevant biological questions.

plant biology↗

Whole genome sequencing elucidates the species-wide diversity and evolution of fungicide resistance in the early blight pathogen Alternaria solani

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

evolutionary biology↗