Together, these findings identify PtGH1and PtCBM1 as distinct virulence factors that act through complementary mechanisms, involving physical facilitation and enzymatic degradation of host cell walls, illustrating how the leaf rust fungus overcomes host immunity and provides potential molecular targets for developing durable wheat resistance.
Abstract
Wheat leaf rust, caused by the biotrophic fungus Puccinia triticina (Pt), is a major threat to global wheat production. Fungal pathogens often deploy plant cell wall-degrading enzymes to breach host barriers, with glycoside hydrolases (GHs) providing hydrolytic activity and carbohydrate-binding modules (CBMs) enabling substrate recognition. However, research on their specific roles in the leaf rust fungus remains limited. Here, we functionally characterized two Pt genes, PtGH1 and PtCBM1. PtCBM1, a carbohydrate-binding module protein, binds cellulose and potentiates cellulase activity despite lacking hydrolase activity, whereas PtGH1 encodes a β-glucanase secreted via a non-classical pathway. Both proteins suppress Bax-induced cell death in Nicotiana benthamiana, suggesting immune-suppressive activity. Silencing either of the two genes in wheat via host-induced gene silencing significantly reduced fungal virulence, impaired hyphal growth, and enhanced host defense. Together, these findings identify PtGH1and PtCBM1 as distinct virulence factors that act through complementary mechanisms, involving physical facilitation and enzymatic degradation of host cell walls. This dual strategy illustrates how the leaf rust fungus overcomes host immunity and provides potential molecular targets for developing durable wheat resistance.
It is shown that expression of AVR2 is strongly induced in root-and xylem-colonizing hyphae three days post inoculation, and it is found that Avr2 has to be nuclear localized to trigger an I-2 -dependent cell death response.
Benavides Ma, Cornelissen F. L. W., Takken· 0 citations
This review examines the defence strategies of rice and provides key insights into host-pathogen interactions that inform the development of durable resistance and improved disease management strategies, including integrating molecular breeding with sustainable agricultural practices to mitigate yield losses caused by BLB.
M. Syed, N. Rajinimala, M. Theradimani et al.· Plant Science Today· 0 citations
Apple rust, caused by the fungal pathogen Gymnosporangium yamadae, leads to substantial yield losses and significant economic damage. In the rust-resistant cultivar Malus ‘Profusion’, rust infection triggers anthocyanin synthesis at infection sites as a defense mechanism to restrict fungal proliferation. Although small noncoding RNAs (miRNAs) play important roles in regulating anthocyanin biosynthesis, their specific functions under rust stress remain poorly characterized. In this study, small RNA sequencing revealed that miR166a is a key rust-responsive regulator. Its direct targeting and negative regulation of MpATHB8 were confirmed through luciferase assays, GUS staining, and gene expression analyses. Functional validation via transient and stable transformation in Malus demonstrated that suppressing miR166a expression using short tandem target mimics or overexpressing MpATHB8 promoted anthocyanin accumulation and enhanced resistance to rust. In contrast, overexpressing miR166a or silencing MpATHB8 suppressed anthocyanin synthesis and increased susceptibility to the pathogen. Further evidence indicates that the MpATHB8 protein activates anthocyanin biosynthesis by binding to and inducing the promoter of MpMYB10b. These findings reveal a miR166a-MpATHB8-MpMYB10b regulatory module that enhances rust resistance through anthocyanin metabolism in M. ‘Profusion’. Our findings provide novel insights into the miRNA-mediated regulation of anthocyanin metabolism and facilitate the breeding of rust-resistant and anthocyanin-enriched Malus cultivars.
Prunus sibirica L., an economically and ecologically significant Asian endemic species, faces severe pathogenic threats, yet its disease resistance mechanisms remain poorly understood. Using RNA-seq of pathogen-infected leaves, we identified PsWRKY75 as a potential resistance gene. Heterologous overexpression in poplars showed that PsWRKY75 enhanced disease resistance, promoting lignin and H₂O₂ accumulation in leaves. Through RNA-seq and promoter analysis, PsWRKY75 was identified as an upstream regulator of the H₂O₂-producing gene PsRbohB and lignin biosynthesis gene PsLFP1, validated by yeast one-hybrid, EMSA, and dual luciferase assays. Pathogen infection upregulates PsWRKY75, which directly activates PsRbohB and PsLFP1 to enhance lignin/H₂O₂ accumulation, thereby strengthening disease resistance. This study reveals PsWRKY75 as a novel integrator of H₂O₂ signaling and lignin biosynthesis, providing genetic resources for woody plant disease resistance improvement via physiological and biochemical engineering.
