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The Pathogenic Mechanisms of Tilletia horrida as Revealed by Comparative and Functional Genomics

Summary

This research provides important insights into how a destructive fungal disease affects rice crops by studying its genetic makeup. The findings help us understand how this fungus infects rice plants and causes disease, which is crucial for developing better control methods. Impacts on everyday life: • Helps protect rice production, which is a staple food for about 20% of the world’s population • Could lead to better methods for controlling crop diseases and improving food security • May help develop more resistant rice varieties that farmers can grow • Could reduce the need for chemical fungicides in rice farming • Has potential implications for reducing crop losses and keeping rice prices stable for consumers

Background

Rice kernel smut (RKS), caused by the soil-borne Basidiomycete fungus Tilletia horrida that infects rice floral organs, was first reported in Japan in 1896. While once considered a minor disease, the increasing cultivation of hybrid rice varieties has led to greater susceptibility and impact, with disease incidence as high as 87-100% reported in some regions. This has resulted in 40-60% prevalence in hybrid rice fields and 5-20% decreases in rice yield, making it an increasing threat to rice cultivation globally.

Objective

To understand the molecular mechanisms involved in the evolution, biotrophy, and pathogenesis of Tilletia horrida through genome sequencing, comparative genomics, and functional analysis of virulence factors.

Results

The T. horrida genome was found to be 23.2 Mb in size, containing 7,729 predicted genes with 6,973 supported by RNA-seq data. The genome contained few repetitive elements (8.45% of total). Two novel effector proteins were identified and validated to trigger cell death in N. benthamiana. The fungus possessed a smaller set of carbohydrate-active enzymes and secondary metabolites compared to other plant pathogens, reflecting its biotrophic lifestyle. Genes encoding secreted proteins, secondary metabolism enzymes, and pathogen-host interaction genes showed high expression during early infection.

Conclusion

The study revealed new molecular mechanisms underlying T. horrida’s evolution and pathogenesis, including the identification of effector proteins and virulence factors. The genome analysis showed adaptations for a biotrophic lifestyle and host specificity, providing insights into the pathogen’s infection strategies and host-pathogen interactions.
  • Published in:Scientific Reports,
  • Study Type:Genomic Analysis,
  • Source: 10.1038/s41598-018-33752-w
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