# Auxin dysregulation: a key early event in sugarcane susceptibility to Sporisorium scitamineum

**Authors:** Xin Hu, Zhengying Luo, Shenglin Ren, Jing Zhang, Chaohua Xu, Chunjia Li, Xinlong Liu

PMC · DOI: 10.1186/s12870-026-08187-5 · BMC Plant Biology · 2026-01-24

## TL;DR

This study shows that auxin, a plant hormone, plays a key role in sugarcane's susceptibility to smut disease by altering host physiology and supporting fungal infection.

## Contribution

The study reveals how fungal-produced auxin manipulates host defenses and promotes infection in sugarcane, offering new targets for disease control.

## Key findings

- IAA promotes infection at low concentrations but inhibits fungal growth at high levels.
- IAA disrupts redox balance and flavonoid metabolism, enhancing susceptibility in sugarcane.
- Resistant sugarcane genotypes maintain redox balance and flavonoid levels, limiting disease progression.

## Abstract

Sugarcane smut, caused by Sporisorium scitamineum, severely limits global sugarcane yield. Although auxin manipulation is a recognized virulence mechanism in plant-pathogen interactions, biological basis and mechanisms in orchestrating host colonization within the sugarcane-smut pathosystem remain elusive. This knowledge gap constrains a mechanistic understanding of auxin-mediated pathogenesis, thereby limiting opportunities to design auxin-based control strategies. Through integrated approaches combining exogenous hormone treatment, physiological profiling, and spatiotemporal gene expression analysis in susceptible and resistant genotypes, we aim to reveal how IAA coordinates an early host-pathogen dialogue. Our findings showed that IAA promoted infection in a dose-dependent manner: it reprogrammed host physiology at low concentrations in planta while inhibiting fungal growth at higher levels in vitro. IAA-mediated susceptibility involved disrupted redox homeostasis through suppressed activities of SOD and CAT, altered flavonoid metabolism, and upregulation of fungal effector genes such as Tin2 and Nkd1. Expression analysis further revealed temporally and genotype-dependent regulation of IAA-biosynthetic genes, with strong late-stage induction of SsIad13 and SsIad16 exclusively in susceptible plants. The resistant genotype demonstrated a superior ability to maintain redox balance and sustain flavonoid accumulation, underscoring the importance of constitutive host defense in limiting disease progression. Together, this study establishes auxin signaling as a key virulence module in S. scitamineum, synchronizing fungal IAA production, host immunity suppression, and effector deployment. These insights advance our understanding of smut disease mechanisms and propose fungal IAA pathway elements as candidate targets for future resistance breeding.

The online version contains supplementary material available at 10.1186/s12870-026-08187-5.

## Linked entities

- **Genes:** TINF2 (TERF1 interacting nuclear factor 2) [NCBI Gene 26277], NKD1 (NKD inhibitor of Wnt signaling pathway 1) [NCBI Gene 85407]
- **Chemicals:** IAA (PubChem CID 802)
- **Species:** Sporisorium scitamineum (taxon 49012)

## Full-text entities

- **Chemicals:** Auxin (MESH:D007210)
- **Species:** Sporisorium scitamineum (species) [taxon 49012]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12914901/full.md

## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC12914901/full.md

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Source: https://tomesphere.com/paper/PMC12914901