Plasmopara viticola is an obligate biotrophic pathogen that infects grapevines, causing downy mildew. It has demonstrated remarkable adaptive capacity, rapidly developing fungicide resistance and repeatedly breaking down grapevine resistance genes including Rpv3.1, Rpv10, Rpv12, and more recently Rpv1. In China, P. viticola populations exhibit high genetic diversity, with significant pathogenic differences observed between isolates from Eurasian Vitis vinifera and wild East Asian V. amurensis. However, earlier genome assemblies based on short-read sequencing failed to fully capture the complex, repeat-rich regions where effector genes often reside, leaving the mechanisms driving this pathogenic variation unresolved. Based on these challenges, there is an urgent need to conduct in-depth research into the genomic architecture underlying effector diversification and host adaptation in this pathogen.
A team led by researchers from the Institute of Plant Protection at the Chinese Academy of Agricultural Sciences, in collaboration with China Agricultural University, the Chinese Academy of Tropical Agricultural Sciences, and Yunnan Agricultural University, has published (DOI: 10.1093/hr/uhag073) two complete genome assemblies of Plasmopara viticola in Horticulture Research (Volume 13, Issue 6, June 2026). The study reveals that structural variations and local gene duplications are the primary drivers of effector gene diversification, providing a genome-resolved framework for understanding intraspecific genomic diversity in this major agricultural pathogen.
Using PacBio HiFi long-read sequencing, the researchers assembled two complete genomes—PvH (115.3 Mb) from V. vinifera and PvS (113.0 Mb) from V. amurensis—each resolved into 17 chromosomes. The assemblies achieved telomere-to-telomere completeness for 14 chromosomes in PvH and 15 in PvS, a substantial improvement over previous fragmented assemblies. Comparative genomic analysis uncovered striking differences in effector repertoires: PvH harbors 379 CRN (Crinkler) effectors compared to 240 in PvS and 219 in the reference isolate PV221—a 1.4-fold increase—and contains 35 strain-specific CRN genes. These effector genes are not randomly distributed but clustered in specific chromosomal regions with elevated transposable element (TE) density. The study further demonstrated that local duplication events—including tandem, proximal, and segmental duplications—are the primary drivers of effector expansion. At known avirulence loci (AvrRpv3.1, AvrRpv10, AvrRpv12), PvS showed effector gene deletions that correlated with loss of expression, while PvH retained multiple novel effector variants, with TEs enriched at these sites. In total, 104 putative effectors—including 21 RxLRs, 59 CRNs, and 24 carbohydrate-active enzymes (CAZymes)—were located within inversion regions.
"The pathogen's genome is far more dynamic than we previously appreciated," the authors said. "We found that structural variations—inversions, duplications, and rearrangements—create hotspots where effector genes are constantly being duplicated, deleted, and reshuffled. This genomic plasticity may be the secret behind P. viticola's ability to rapidly adapt to new grapevine hosts and overcome resistance. What surprised us most was the extent of isolate-specific effector differences: two strains of the same species can have dramatically different arsenals of these virulence genes."
These findings have direct implications for grapevine breeding and disease management. By identifying the genomic regions and mechanisms driving effector diversification, the study provides a roadmap for predicting how P. viticola might evolve in response to new resistant grapevine varieties. The complete genome assemblies also establish a reference for future population-level studies aimed at linking specific structural variants to pathogenic outcomes. Understanding which effector genes are lost or gained as the pathogen adapts to different hosts could inform the design of more durable resistance strategies—for instance, by stacking resistance genes that target effectors unlikely to be deleted without compromising pathogen fitness. The work also provides a foundation for functional validation of candidate effectors and the development of novel fungicide targets.
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References
DOI
10.1093/hr/uhag073
Original Source URL
https://doi.org/10.1093/hr/uhag073
Funding information
This work was supported by the National Key Research and Development Program of China (2023YFD1401405), the China Agricultural Research System (CARS-29), the Expert Workstation Project in Yunnan Province (202305AF150129), and Central Public-interest Scientific Institution Basal Research Fund (82025X131).
About Horticulture Research
Horticulture Research is an open access journal of Nanjing Agricultural University and ranked number one in the Horticulture category of the Journal Citation Reports ™ from Clarivate, 2023. The journal is committed to publishing original research articles, reviews, perspectives, comments, correspondence articles and letters to the editor related to all major horticultural plants and disciplines, including biotechnology, breeding, cellular and molecular biology, evolution, genetics, inter-species interactions, physiology, and the origination and domestication of crops.