Pathogenic Mechanisms of Curvularia Species in Maize

Curvularia species, notably C. lunata, constitute a major threat to global maize production through complex infection strategies. Initial colonisation relies on specialised infection structures that breach the leaf surface, facilitating biotrophic and necrotrophic stages. Once inside the host, these fungi deploy an array of secondary metabolites, including host-selective toxins such as methyl-(5-hydroxymethyl) furan-2-carboxylate, to induce cell death and nutrient leakage. Melanin deposition in the cell wall and regulatory networks involving velvet proteins and GTPase-mediated signal transduction underpin fungal survival under oxidative and osmotic stress, ensuring both reproduction and lesion expansion. Adaptation to host-derived iron constraints further fine-tunes virulence by modulating iron assimilation pathways. Transcriptomic and genomic analyses have revealed expansions in transporter families, polyketide synthases and regulatory kinases, reflecting evolutionary plasticity that enables rapid emergence of new virulent strains under variable environmental conditions. A detailed understanding of these mechanisms is essential for breeding resistant maize varieties and for developing targeted antifungal strategies.

Research from Nature Portfolio

Recent studies have elucidated key regulators of Curvularia pathogenicity. A master regulator known as ClVelB, a member of the velvet protein family, coordinates conidiation, secondary toxin production and stress responses; disruption of this regulator impairs melanin synthesis and toxin accumulation, leading to reduced host colonisation. Another investigation has characterised a small GTPase homologue, Clg2p, which interacts with MAP kinase kinase kinase–like and urate oxidase partners to control appressorium formation and spore morphology. Mutants lacking Clg2p form defective infection structures and exhibit diminished lesion development, confirming the importance of this signalling axis in fungal invasion.

Pathogenic Mechanisms of Curvularia Species in Maize publication trend

The graph below shows the total number of articles in pathogenic mechanisms of curvularia species in maize across all publications each year (not limited to Nature Index journals).

Technical terms

Appressorium: A specialised fungal structure that generates mechanical force to penetrate the host epidermis.

Conidium: A non-motile asexual spore involved in dispersal and infection initiation.

Velvet protein: A regulatory protein family that coordinates fungal development, secondary metabolism and stress tolerance.

Polyketide synthase: An enzyme complex that assembles polyketide secondary metabolites, including host-selective toxins.

GATA transcription factor: A DNA-binding protein that regulates gene expression in response to iron availability.

References

1. SreC‐dependent adaption to host iron environments regulates the transition of trophic stages and developmental processes of Curvularia lunata. Molecular Plant Pathology (2024).
2. Elucidating the Fundamental Process of Methyl-(5hydroxymethyl) Furan-2-Carboxylate Toxin Biosynthesis in Curvularia lunata Causing Maize Leaf Spot. Journal of Fungi (2024).
3. Involvement of a velvet protein ClVelB in the regulation of vegetative differentiation, oxidative stress response, secondary metabolism, and virulence in Curvularia lunata. Scientific Reports (2017).
4. Clg2p interacts with Clf and ClUrase to regulate appressorium formation, pathogenicity and conidial morphology in Curvularia lunata. Scientific Reports (2016).
5. Genome sequence and virulence variation-related transcriptome profiles of Curvularia lunata, an important maize pathogenic fungus. BMC Genomics (2014).
6. The Interpretation of the Role of a Polyketide Synthase ClPKS18 in the Pathogenicity of Curvularia lunata. Frontiers in Microbiology (2022).