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Main conclusion <p><Emphasis Type="BoldItalic">S. sclerotiorum</Emphasis><b> virulence is mediated by oxalic acid-induced redox imbalance. Resistant Brassica genotypes sustain antioxidant capacity and NPR1-dependent systemic acquired resistance, unlike susceptible genotypes showing transient defense responses.</b></p> Abstract <p>Stem rot caused by <i>Sclerotinia sclerotiorum</i> represents a major constraint to <i>Brassica</i> production, with oxalic acid (OA) acting as a key virulence determinant. This study elucidates the role of OA in modulating disease progression, redox homeostasis, antioxidant defenses, and systemic acquired resistance (SAR) signaling in <i>Brassica</i> genotypes contrasting in resistance. Exogenous application of OA significantly exacerbated lesion expansion and disease severity, particularly in susceptible genotypes, which exhibited rapid symptom development, pronounced chlorophyll degradation, excessive reactive oxygen species (ROS) accumulation, elevated lipid peroxidation, and compromised antioxidant enzyme activities. In contrast, resistant genotypes maintained higher antioxidant capacity and displayed tightly regulated ROS dynamics, indicative of effective redox control. Temporal expression profiling of <i>NONEXPRESSOR OF PATHOGENESIS-RELATED GENES 1 (NPR1)</i> revealed distinct cultivar-specific regulatory patterns. Susceptible genotypes showed strong but transient early <i>NPR1</i> induction (up to 5.26-fold), which was not sustained during disease progression, whereas resistant genotypes exhibited intrinsic and temporally coordinated <i>NPR1</i> activation (3.37- and 9.84-fold at 7 and 14&#xa0;days post-inoculation, respectively), largely independent of OA treatment. Late-stage <i>NPR1</i> induction in susceptible genotypes was delayed and insufficient to restrict pathogen spread. Collectively, these findings demonstrate that OA-mediated disruption of redox homeostasis differentially impacts antioxidant defenses and <i>NPR1</i>-dependent SAR signaling, thereby governing cultivar-specific resistance to <i>S. sclerotiorum</i> in <i>Brassica</i> crops.</p>

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Oxalic acid-driven redox reprogramming modulates NPR1-mediated defense and disease progression in Brassica–Sclerotinia interactions

  • 期刊论文

  • 发表日期：

    2026年6月29日

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  • Rakesh Punia,
  • Pavitra Kumari,
  • Sapna,
  • Shubham Saini,
  • Ram Avtar,
  • Manoj Kumar Buswal,
  • Dalip Kumar,
  • Aakash,
  • Neeraj Kumar,
  • Mahavir Bishnoi,
  • Vinod Chouhan

摘要

Main conclusion

S. sclerotiorum virulence is mediated by oxalic acid-induced redox imbalance. Resistant Brassica genotypes sustain antioxidant capacity and NPR1-dependent systemic acquired resistance, unlike susceptible genotypes showing transient defense responses.

Abstract

Stem rot caused by Sclerotinia sclerotiorum represents a major constraint to Brassica production, with oxalic acid (OA) acting as a key virulence determinant. This study elucidates the role of OA in modulating disease progression, redox homeostasis, antioxidant defenses, and systemic acquired resistance (SAR) signaling in Brassica genotypes contrasting in resistance. Exogenous application of OA significantly exacerbated lesion expansion and disease severity, particularly in susceptible genotypes, which exhibited rapid symptom development, pronounced chlorophyll degradation, excessive reactive oxygen species (ROS) accumulation, elevated lipid peroxidation, and compromised antioxidant enzyme activities. In contrast, resistant genotypes maintained higher antioxidant capacity and displayed tightly regulated ROS dynamics, indicative of effective redox control. Temporal expression profiling of NONEXPRESSOR OF PATHOGENESIS-RELATED GENES 1 (NPR1) revealed distinct cultivar-specific regulatory patterns. Susceptible genotypes showed strong but transient early NPR1 induction (up to 5.26-fold), which was not sustained during disease progression, whereas resistant genotypes exhibited intrinsic and temporally coordinated NPR1 activation (3.37- and 9.84-fold at 7 and 14 days post-inoculation, respectively), largely independent of OA treatment. Late-stage NPR1 induction in susceptible genotypes was delayed and insufficient to restrict pathogen spread. Collectively, these findings demonstrate that OA-mediated disruption of redox homeostasis differentially impacts antioxidant defenses and NPR1-dependent SAR signaling, thereby governing cultivar-specific resistance to S. sclerotiorum in Brassica crops.