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RNA Interference of Effector Gene Mc16D10L Confers Resistance Against Meloidogyne chitwoodi in Arabidopsis and Potato

October 2014 , Volume 104 , Number  10
Pages  1,098 - 1,106

Phuong T. Y. Dinh, Charles R. Brown, and Axel A. Elling

First and third authors: Department of Plant Pathology, Washington State University, Pullman 99164; and second author: Vegetable and Forage Crops Research Unit, U.S. Department of Agriculture-Agricultural Research Service, Prosser, WA 99350.


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Accepted for publication 9 April 2014.
ABSTRACT

Meloidogyne chitwoodi, a quarantine pathogen, is a significant problem in potato-producing areas worldwide. In spite of considerable genetic diversity in wild potato species, no commercial potato cultivars with resistance to M. chitwoodi are available. Nematode effector genes are essential for the molecular interactions between root-knot nematodes and their hosts. Stable transgenic lines of Arabidopsis and potato (Solanum tuberosum) with resistance against M. chitwoodi were developed. RNA interference (RNAi) construct pART27(16D10i-2) was introduced into Arabidopsis thaliana and potato to express double-stranded RNA complementary to the putative M. chitwoodi effector gene Mc16D10L. Plant-mediated RNAi led to a significant level of resistance against M. chitwoodi in Arabidopsis and potato. In transgenic Arabidopsis lines, the number of M. chitwoodi egg masses and eggs was reduced by up to 57 and 67% compared with empty vector controls, respectively. Similarly, in stable transgenic lines of potato, the number of M. chitwoodi egg masses and eggs was reduced by up to 71 and 63% compared with empty vector controls, respectively. The relative transcript level of Mc16D10L was reduced by up to 76% in M. chitwoodi eggs and infective second-stage juveniles that developed on transgenic pART27(16D10i-2) potato, suggesting that the RNAi effect is systemic and heritable in M. chitwoodi.



This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 2014.