Plants defend themselves through a layered innate immune system: pathogen-associated molecular pattern-triggered immunity (PTI) and effector-triggered immunity (ETI), mediated by pattern recognition receptors (PRRs) and nucleotide-binding leucine-rich repeat (NLR) receptors, respectively.
Transcription factors—proteins that switch defense genes on and off—are central to this process. Yet fungal pathogens have evolved effector proteins designed to sabotage these regulators.
While scientists knew that V. mali secretes effectors to undermine plant immunity, exactly how these molecular saboteurs operate at the molecular level remained unclear. Due to these challenges, there is an urgent need for in-depth research into the specific mechanisms by which fungal effectors disable host transcription factors during infection.
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Researchers from the State Key Laboratory for Crop Stress Resistance and High-Efficiency Production at Northwest A&F University in China report their findings published (DOI: 10.1093/hr/uhag054) online on February 26, 2026, in Horticulture Research. The team identified a ribonuclease T2-like effector protein, VmRnt2, that V. mali deploys during infection. Their work reveals that VmRnt2 physically binds to and disables an apple transcription factor called MdMYB44, effectively silencing the tree’s defense gene MdPR1A and rendering the plant more vulnerable to infection.
Essential for virulence
The research team began by demonstrating that VmRnt2 is essential for the fungus’s full virulence. When they knocked out the VmRnt2 gene, the mutant fungus caused significantly smaller lesions on apple twigs without any impact on its growth or spore production—proving this protein is a dedicated weapon, not a general-purpose tool.
Further experiments showed that VmRnt2 suppresses multiple layers of plant immunity, including reactive oxygen species (ROS) bursts, callose deposition, and programmed cell death triggered by immune elicitors. Critically, the team discovered that VmRnt2 physically interacts with MdMYB44, an apple transcription factor belonging to the myeloblastosis (MYB) family of proteins. Overexpressing MdMYB44 in apple plants enhanced resistance to V. mali, confirming its role as a positive immune regulator.
MdMYB44 normally binds to the promoter of the defense gene MdPR1A and activates its transcription. But when VmRnt2 is present, it disrupts MdMYB44’s DNA-binding activity—effectively pulling the plug on the tree’s immune signaling. Even more revealing, when the researchers mutated the catalytic site of VmRnt2, the protein lost its ability to inhibit MdMYB44, proving that the interaction is specific and functionally critical.
Master switch
“We were surprised to find that a single effector protein from the fungus could so precisely target a key transcriptional regulator in the apple tree,” the authors said. “It’s like the pathogen has found the master switch for the plant’s immune response and figured out exactly how to turn it off. Understanding this arms race at the molecular level gives us a real opportunity to tip the balance back in favor of the tree.”
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These findings have immediate implications for apple breeding and disease management. By identifying MdMYB44 as a critical resistance factor, breeders now have a molecular marker to select for canker-resistant apple varieties. Moreover, the discovery that VmRnt2 targets the DNA-binding domain of MdMYB44 suggests that engineering variants of this transcription factor resistant to fungal interference could be a viable strategy.
The research also highlights the salicylic acid (SA) defense pathway as a promising target for enhancing broad-spectrum resistance. With apple Valsa canker causing devastating losses across orchards worldwide, these insights could translate into more resilient trees and more sustainable farming practices.
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