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Home Science News Agriculture

Fungal enzyme strips chitin disguise to let wheat bunt pathogen slip past plant defenses

October 18, 2026
in Agriculture
Alan Morgan
By Alan Morgan Scienmag Editorial Profile - Precision Agriculture
Reading Time: 4 mins read
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Fungal enzyme strips chitin disguise to let wheat bunt pathogen slip past plant defenses

Fungal enzyme strips chitin disguise to let wheat bunt pathogen slip past plant defenses

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Wheat growers around the world have long battled common bunt, a disease caused by the fungus Tilletia laevis that replaces healthy grains with dark, fishy-smelling galls and can devastate both yield and flour quality. Now researchers have identified a single fungal enzyme that appears to be central to how this pathogen slips past the plant’s immune system, offering a promising new target for chemical control of one of the most destructive wheat diseases worldwide.

The enzyme, named TlCDA, is a chitin deacetylase produced by T. laevis. Chitin deacetylases catalyze the conversion of chitin, a structural polysaccharide found in fungal cell walls, into chitosan by removing acetyl groups. This chemical modification matters because chitin is a potent pathogen-associated molecular pattern, or PAMP, that plant pattern-recognition receptors detect to launch pattern-triggered immunity, the first line of defense against invading fungi. By deacetylating chitin, the fungus effectively converts an alarm signal into a molecule that plant receptors no longer recognize.

In the new study, published in BMC Plant Biology, a team led by Zhaoyu Ren and Li Gao at the Chinese Academy of Agricultural Sciences identified TlCDA from T. laevis and confirmed that it possesses genuine chitin deacetylase activity. Critically, the researchers found that expression of the TlCDA gene is upregulated during the early infection stage of T. laevis in wheat, precisely the window when the pathogen must establish itself before the plant mounts an effective response.

To probe what TlCDA does inside plant tissue, the team used transient expression assays in Nicotiana benthamiana, a widely used model plant for studying pathogen virulence factors. When TlCDA was expressed in the model plant, it inhibited programmed cell death, suppressed the accumulation of reactive oxygen species, and reduced the expression level of defense-related genes. These three outcomes together indicate that TlCDA actively dampens the plant’s immune defense response rather than merely avoiding it.

Reactive oxygen species, or ROS, are a rapid and essential component of plant immunity. Upon recognizing a pathogen, plants produce an oxidative burst that can directly damage the invader and also serves as a signal to activate broader defense pathways, including mitogen-activated protein kinase cascades and the expression of pathogenesis-related genes. Programmed cell death at the infection site, meanwhile, is a strategy plants use to sacrifice cells and starve biotrophic pathogens of living tissue. By suppressing both ROS accumulation and programmed cell death, TlCDA undermines two of the most important weapons in the plant’s arsenal.

The researchers also generated a deletion mutant of TlCDA in T. laevis to test whether the enzyme is required for pathogenicity. Loss of TlCDA suppressed both the growth and the pathogenicity of the fungus, highlighting the significance of this enzyme in the host-pathogen interaction. This result elevates TlCDA from a correlated virulence factor to a demonstrated requirement for full disease development, a distinction that matters for any future control strategy.

Beyond its role in suppressing plant immunity, TlCDA appears to serve a second protective function for the pathogen. In vitro experiments showed that TlCDA can protect teliospores, the thick-walled survival structures of T. laevis, from being damaged by chitinase, the enzyme plants and other organisms use to break down chitin in fungal cell walls. This suggests that deacetylating the spore surface converts it into a chitosan-rich layer that chitinase cannot efficiently degrade, shielding the pathogen during its most vulnerable phase.

Common bunt is prevalent in wheat-growing regions across the globe, and diseased grains emit a distinctive fishy odor due to trimethylamine produced by the pathogen, seriously affecting the quality of flour. The disease is particularly difficult to manage because teliospores can survive in soil and on seed for years, and chemical seed treatments face increasing regulatory pressure. Identifying a key virulence factor like TlCDA opens the possibility of designing inhibitors that specifically block the enzyme’s activity, preventing the pathogen from disguising itself and allowing the plant’s immune system to recognize and respond to the invader.

The findings collectively identify TlCDA as a key virulence factor of T. laevis and a promising target for chemical control of common bunt. Because chitin deacetylases are fungal enzymes with no direct equivalent in plant metabolism, inhibitors directed against TlCDA could in principle be selective for the pathogen while sparing the host, reducing off-target effects compared with broader-spectrum fungicides. The work also adds to a growing body of research showing that pathogens manipulate PAMP chemistry as a central immune-evasion strategy, a theme now documented across fungal, oomycete, and bacterial plant pathogens.

For wheat breeders and plant pathologists, the study provides a molecular handle on a disease that has historically been managed through seed treatment and quarantine rather than through targeted intervention. If future research can validate TlCDA as a control point in the field, whether through small-molecule inhibitors, RNA-based silencing, or breeding for host factors that interfere with the enzyme, the discovery could translate into practical protection for a staple crop that feeds billions. The research was supported by the Central Public-interest Scientific Institution Basal Research Fund, the Agricultural Science and Technology Innovation Program, Xinjiang Major Science and Technology Projects, and the Nanfan Special Project of the Chinese Academy of Agricultural Sciences.

Subject of Research: Plant Pathology

Article Title: The chitin deacetylase TlCDA from Tilletia laevis facilitates pathogen infection by suppressing plant immunity

Article References: Ren, Z., Weng, H., Jia, H., Liu, T., Chen, W., & Gao, L. (2026). The chitin deacetylase TlCDA from Tilletia laevis facilitates pathogen infection by suppressing plant immunity. BMC Plant Biology. https://doi.org/10.1186/s12870-026-09998-2

Image Credits: AI Generated

DOI: 10.1186/s12870-026-09998-2

Keywords: Tilletia laevis, common bunt, chitin deacetylase, plant immunity, wheat disease, virulence factor, chitin, deacetylase, TlCDA, Tilletia, laevis, facilitates

Cite Scienmag News

Alan Morgan. (October 18, 2026). Fungal enzyme strips chitin disguise to let wheat bunt pathogen slip past plant defenses. Scienmag. https://scienmag.com/fungal-enzyme-strips-chitin-disguise-to-let-wheat-bunt-pathogen-slip-past-plant-defenses/

Alan Morgan. "Fungal enzyme strips chitin disguise to let wheat bunt pathogen slip past plant defenses." Scienmag, 18 October 2026, https://scienmag.com/fungal-enzyme-strips-chitin-disguise-to-let-wheat-bunt-pathogen-slip-past-plant-defenses/. Accessed 18 October 2026.

Alan Morgan. "Fungal enzyme strips chitin disguise to let wheat bunt pathogen slip past plant defenses." Scienmag. October 18, 2026. https://scienmag.com/fungal-enzyme-strips-chitin-disguise-to-let-wheat-bunt-pathogen-slip-past-plant-defenses/

Tags: chemical control of wheat diseaseschitinchitin deacetylasechitin deacetylation in fungicommon buntcrop disease managementdeacetylasefacilitatesfungal cell wall modificationfungal enzyme chitin deacetylasefungal pathogenicity factorslaevispattern-triggered immunity suppressionplant immune evasion mechanismsplant immunityplant-pathogen interactionsTilletiaTilletia laevisTilletia laevis pathogenTlCDAvirulence factorwheat bunt diseasewheat diseasewheat disease resistance
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