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Publication

Host-pathogen interaction between Ophiosphaerella korrae and symptomatic and asymptomatic hosts plants

Cevallos Navarrete, Felipe Gabriel
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Abstract

Ophiosphaerella korrae (J. Walker & A.M. Sm. bis) a soilborne necrotrophic fungal pathogen, is the causal agent of spring dead spot on warm season bermudagrasses (Cynodon spp.) and necrotic ring spot on the cool season Kentucky bluegrass (Poa pratensis L.). Symptoms in susceptible turfgrass varieties include circular dead patches with bleached foliage ranging from a few inches to several feet in diameter. Grass stolons, roots, and rhizomes are the primary organs where the fungus infects and colonizes, causing necrosis. O. korrae infection in tolerant bermudagrass cultivars and asymptomatic hosts including creeping bentgrass (Agrostis stolonifera L.) and wheat (Triticum aestivum L.) display cortex and vascular root colonization without necrosis. Molecular mechanisms underlying the host-pathogen interaction and fungal pathogenicity in different hosts plants are not yet fully understood. To elucidate differences in gene expression profiles in both fungal infection and host (symptomatic and asymptomatic) defense mechanisms, a transcriptome analysis was used. To achieve this, O. korrae was in vitro inoculated on symptomatic hosts: tolerant bermudagrass U3 biotype, susceptible hybrid bermudagrass Tifway 419, Kentucky bluegrass (incubated at warm and cool temperatures), Brachypodium distachyon, and asymptomatic hosts: creeping bentgrass and wheat. RNA was extracted from inoculated and non-inoculated root samples after 10 dpi. RNA was sequenced using an Illumina platform. The upregulation of U3 biotype and Kentucky bluegrass genes encoding putative cysteine-rich receptor-like protein kinases (CRK) may play important roles resembling PAMP-triggered immunity (PTI) defense mechanisms. Susceptible Tifway 419 upregulated genes in response to effector triggered susceptibility (ETS) mediated by the Jasmonic acid accumulation triggering hypersensitive response. Upregulation of B. distachyon genes related to the response of jasmonic acid might contribute to the activation of the MAPK cascade during root infection. Asymptomatic hosts (creeping bentgrass and wheat) revealed an upregulation on genes related to basal defense responses (PTI) such as pathogenesis-related proteins synthesis of antimicrobial compounds and ROS production. Gene expression profiles of O. korrae in infected asymptomatic and symptomatic hosts revealed upregulation of genes encoding cell wall degrading enzymes, which play a role in the activation of pathogen-associated molecular patterns (PAMP)-triggered immunity (PTI) suggesting that the fungus can suppress PTI pathways using necrotrophic effectors and cell wall degrading enzymes to induce cell death in the hosts. These findings will be an important resource for turfgrass breeding programs to design more effective control strategies for soilborne diseases caused by Ophiosphaerella spp.

Date
2024-05