Skip to main content
ARS Home » Northeast Area » Ithaca, New York » Robert W. Holley Center for Agriculture & Health » Emerging Pests and Pathogens Research » Research » Research Project #443189

Research Project: PCN Immunity

Location: Emerging Pests and Pathogens Research

Project Number: 8062-22000-023-010-A
Project Type: Cooperative Agreement

Start Date: Sep 1, 2022
End Date: Jun 30, 2023

Objective:
1) Use pot bioassay to determine if the candidate clones confer resistance to G. pallida, 2) Use in-vitro nematode infection assay coupled with staining and microscopic observation to re-evaluate plant responses to G. pallida infection, and 3) Test the Y1-5-derived F1 population for Ro2 resistance using in-vitro infection assay.

Approach:
Objective 1: We have established plant growing conditions that allow a good production of tubers from wild potato species. Once tubers are collected, pot bioassay test will be conducted in the Dandurand lab (U. of Idaho) and the Wang lab (Cornell University, NY) using standard protocols that are routinely performed in both labs. In the bioassay test, ‘Russet Burbank’ and ‘Desiree’ (susceptible cultivars) as well as ‘Innovator’ (resistant cultivar) will be included as controls and a final cyst count will be used to determine the level of resistance for each clone. Objective 2: Nematode resistance in host plants mediated by resistance (R) genes is often associated with a hypersensitive response (HR) that occurs around nematode infection sites. To evaluate whether the resistance observed in the resistant clones is potentially mediated by an R gene, we will conduct the in-vitro nematode infection assay coupled with staining and microscopic observations of infected roots to determine if HR occurs during nematode infection. Clones producing HR phenotype likely express novel R genes, which can then be introduced into breeding programs to pyramid resistance genes in U.S. potato cultivars. Objective 3: We will use an in-vitro infection assay to evaluate the progenies of the Y1-5-derived F1 population for their responses to Ro2 infection. The collected phenotypic data will guide the downstream identification and cloning of the endogenous R genes expressed in Y1-5.