Skip to content
Open access

A putative rRNA methyltransferase Mrm1 regulates mitochondrial dynamics and pathogenicity in Magnaporthe oryzae

Aug 2026 · Virulence · Vol 17 · 0 citations · 25 references
Medicine

TL;DR

The findings deepen the understanding of epitranscriptomic regulation in fungal pathogenicity and represent a potential candidate for future target-based intervention strategies, pending validation through chemical or genetic approaches.

Abstract

ABSTRACT Rice blast disease, a major global threat to staple crops, is caused by the ascomycete fungus Magnaporthe oryzae. This pathogen has complex mechanisms to invade rice, with mitochondrial function crucial for infection energy. Our study looks at the impact of Mrm1, a putative rRNA methyltransferase, on mitochondrial dynamics and pathogenicity of M. oryzae. Mrm1 deficiency delays appressorium formation and reduces turgor pressure for host penetration and infection hypha expansion. The N-terminal sequence of Mrm1, with a mitochondrial targeting sequence (MTS), is vital for its localization and function. Deletions cause impaired growth and lower pathogenicity. Deleting MRM1 leads to abnormal mitochondrial morphology, with more filamentous mitochondria during invasive growth, disrupting the balance of fission and fusion. This imbalance reduces the fungus’s infection ability. Furthermore, loss of Mrm1 alters the steady-state protein levels of mitochondrial dynamics regulators Dnm1 and Fzo1, likely through translational regulation, while their transcript abundances remain unchanged. In the absence of Mrm1, the levels of these proteins are significantly reduced. Our findings deepen the understanding of epitranscriptomic regulation in fungal pathogenicity and represent a potential candidate for future target-based intervention strategies, pending validation through chemical or genetic approaches.

Read PDF

Similar papers

Open access Aug 2026

MoSun4 Contributes to Pathogenicity and Is Associated with Altered Expression of Virulence-Related Genes in Magnaporthe oryzae

The SUN family protein MoSun4 in Magnaporthe oryzae has been previously implicated in mitophagy and has potential as a target for reducing rice blast, but its role as a secreted protein remains poorly understood. In this study, signal peptide prediction and yeast secretion assays confirmed MoSun4 signal peptide function, and co-localization revealed the localization of the extra-invasive hyphal membrane (EIHM)-associated apoplastic compartment or matrix, establishing MoSun4 as a secreted protein. In addition, deletion of the MoSUN4 gene reduced the hyphal growth, conidiation and virulence of M. oryzae. We further showed that MoSun4 is involved in regulating the expression of virulence-related genes, including multiple genes involved in cell wall degradation (eglC, eglD), secondary metabolism (gliK), and melanin biosynthesis (SDH1, BUF1, Cmr1, ALB1). Collectively, our study reveals that MoSun4 is a secreted protein that contributes to pathogenicity and is associated with altered expression of virulence-related genes, providing new insights into the functions of SUN family proteins.

Huimin Li, Zhenhe Su, Xiaomeng Liu et al. · 0 citations
Open access Jul 2026

Transcriptome and Metabolome Dissection of Multilayered Pydiflumetofen Resistance Mechanisms in Fusarium graminearum

Wheat Fusarium head blight (FHB) is a globally prevalent and destructive fungal disease predominantly caused by Fusarium graminearum. Pydiflumetofen, a novel succinate dehydrogenase inhibitor (SDHI) fungicide, exhibits strong inhibitory activity against F. graminearum; however, the molecular regulatory mechanisms underlying the field-developed resistance in this pathogen remain poorly defined. In the present study, a field-evolved resistant isolate W24-039 and a sensitive isolate W24-016 were subjected to multi-omics analysis. The sequencing results identified compound mutations C89S/A93V in SdhC2, and A21T/S30F in SdhD of the resistant strain, which confer stable fungicide resistance without any detectable fitness costs. Physiological tests revealed that these target mutations sustain the homeostasis of succinate dehydrogenase (SDH) activity and intracellular ATP production. Following pydiflumetofen treatment, the sensitive isolate displayed remarkable declines in SDH activity, intracellular ATP content and deoxynivalenol (DON) biosynthesis, accompanied by markedly elevated cell membrane permeability. Transcriptomic sequencing uncovered 2221 differentially expressed genes (DEGs) in the sensitive strain under fungicide stress, and 2566 DEGs in the resistant isolate under the same conditions. The genes associated with detoxification and drug efflux, including cytochrome P450, glutathione S-transferase (GST), ABC and MFS transporters, were significantly upregulated in the resistant isolate. Metabolomic analysis indicated that differential metabolites were mainly enriched in the tricarboxylic acid (TCA) cycle, amino acid metabolism and membrane lipid biosynthesis pathways. The resistant strain maintained intact TCA cycle operation and accumulated high levels of pivotal metabolites such as phosphatidylcholine, unsaturated fatty acids and reduced glutathione. Integrated multi-omics analysis verified that the ABC transporter and glutathione metabolism pathways serve as core regulatory modules governing fungicide resistance. Collectively, F. graminearum develops resistance via the synergistic effects of SDH compound mutations, enhanced detoxification and efflux, and global metabolic remodeling, demonstrating that target-site mutation alone is not the sole driver of resistance, which is instead controlled by an intricate regulatory network involving multiple coordinated pathways. This study systematically characterizes the resistance regulatory network of F. graminearum against pydiflumetofen, and provides theoretical guidance for the rational application and sustainable field resistance management of this fungicide.

Yun Wang, Dongmei Liu, Haiyan Yin et al. · 0 citations
Open access Aug 2026

FpLaeA Coordinates Fusarium proliferatum Pathogenesis by Orchestrating Mycotoxin Biosynthesis and Host Immune Subversion

It is reported that the methyltransferase FpLaeA is a global regulator essential for F. proliferatum pathogenicity and a target for integrated control of F. proliferatum and its associated mycotoxin risk.

Ling Wang, Shaoqing Tang, Weiyang Liao et al. · 0 citations
Open access Aug 2026

VdPRMT1 Is Required for Fungal Growth, Metabolism, and Pathogenicity in Verticillium dahliae

Highlights This VdPRMT1 is a conserved arginine methyltransferase in Verticillium dahliae. VdPRMT1 contributes to fungal growth, stress adaptation, carbon utilization, and virulence. HIGS-mediated silencing of VdPRMT1 reduces Verticillium wilt severity in cotton. VdPRMT1 interacts with VdLuc7, indicating a potential link to RNA processing. Abstract Protein arginine methyltransferases (PRMTs) are key regulators of diverse cellular processes in eukaryotes, including transcriptional regulation, RNA processing, signal transduction and DNA repair. However, the biological functions of PRMTs in Verticillium dahliae remain largely unexplored. In this study, we identified a PRMT1 homolog in V. dahliae. Targeted deletion of VdPRMT1 resulted in severely impaired hyphal growth, sporulation, stress responses and pathogenicity. Subcellular localization analysis showed that VdPRMT1 is distributed in both the nucleus and cytoplasm of hyphae. Host-induced gene silencing (HIGS) of VdPRMT1 in cotton significantly reduced disease severity, supporting its important role in pathogenicity. Furthermore, VdLuc7, a U1 snRNP-associated protein containing multiple RG/RGG motifs, was identified as a putative interacting partner of VdPRMT1 through yeast two-hybrid (Y2H) screening, bimolecular fluorescence complementation (BiFC) and luciferase complementation imaging (LCI) assays. Together, our results demonstrate that VdPRMT1 is required for normal fungal development and full virulence in V. dahliae, and suggest that arginine methylation may contribute to pathogenicity through regulation of RNA processing-related pathways. These findings provide new insights into the molecular mechanisms underlying fungal virulence and identify VdPRMT1 as a potential target for disease control.

Wenwen Li, Suoxian Li, Siyuan Wu et al. · 0 citations
Open access Aug 2026

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

It is shown that the understudied bZIP transcription factor PnAda1 is an important downstream component of this PnPf2-regulatory network, and current understanding of the transcriptional network underlying virulence, metabolism and stress adaptation in an important fungal wheat pathogen is expanded.

S. Morikawa, Leon Lenzo, Keshara Colomba Thanthrige et al. · 0 citations