Biology subjects

Lenzo, L. V.

Publications and source records attributed to Lenzo, L. V..

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

The bZIP transcription factor PnAda1 functions as a regulator of virulence, fungicide tolerance and necrotrophy in the wheat pathogen Parastagonospora nodorum

Ada1 (All Development Altered-1) is a conserved but poorly characterised basic leucine zipper (bZIP) transcription factor found throughout filamentous fungi. In the wheat pathogen Parastagonospora nodorum, PnAda1 is required for full virulence and is transcriptionally associated with the virulence regulator PnPf2, but its biological functions remain unclear. Here, we combined comparative RNA sequencing with targeted phenotypic analyses to define the role of PnAda1 during vegetative growth and host infection. Deletion of PnAda1 did not abolish pathogenicity but delayed disease progression, with the PnAda1-deletion mutant transcriptome at 7 days post-inoculation resembling that of the wildtype SN15 at 3 days. This developmental delay was associated with impaired activation of early infection-associated genes, including putative carbohydrate-active enzymes, proteases, transporters and other host-colonisation factors. In contrast, expression of major necrotrophic effector genes was not reduced and instead remained elevated during later stages of infection, indicating that PnAda1 is required for the timely progression of infection-associated transcriptional regulation rather than direct activation of effector genes. Beyond virulence, transcriptomic and phenotypic analyses revealed roles for PnAda1 in nitrogen assimilation, carbon utilisation, abiotic stress responses and fungicide sensitivity. Notably, PnAda1 deletion increased sensitivity to succinate dehydrogenase inhibitor fungicides and reduced expression of succinate dehydrogenase subunit genes. Collectively, our findings identify PnAda1 as a broad regulator of developmental and infection-associated transitions in P. nodorum and expand current understanding of the transcriptional network underlying virulence, metabolism and stress adaptation in an important fungal wheat pathogen.

molecular biology↗

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↗

bioRxiv2025

Fair-weather friends: Unequal partnerships between Parastagonospora nodorum and Pyrenophora tritici-repentis define disease dynamics in wheat

Parastagonospora nodorum and Pyrenophora tritici-repentis are the causal agents of septoria nodorum blotch and tan spot of wheat, respectively. Though these fungal phytopathogens have been found to frequently cohabitate the same leaf, their interaction dynamics in the manifestation of disease remain poorly understood due to limitations in species-specific detection methods. We developed a digital PCR based model targeting conserved regions of the -tubulin gene, enabling biomass quantification of both pathogens during infection. Field surveys revealed up to two in three symptomatic infections involved both pathogens, with co-infected plants showing significantly higher individual pathogen biomass than single-species infections. Host plants in the field with moderate resistance to both pathogens were found to be significantly more necrotic under co-infection, with individual pathogen biomass up to twice that observed value for single infections. However, like fair-weather friends the partnership between these two pathogens seems to be conditional.When P. tritici-repentisestablished first, secondary P. nodorumcolonisationled to a breakdown of host resistance. Conversely, when P. nodorum established on the host first, it suppressed P. tritici-repentis colonisation regardless of host resistance. To our knowledge this is the first description of asymmetric priority effects overcoming host resistance in a plant pathosystem. Resistance breeding strategies evaluating single pathogen challenges may inadvertently select for cultivars vulnerable to sequential co-infection, necessitating integrated disease complex approaches for durable resistance development.

microbiology↗