Pathogenic Mechanisms of Ustilago Maydis in Plant Systems

Ustilago maydis is a biotrophic basidiomycete fungus that causes common smut in maize by establishing intimate, long‐term interactions with its host without immediately killing plant cells. Central to its pathogenic success is a diverse arsenal of secreted effector proteins that manipulate host physiology. These effectors suppress immune responses—for example by inhibiting oxidative‐burst enzymes and apoplastic proteases—reprogramme host transcriptional networks to induce hyperplasia and hypertrophy, and divert metabolic fluxes towards pathways that favour fungal proliferation. Tumour formation on aerial maize tissues arises from coordinated cell‐cycle re‐entry of bundle‐sheath and leaf epidermal cells, driven by effector‐mediated activation of plant developmental regulators. Prior to penetration, U. maydis senses plant surface cues via specialised receptors, triggering filamentous growth and appressorium formation. Following entry, fungal hyphae grow intercellularly, deriving nutrients through a specialised interface. The interplay between early immune suppression and later nutrient acquisition underpins U. maydis virulence, offering a model for understanding biotrophic fungal pathogens and guiding breeding of resistant crops.

Research from Nature Portfolio

Recent studies have elucidated novel effector functions. One investigation characterised the Small Tumour on Seedlings 2 (Sts2) effector, revealing its translocation into the maize‐cell nucleus where it acts as a transcriptional activator of leaf developmental genes to drive hyperplasia and tumour growth. Disruption of its transactivation domain abolishes virulence, underlining the centrality of host transcriptional reprogramming. A separate analysis defined the repetitive secreted protein Rsp3, which coats fungal hyphae and interacts with mannose‐binding DUF26‐domain host proteins. By neutralising these antifungal host factors, Rsp3 protects the pathogen from host‐derived defence peptides, illustrating a novel strategy by which surface‐associated effectors shield invasive hyphae.

Pathogenic Mechanisms of Ustilago Maydis in Plant Systems publication trend

The graph below shows the total number of articles in pathogenic mechanisms of ustilago maydis in plant systems across all publications each year (not limited to Nature Index journals).

Technical terms

Effector protein: secreted fungal molecule that manipulates host cell processes to facilitate infection.

Biotrophic interaction: a parasitic relationship in which the pathogen derives nutrients from living host cells without killing them immediately.

Hyperplasia: increased cell division leading to tissue overgrowth, as seen in tumour formation.

Apoplast: the extracellular space in plant tissues through which water and solutes move and where many effectors act.

Transcriptional activator: a protein that binds host DNA and enhances expression of target genes.

References

1. A transcriptional activator effector of Ustilago maydis regulates hyperplasia in maize during pathogen-induced tumor formation. Nature Communications (2023).
2. The Ustilago maydis repetitive effector Rsp3 blocks the antifungal activity of mannose-binding maize proteins. Nature Communications (2018).
3. Combination of in vivo proximity labeling and co-immunoprecipitation identifies the host target network of a tumor-inducing effector in the fungal maize pathogen Ustilago maydis. Journal of Experimental Botany (2023).
4. The Ustilago maydis Effector Pep1 Suppresses Plant Immunity by Inhibition of Host Peroxidase Activity. PLOS Pathogens (2012).
5. Compatibility in the Ustilago maydis–Maize Interaction Requires Inhibition of Host Cysteine Proteases by the Fungal Effector Pit2. PLOS Pathogens (2013).
6. Plant Surface Cues Prime Ustilago maydis for Biotrophic Development. PLOS Pathogens (2014).