Apple Disease Gene VmRDR2 Weakens Resistance Through RNA Interference

Jim Crocker
2nd June, 2024

Apple Disease Gene VmRDR2 Weakens Resistance Through RNA Interference

Image Source: Natural Science News, 2024

Key Findings

  • Researchers from Northwest A&F University studied how the fungus Valsa mali infects apple trees using RNA interference (RNAi)
  • The fungus uses an enzyme called VmRDR2 to produce small interfering RNAs (siRNAs) that target and degrade the apple gene MdLRP14
  • By degrading MdLRP14, the fungus suppresses the apple tree's immune response, making it more susceptible to infection
Cross-kingdom RNA interference (RNAi) is a significant mechanism in the interactions between hosts and pathogens, particularly in the context of plant-pathogen dynamics. Researchers from Northwest A&F University have recently uncovered critical insights into how pathogenic fungi utilize RNAi to suppress plant immune responses, focusing on the role of RNA-dependent RNA polymerase (RdRP) in this process[1]. RNAi is a biological process where RNA molecules inhibit gene expression by neutralizing targeted mRNA molecules. This mechanism plays a crucial role in defending against viruses and regulating gene expression. In this study, the researchers aimed to understand the role of two specific RdRP enzymes, VmRDR1 and VmRDR2, in the pathogenicity of the fungus Valsa mali, which infects apple trees. The study revealed that VmRDR2 is particularly important in generating small interfering RNAs (siRNAs), including an infection-related siRNA named VmR2-siR1. These siRNAs are crucial because they can silence specific genes in the host plant. In this case, VmR2-siR1 targets and degrades the apple gene MdLRP14, which encodes an intracellular leucine-rich repeat (LRR) protein. LRR proteins are known for their role in protein-protein interactions and are vital for the plant's immune response[2]. By degrading MdLRP14, VmR2-siR1 effectively suppresses the apple tree's resistance to V. mali. The study demonstrated that overexpression of MdLRP14 in apple trees enhanced their resistance to the fungus, while knockdown of MdLRP14 reduced this resistance. This indicates that VmR2-siR1 plays a pivotal role in the pathogenicity of V. mali by silencing a key resistance gene in the host plant. The researchers employed deep sequencing, molecular, genetic, and biochemical approaches to elucidate these mechanisms. Deep sequencing allowed them to identify the specific siRNAs generated during infection. Genetic and molecular techniques were used to manipulate the expression of VmRDR1, VmRDR2, and MdLRP14 to observe the effects on fungal pathogenicity and plant resistance. Biochemical methods helped to confirm the interactions between VmR2-siR1 and MdLRP14 mRNA. This study builds on previous findings about the role of RNAi and RdRPs in fungal pathogenesis. For instance, earlier research in Mucor circinelloides, a fungus causing mucormycosis, highlighted the role of RdRP in generating drug-resistant strains through RNAi pathways[3]. Additionally, it was shown that different RdRPs have distinct roles in the initiation and amplification of the RNA silencing signal in M. circinelloides[4]. The current study expands this understanding by demonstrating a similar mechanism in a plant-pathogen interaction, where fungal RdRPs generate siRNAs to suppress host immune responses. In summary, the study from Northwest A&F University provides valuable insights into how Valsa mali utilizes the RNAi machinery to enhance its pathogenicity in apple trees. By generating siRNAs like VmR2-siR1, the fungus can silence crucial resistance genes in the host, thereby overcoming the plant's immune defenses. These findings not only enhance our understanding of fungal pathogenesis but also open up potential avenues for developing new strategies to improve plant resistance against fungal infections.

GeneticsBiochemPlant Science


Main Study

1) VmRDR2 of Valsa mali mediates the generation of VmR2-siR1 that suppresses apple resistance by RNA interference.

Published 1st June, 2024

Related Studies

2) The leucine-rich repeat structure.

3) A non-canonical RNA degradation pathway suppresses RNAi-dependent epimutations in the human fungal pathogen Mucor circinelloides.

4) Two distinct RNA-dependent RNA polymerases are required for initiation and amplification of RNA silencing in the basal fungus Mucor circinelloides.

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