ArticleThe Plant journal : for cell and molecular biology2016
Differential effector gene expression underpins epistasis in a plant fungal disease.
Article in The Plant journal : for cell and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 98 citations in OpenAlex.
- Identification of septoria nodorum blotch susceptibility genes in hard winter wheat.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2026Article
- Genome-wide association mapping for resistance against Septoria nodorum blotch and tan spot in a diverse wheat panel.Molecular breeding : new strategies in plant improvement · 2025Article
- Abscisic Acid Can Play a Dual Role in thePlants (Basel, Switzerland) · 2025Article
- Genetic dissection of Septoria tritici blotch and Septoria nodorum blotch resistance in wheat using GWAS.Frontiers in plant science · 2025Article
- Repeat-induced point mutations driving Parastagonospora nodorum genomic diversity are balanced by selection against non-synonymous mutations.Communications biology · 2024Article
- The Role of Salicylic, Jasmonic Acid and Ethylene in the Development of the Resistance/Susceptibility of Wheat to the SnTox1-Producing Isolate of the Pathogenic FungusPlants (Basel, Switzerland) · 2024Article
- Regulatory insight for a Zn2Cys6 transcription factor controlling effector-mediated virulence in a fungal pathogen of wheat.PLoS pathogens · 2024Article
- Article
- The Role of Cytokinins and Abscisic Acid in the Growth, Development and Virulence of the Pathogenic FungusBiomolecules · 2024Article
- Identification of WheatPlants (Basel, Switzerland) · 2024Article
- Genome-wide association mapping of resistance to the foliar diseases septoria nodorum blotch and tan spot in a global winter wheat collection.Molecular breeding : new strategies in plant improvement · 2023Article
- Genetics and breeding for resistance against four leaf spot diseases in wheat (Frontiers in plant science · 2023Review
- Assessment of Indian wheat germplasm for Septoria nodorum blotch and tan spot reveals new QTLs conferring resistance along with recessive alleles ofFrontiers in plant science · 2023Article
- Genome-wide association mapping of septoria nodorum blotch resistance in Nordic winter and spring wheat collections.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2022Article
- Variability in an effector gene promoter of a necrotrophic fungal pathogen dictates epistasis and effector-triggered susceptibility in wheat.PLoS pathogens · 2022Article
- Analysis of plant cell death-inducing proteins of the necrotrophic fungal pathogensFrontiers in plant science · 2022Article
- A triple threat: the Parastagonospora nodorum SnTox267 effector exploits three distinct host genetic factors to cause disease in wheat.The New phytologist · 2022Article
- Article
- Review
- Extracellular Vesicles fromJournal of fungi (Basel, Switzerland) · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fungal effector-host sensitivity gene interactions play a key role in determining the outcome of septoria nodorum blotch disease (SNB) caused by Parastagonospora nodorum on wheat. The pathosystem is complex and mediated by interaction of multiple fungal necrotrophic effector-host sensitivity gene systems. Three effector sensitivity gene systems are well characterized in this pathosystem; SnToxA-Tsn1, SnTox1-Snn1 and SnTox3-Snn3. We tested a wheat mapping population that segregated for Snn1 and Snn3 with SN15, an aggressive P. nodorum isolate that produces SnToxA, SnTox1 and SnTox3, to study the inheritance of sensitivity to SnTox1 and SnTox3 and disease susceptibility. Interval quantitative trait locus (QTL) mapping showed that the SnTox1-Snn1 interaction was paramount in SNB development on both seedlings and adult plants. No effect of the SnTox3-Snn3 interaction was observed under SN15 infection. The SnTox3-Snn3 interaction was however, detected in a strain of SN15 in which SnTox1 had been deleted (tox1-6). Gene expression analysis indicates increased SnTox3 expression in tox1-6 compared with SN15. This indicates that the failure to detect the SnTox3-Snn3 interaction in SN15 is due - at least in part - to suppressed expression of SnTox3 mediated by SnTox1. Furthermore, infection of the mapping population with a strain deleted in SnToxA, SnTox1 and SnTox3 (toxa13) unmasked a significant SNB QTL on 2DS where the SnTox2 effector sensitivity gene, Snn2, is located. This QTL was not observed in SN15 and tox1-6 infections and thus suggesting that SnToxA and/or SnTox3 were epistatic. Additional QTLs responding to SNB and effectors sensitivity were detected on 2AS1 and 3AL.
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