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ARS Home » Midwest Area » Madison, Wisconsin » Vegetable Crops Research » Research » Publications at this Location » Publication #364159

Research Project: Maximizing the Impact of Potato Genebank Resources: Development and Evaluation of a Wild Species Genotype Diversity Panel

Location: Vegetable Crops Research

Title: Dissecting the molecular basis of strain- and temperature-sensitivity to PVY conferred by the potato Nytbr resistance gene

Author
item Halterman, Dennis
item RAKOTONDRAFARA, AURELIE - University Of Wisconsin
item CHOWDHURY, RAWNAQ - University Of Wisconsin
item Karki, Hari

Submitted to: American Phytopathological Society Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 9/13/2019
Publication Date: 9/18/2019
Citation: Halterman, D.A., Rakotondrafara, A., Chowdhury, R., Karki, H.S. 2019. Dissecting the molecular basis of strain- and temperature-sensitivity to PVY conferred by the potato Nytbr resistance gene. American Phytopathological Society Annual Meeting. https://doi.org/10.1094/PHYTO-07-19-0229-FI.
DOI: https://doi.org/10.1094/PHYTO-07-19-0229-FI

Interpretive Summary:

Technical Abstract: Potato Virus Y (PVY) is one of the most important plant viruses affecting potato production and enters in the list of the top 10 plant viruses in molecular plant pathology. Here we have investigated the nature of Nytbr-mediated resistance against PVY in potato (Solanum tuberosum). The Nytbr gene is strain specific and sensitive to increased temperature. While effective in controlling PVYO at 21°C, elevated growth temperature was sufficient to trigger systemic spread of PVYO throughout of the Nytbr-bearing potatoes. To shed light on the interplay of elevated temperature and susceptibility, we dissected the earlier step of viral infection in both Nytbr-bearing cultivar Premier Russet (PR) and PVY-susceptible plants. We established that the PVYO helper component proteinase (HCPro) alone is sufficient to induce a hypersensitive cell death response in PR plants. Remarkably, cell death was enhanced at 28°C, suggesting that the failure of blocking virus spread at higher temperature is not linked to a failure of recognition of the pathogen and/or activation of HR. We uncovered that the production of callose was part of the Nytbr-mediated response and occurs at a very earlier time point in the signal cascade prior to the appearance of local necrosis. Callose accumulation was delayed up to 24 hours at elevated temperature. We propose that callose deposition is a key component of the Nytbr-resistance response and may be a target of virulent PVY strains.