Biology subjects

Furuki, E.

Publications and source records attributed to Furuki, E..

4 recordsLinked to original sources

bioRxiv2026

Major effector loss reveals compensatory pathogenicity networks in a necrotrophic wheat pathogen

Necrotrophic effectors (NEs) are key determinants of virulence in the necrotrophic fungal pathogen Parastagonospora nodorum that causes septoria nodorum blotch of wheat. However, targeted removal of three important NEs SnToxA, SnTox1, and SnTox3 in the mutant{Delta} toxa13 previously revealed a redundancy mechanism is triggered, whereby pathogenicity on wheat is maintained. In this study, we investigated the gene regulatory profile underpinning this phenomenon and discover that virulence is not dependent on a fixed set of dominant effectors but instead arises from a flexible, epistatic compensatory network. Although host transcriptional responses to the P. nodorum wildtype SN15 and{Delta} toxa13 infection remained largely conserved, consistent with an overlapping disease-susceptibility pathway, a significant upregulation of candidate effector genes was observed in{Delta} toxa13. This included the recently characterised NE SnTox267, and several other candidate effectors able to induce necrosis in the non-host Nicotiana benthamiana, each carrying a predicted structural fold conserved across other pathogens. We therefore provide further direct evidence that virulence is maintained in P. nodorum lacking three NEs by an epistatic and compensatory effector network, underpinned by changes in pathogen gene expression. Targeting conserved effector-mediated virulence mechanisms rather than individual host-specific gene-for-gene interactions may provide a more tractable route to host resistance.

molecular biology↗

bioRxiv2026

Transcriptomic analysis reveals SnTox8-mediated reprogramming of wheat defence signalling

Parastagonospora nodorum (Berk.) Quaedvlieg, Verkley & Crousis, a necrotrophic fungal pathogen, is the causal agent for septoria nodorum blotch, a major constraint on global wheat production. Pathogen-produced necrotrophic effectors (NEs) that interact with host-sensitivity genes in an inverse gene-for-gene manner, collectively leading to effector-triggered susceptibility (ETS). Here, we investigated the transcriptional responses of two Triticum aestivum L. genotypes, Mace and Lancer, following infiltration with a novel NE, SnTox8. A total of 12,679 unique differentially expressed genes in Mace and 149 in Lancer were detected from transcriptomic analysis. In the SnTox8-sensitive cultivar, Mace, numerous defence-related genes were induced, including protein phosphorylation cascades, reactive oxygen species bursts, calcium signalling, phytohormone modulation, and suppression of photosynthesis, consistent with findings from other ETS models, in which necrotrophic fungal pathogens hijack host defence systems to proliferate. The interaction also activated genes involved in signal transduction, metabolism, membrane modification, and molecular transport, reflecting a coordinated host reprogramming that promotes cellular dysfunction and cell death, thereby facilitating necrotrophic pathogenesis. In contrast, Lancer, an SnTox8-insensitive cultivar, exhibited minimal transcriptional changes with no evidence of effector recognition or downstream defence-related activities. Overall, this study exhibited that SnTox8 manipulates kinase-mediated immune signalling and metabolic reprogramming to convert defence activation into host cell death, revealing a mechanistic basis for ETS in wheat. The identified SnTox8-Snn8-triggered processes were confirmed through additional transcriptome analysis of Mace mutants. Outcomes from this study establish a foundation for identifying, functionally characterising and validating the corresponding host susceptibility gene Snn8.

molecular biology↗

bioRxiv2026

Transposon-associated genetic structure of a fungal phytopathogen population of wheat

Septoria nodorum blotch (SNB) is an economically important fungal disease of wheat caused by Parastagonospora nodorum. It is primarily controlled by the breeding of resistant wheat cultivars, but experience over the last 50 years shows that new pathogen populations soon evolve that are more virulent on the current popular cultivars. In this study, we assembled a panel of 360 P. nodorum isolates. The collection resolved into eight subpopulations. One core and seven transient populations were found possessing contrasting characters in term of spatial and temporal distribution, mating-type, effector haplotypes and patterns of intact and degraded copies of a Tc-1 mariner transposon, called Molly. Molly can proliferate and randomly insert throughout the fungal genome. Its multiplication in sexual population likely triggered RIP which partially explains the extensive genetic diversity and explains the ability to form new adapted lineages and the observed population structure of this important pathogen of wheat. When tested on wheat, the recently emerged groups exhibited greater pathogenicity on modern elite cultivars consistent with the low-amplitude boom-and-bust cycle observed previously. It is possible that active copies of Molly transpose and contribute to both the birth and death of the transient groups. This study identified and characterised a fungal specific transposable element (TE) which plays a vital role in shaping Australian P. nodorum population structure and creating extensive genetic diversity which potentially leads to the pathogens better adaptation. The study suggests practical measures to improve the efficiency and longevity of resistance breeding for SNB.

pathology↗

bioRxiv2026

Differential genetic resistance identified in Parastagonospora nodorum and Pyrenophora tritici-repentis-wheat pathosystems

Septoria nodorum blotch (SNB) and tan spot (TS) wheat diseases are caused by necrotrophic fungal pathogens Parastagonospora nodorum (Pn) and Pyrenophora tritici-repentis (Ptr), respectively. Although recognised as premier model pathosystems for our understanding of necrotrophic effectors, no resistance mechanism has been reported in both diseases. Here, two SNB and TS resistance wheat lines ( 56:ZWB11 and 105:ZIF14) derived from the Australian national germplasm evaluation programme (CAIGE) were used to develop a double haploid mapping population. Two Pn and Ptr isolates of different pathotypes, their respective culture filtrates and effector SnTox267 were evaluated on the population. Genetic analysis of Ptr conidial inoculation of race 1 and race 2 identified a major resistance quantitative trait locus (QTL) (QTs.cur-1B) on chromosome 1B, while resistance to SNB was explained by several minor QTL. SnTox267 sensitivity was mapped to six locations (2A2, 2A3, 2B1, 2D3, 5B and 7B1) with only one QTL co-localized to known corresponding gene Snn7. Sensitivity loci 5B and 7B1 also conferred SNB resistance at seedling and adult stages. Two QTL on chromosome 2D1 and 7B2 were common in both SNB and TS, associated with disease at seedling stage and culture filtrate bioactivity, respectively. Resistance responses of 56:ZWB11 and 105:ZIF14 were confirmed cytologically, however, distinct responses were observed on wounded leaves. The defence responses were more effective against Ptr, while resistance to Pn infection was likely a combination of lack of susceptibility and effective physical barriers. Overall results demonstrated the distinction between the underlying resistance mechanisms to TS and SNB.

genetics↗