Skip to main content
ARS Home » Pacific West Area » Wapato, Washington » Temperate Tree Fruit and Vegetable Research » Research » Publications at this Location » Publication #316450

Title: RNA interference of effector gene 16D10 leads to broad meloidogyne resistance in potato

Author
item DINH, PHOUNG - Washington State University
item ZHANG, LIN-HAI - Washington State University
item MOJTAHEDI, HASSAN - US Department Of Agriculture (USDA)
item Brown, Charles
item ELLING, AXEL - Washington State University

Submitted to: Journal of Nematology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/15/2015
Publication Date: 4/13/2015
Citation: Dinh, P., Zhang, L., Mojtahedi, H., Brown, C.R., Elling, A. 2015. RNA interference of effector gene 16D10 leads to broad meloidogyne resistance in potato. Journal of Nematology. 47:71-78.

Interpretive Summary: Plant Parasitic Nematodes are microscopic worms that live in the soil and feed on plants. One of these, the root-knot nematode, enters the root system of the potato, and must be controlled by the application of pesticides to the plants or soil. The root-knot nematode migrates within the root to a specific location where it takes over the plant growth process and provides itself with a giant cell (the root-knot) that supplies its food. The interaction between nematode and plant resulting in the root-knot involves nematode chemicals called effectors. Effectors are produced in the nematode salivary glands and are spit into plant root cells through the nematode stylet which is like a straw. The effector chemicals are produced by the expression of a gene in the nematode. Plant root cells are very responsive to the effector. It is the strategy of the nematode to transform the potato root into a nematode cafeteria. USDA, ARS researchers at Prosser, Washington, in collaboration with scientists at Washington State University transformed potato plants to express an RNA which interfered with the nematode effector called "16D10" The interference reduced the quantity of the effector, which reduced the nematode food supply and the numbers of eggs produced by the nematode. These results demonstrate a potential for RNA interference of 16D10 to inhibit the plant parasitism process of root-knot nematode species. Potato plants that are genetically altered to reduce the effectiveness of the nematode effector could be grown with reduced application of pesticides, a benefit to the environment and consumer, and a cost reduction for the farmer.

Technical Abstract: Root-knot nematodes (Meloidogyne spp.) are a significant problem in potato (Solanum tuberosum) production. There is no known Meloidogyne resistance gene in cultivated potato, even though sources of resistance were identified in wild potato species. The objective of this study was to generate stable transgenic potato lines in a cv. ‘Russet Burbank’ background that carry an RNA interference (RNAi) transgene capable of silencing the 16D10 Meloidogyne effector gene, and to test for resistance against some of the most important root-knot nematodes in potato, i.e., M. arenaria, M. chitwoodi, M. hapla, M. incognita, and M. javanica. At 35 days after inoculation (DAI), the number of egg masses per plant was significantly reduced by 65 to 97% (P < 0.05) in the RNAi line compared to wild type and empty vector controls. The strongest reduction in the number of egg masses was observed in M. hapla, whereas M. javanica showed the smallest resistance effect. Similarly, the number of eggs per plant was significantly reduced between 66% in M. arenaria and 87% in M. hapla (P < 0.05) compared to wild type and empty vector control plants. Plant-mediated RNAi silencing of the 16D10 effector gene resulted in significant resistance against all root-knot nematode species tested, whereas RMc1(blb), the only known Meloidogyne resistance gene in potato, did not have a broad resistance effect. Silencing of 16D10 did not interfere with the attraction of M. incognita second-stage juveniles to roots, nor did it reduce root invasion.