Novel Epigenetic Regulator Enhances Downy Mildew Resistance in Brassica rapa

Downy mildew is a major constraint on Brassica crop production worldwide, especially during early developmental stages when plants are highly vulnerable to infection. Effective plant immunity relies on tightly regulated defense signaling networks, among which salicylic acid plays a central role in resistance to biotrophic pathogens. Epigenetic regulators such as histone deacetylases are known to influence plant stress responses by altering chromatin structure and gene expression. However, most previous studies have focused on histone modification, leaving the role of nonhistone protein deacetylation largely unexplored in plant–pathogen interactions. These gaps highlight the need for deeper investigation into unconventional epigenetic mechanisms that fine-tune plant immune responses.

Researchers from the Beijing Academy of Agriculture and Forestry Science and collaborating institutions report new insights into plant immune regulation in a study published (DOI: 10.1093/hr/uhaf136) on May 21, 2025, in Horticulture Research. By combining genetic, biochemical, and multi-omics approaches, the team investigated how epigenetic regulators influence resistance to downy mildew in Brassica rapa. The study identifies BrHDA6 as a positive regulator of disease resistance and demonstrates that it enhances immunity by modifying a key enzyme in salicylic acid metabolism rather than acting solely through chromatin remodeling.

The study first showed that chemical inhibition of histone deacetylases increased susceptibility to downy mildew, indicating that deacetylation is essential for basal resistance. Transcriptome profiling of resistant and susceptible lines then identified BrHDA6 as a candidate gene strongly associated with disease resistance. Functional analyses using transgenic plants confirmed that overexpression of BrHDA6 enhanced resistance, while gene silencing led to severe disease symptoms.

Beyond histone regulation, the researchers discovered that BrHDA6 directly interacts with the sulfotransferase BrSOT12. Proteomic and acetylome analyses revealed that BrHDA6 reduces the acetylation level of BrSOT12, particularly at a key lysine residue. This deacetylation is associated with increased sulfotransferase activity, which in turn promotes early accumulation of salicylic acid following pathogen infection. Elevated salicylic acid levels were accompanied by rapid activation of defense-related genes, reinforcing immune responses.

Together, these results define a previously unrecognized epigenetic pathway in which a histone deacetylase regulates plant immunity through nonhistone protein modification, linking epigenetic control directly to hormone-mediated defense signaling.

"This work changes how we think about epigenetic regulation in plant immunity," said the study's senior author. "Instead of acting only at the level of chromatin, BrHDA6 directly modifies a metabolic enzyme that controls salicylic acid signaling. This dual role allows plants to respond rapidly and precisely to pathogen attack. Understanding such mechanisms opens new opportunities to improve disease resistance without compromising growth, which is a long-standing challenge in crop breeding."

The identification of the BrHDA6–BrSOT12 regulatory module provides a promising molecular target for breeding disease-resistant Brassica crops. By enhancing salicylic acid-mediated immunity through epigenetic fine-tuning rather than broad transcriptional changes, this pathway may allow more durable resistance with fewer trade-offs in plant development. The findings also suggest that nonhistone deacetylation is an underexplored layer of immune regulation in plants. Beyond Brassica, similar mechanisms may operate in other crops, offering new strategies for improving resilience against pathogens in sustainable agriculture.

Source:
Journal reference:

Wang, J., et al. (2025). BrHDA6 mediates nonhistone deacetylation of BrSOT12 to positively regulate downy mildew resistance in Brassica rapaHorticulture Research. DOI: 10.1093/hr/uhaf136. https://academic.oup.com/hr/article/12/8/uhaf136/8139763

Comments

The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of AZoLifeSciences.
Post a new comment
Post

While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. We do not provide medical advice, if you search for medical information you must always consult a medical professional before acting on any information provided.

Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles.

Please do not ask questions that use sensitive or confidential information.

Read the full Terms & Conditions.

You might also like...
Mapping the Human E3 Ligase Landscape