Transcriptional profiling of Fraxinus excelsior leaves during the early infection phase of ash dieback

Abstract

Ash dieback (ADB) has been causing the progressive decline of Fraxinus excelsior trees throughout Europe, urging research and forest management to develop strategies to combat ADB. A genetically heritable component in susceptibility to this fungal disease was reported in common gardens. Thus, exploring the molecular basis of ADB susceptibility will further support breeding initiatives in the future. We performed transcriptional profiling of infected and uninfected leaves from two ash genotypes with different susceptibility to Hymenoscyphus fraxineus . Leaf rachises were sampled one week following inoculation. Differential gene expression analysis was performed to compare between treatments in each genotype (individual response) or in genotypes and treatments combined (common response). Due to the heterogeneity in the response, only DEGs were discussed that passed stringent assessment. Our results revealed that UW1, the most susceptible genotype, showed a total of 515 differentially expressed genes (DEGs), some of them possibly suggesting a self-control mechanism, hindering an effective immune response and causing increased susceptibility. On the other hand, FAR3, the least susceptible genotype with 230 DEGs, seemed to induce a contained but more efficient response, hinting toward a salicylic acid-mediated process and activating pathogen-related (like) proteins as thaumatin-like, peroxidases, and chitinases. In the common response, 512 DEGs were modulated and transcripts from the phenylpropanoid pathway were commonly altered in both genotypes. Altogether, this work comprised an initial transcriptional exploration including two selected genotypes with distinct susceptibility to ADB, however, the heterogenous response indicated the need to further improve the experimental inoculation approach. Exploring gene expression patterns in ADB susceptibility holds promise to reveal early response mechanisms, and new markers related to susceptibility, as well as to contribute to developing strategies that may help contain ADB.

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