Soil bacterium wields two-pronged attack to disarm devastating sunflower pathogen

A soil-dwelling bacterium isolated from the roots of healthy sunflower plants has emerged as a remarkably versatile weapon against one of agriculture’s most stubborn fungal enemies. In a study published in BMC Plant Biology, researchers in China report that Bacillus velezensis strain SGTSH 0811 suppresses sunflower sclerotiniose, a destructive disease caused by the fungus Sclerotinia sclerotiorum, through a dual strategy: it directly attacks the pathogen with antifungal metabolites while simultaneously switching on the plant’s own immune defenses. The work, led by Saisai Wang of Shanghai Jiao Tong University together with colleagues from Silicon Gene Technologies and the Shanghai Agricultural Technology Extension Service Center, offers one of the most complete molecular pictures yet of how a single biocontrol strain can fight a pathogen on two fronts at once.

Sunflower sclerotiniose is a global threat to sunflower production. Sclerotinia sclerotiorum, the fungus responsible, is notorious among plant pathologists for its breadth of hosts and its persistence in soil. It survives unfavorable conditions as sclerotia, compact masses of hardened fungal tissue that can lie dormant for years before germinating and launching new infections. Because the pathogen attacks stems, heads, and roots, and because its resting structures endure in the field, chemical fungicides often deliver only partial and temporary relief. That persistence, combined with growing pressure to reduce agricultural chemical inputs, has driven researchers to search the rhizosphere, the microbially dense zone of soil surrounding plant roots, for natural antagonists capable of durable disease suppression.

The Shanghai-led team began by isolating bacteria from the rhizosphere soil of healthy sunflowers and screening the isolates for activity against S. sclerotiorum. One strain, designated SGTSH 0811 and identified as Bacillus velezensis, stood out. In laboratory assays, the bacterium strongly inhibited both the vegetative growth of the fungus and the germination of its sclerotia, striking at two distinct stages of the pathogen’s life cycle. That combination matters: killing hyphae stops an infection in progress, while preventing sclerotial germination interrupts the disease cycle before it can even begin. The strain also showed activity against a range of other fungal pathogens in vitro, including Fusarium graminearum, Fusarium oxysporum, Alternaria solani, and Magnaporthe oryzae, hinting at a broad-spectrum antifungal repertoire.

To understand where that repertoire comes from, the researchers sequenced the strain’s complete genome using Oxford Nanopore Technologies and mined it for secondary metabolite biosynthetic gene clusters, the genetic blueprints bacteria use to manufacture bioactive small molecules. The analysis identified twelve such clusters, six of which correspond to compounds with previously verified antifungal functions. Among the predicted machinery were non-ribosomal peptide synthetases and polyketide synthases, enzyme families famous for producing lipopeptides and related antibiotics. Comparative genomic checks, including average nucleotide identity and digital DNA-DNA hybridization analyses, confirmed the strain’s placement within B. velezensis, a species already celebrated in biocontrol circles but whose full antagonistic mechanisms often remain murky.

The mechanistic heart of the study focused on lipopeptides, cyclic molecules that combine lipid tails with peptide rings and are among the best-known antifungal weapons of Bacillus species. Using liquid chromatography coupled with quadrupole time-of-flight mass spectrometry, the team characterized a crude lipopeptide extract from the strain’s cell-free culture filtrate. Crucially, the antifungal activity proved thermostable, surviving heat treatment that would destroy most proteins, which pointed squarely at small-molecule metabolites rather than enzymes as the active agents. When the extract was applied to S. sclerotiorum, microscopy told a vivid story of structural collapse: propidium iodide, a dye that only enters cells with compromised membranes, flooded into fungal cells, while Calcofluor white staining and scanning electron microscopy revealed damage to the fungal cell wall and visible distortion of hyphal surfaces.

The damage went deeper than punctured membranes. Transcriptomic profiling of the fungus after exposure to the bacterial metabolites revealed global transcriptional reprogramming, with large numbers of differentially expressed genes falling into pathways that govern virulence and stress resistance. The pathogen’s ability to deploy cell wall-degrading enzymes, its arsenal for breaching plant tissue, and its machinery for coping with oxidative and other stresses were both suppressed. In effect, the lipopeptides did not merely wound the fungus; they undermined its capacity to fight back and to infect. This dual blow, physical disruption of the cell envelope combined with transcriptional silencing of virulence programs, helps explain why the strain’s inhibition was so potent in vitro.

Yet direct antagonism is only half of the story. The researchers also tested what SGTSH 0811 does to the sunflower plants themselves, and here the results shifted from warfare to cultivation. Plants treated with the bacterium grew better than untreated controls, consistent with the strain’s membership in the plant growth-promoting rhizobacteria, a loosely defined group of root-associated microbes that boost host vigor. More strikingly, when challenged by S. sclerotiorum, bacterium-treated sunflowers mounted measurably stronger defensive physiology. The team documented increased activities of antioxidant enzymes, the plant’s first-line detoxifiers of reactive oxygen species generated during infection, alongside elevated accumulation of proline, an osmoprotective amino acid that plants commonly stockpile under stress. Together these changes point to induced systemic resistance, a priming of the plant’s innate immune system by beneficial microbes.

The laboratory findings translated to the field. In field trials, the strain achieved stable suppression of sunflower sclerotiniose, demonstrating that the dual mechanism observed in petri dishes and growth chambers holds up under the messier conditions of real agriculture. Field performance is the perennial stumbling block for biocontrol candidates, which often shine in vitro but fade in soil, where competition, pH, moisture, and microbial neighbors can erode their activity. The authors argue that SGTSH 0811’s combination of traits, pathogen inhibition, sclerotial suppression, plant growth promotion, and host resistance induction, gives it multiple redundant routes to protection, a robustness that single-mechanism agents often lack.

The study’s broader significance lies in its systems-level approach. Rather than cataloguing a single antifungal compound, the researchers connected genome sequence, metabolite chemistry, fungal cytology, fungal transcriptomics, and plant physiology into one coherent causal chain. The twelve biosynthetic gene clusters identified in the genome now constitute a roadmap for future work: individual lipopeptides can be purified, their specific contributions quantified, and the clusters expressed heterologously or engineered to enhance activity. The transcriptional data on the pathogen likewise open questions about which fungal regulatory networks are most vulnerable to lipopeptide attack, knowledge that could inform both biocontrol design and the search for new drug targets in fungal pathogens of crops.

For agriculture, the implications are timely. Soil-borne diseases such as sclerotiniose are among the hardest to manage precisely because the pathogen lurks in the ground where fungicides penetrate poorly and persist badly. A multi-functional biopesticide built on a rhizosphere strain like SGTSH 0811 would attack the problem where it lives, in the soil, while avoiding the residue and resistance concerns that shadow chemical fungicides. The authors frame their results as a theoretical foundation for developing eco-friendly biopesticides against soil-borne sclerotiniose, and the strain’s dual mode of action, killing the fungus while strengthening its host, is exactly the kind of synergistic design that next-generation biologicals aim to replicate. As pressure mounts to sustain sunflower yields with fewer synthetic inputs, a heat-stable lipopeptide arsenal and a primed plant immune system may prove to be a formidable pairing, courtesy of a bacterium found quietly thriving at the sunflower’s roots.

Subject of Research: Biological control of sunflower sclerotiniose using Bacillus velezensis strain SGTSH 0811 through lipopeptide-mediated pathogen inhibition and induced host resistance

Article Title: Bacillus velezensis SGTSH 0811 suppresses sunflower sclerotiniose by pathogen inhibition and host resistance induction

Article References: Wang, S., Yan, X., Gao, Y., Yu, G., Ma, Y., Gao, Y., Huang, Y., & Tang, X. (2026). Bacillus velezensis SGTSH 0811 suppresses sunflower sclerotiniose by pathogen inhibition and host resistance induction. BMC Plant Biology. https://doi.org/10.1186/s12870-026-09784-0

Image Credits: AI Generated

DOI: 10.1186/s12870-026-09784-0

Keywords: Bacillus velezensis, Sclerotinia sclerotiorum, sunflower sclerotiniose, biological control, lipopeptides, biosynthetic gene clusters, induced systemic resistance, plant growth-promoting rhizobacteria, antifungal activity, soil-borne disease, transcriptomics, sustainable agriculture