Studies on resistance phenotypes to Turnip mosaic virus in five species of Brassicaceae, and identification of a virus resistance gene in Brassica juncea

Abstract

Studies were done to: (i) establish the occurrence of different types of Turnip mosaic virus (TuMV) resistance phenotypes in 69 Brassica juncea, 11 Camelina sativa, 11 B. oleracea, five B. rapa and three Raphanus sativus lines, and (ii) characterise a TuMV resistance gene in B. juncea. An isolate of TuMV pathotype 8 (WA-Ap1) was employed to inoculate plants, except in one instance where isolates of pathotypes 1 (isolate NSW-2) and 7 (isolate NSW-1) were also used. The resistance phenotypes found were O (extreme resistance), RN (localised hypersensitivity), R (resistance to systemic movement without necrosis), +N (systemic infection with some necrosis), +N 1 (mild variant of +N), +ND (systemic hypersensitivity and plant death), + (susceptibility), +st (severe stunting variant of +), RN/+ (systemic infection with necrosis limited to inoculated leaves), and RN/st/+ (severe variant of RN/+). Seven different resistance or susceptibility phenotypes were found in B. juncea (codes: +N, RN/+, RN/st/+, +ND, +N 1, + and +st), 22 lines developing only one phenotype and the remaining 47 segregating for 2–3 different phenotypes. Ten B. oleracea cultivars developed phenotype O alone, and one segregated for phenotypes R and O. One B. rapa cultivar produced uniform phenotype +, but four segregated for phenotypes +, RN, O, RN/+, +N, or +st. Two R. sativus cultivars developed phenotype O alone, and one segregated for phenotypes O and RN. All 11 C. sativa lines developed uniform phenotype +ND. Increasing temperature from 16 to 28 °C decreased the time lag between inoculation and symptom development without altering overall phenotypic responses in B. juncea, B. oleracea, B. rapa and C. sativa plants. When one line each of these four species were inoculated with two other TuMV isolates, NSW-1 and NSW-2 belonging to pathotypes 7 and 1 respectively, phenotypic responses remained the same in the B. juncea, B. oleracea and B. rapa lines, but pathotype 8 caused a different phenotypic response in C. sativa. The genetics of resistance to TuMV was studied in a cross between two B. juncea parents with uniform phenotypes, JM 06006 (+) and Oasis Cl (+ND). The results of four tests on F2 progeny plants and three types of control plants (JM 06006, Oasis Cl and mock-inoculated F2 progeny plants) were analysed for their responses to inoculation with TuMV isolate WA-Ap1. Segregation of F2 progeny plants from B. juncea Oasis Cl X JM 06006 fitted a 3:1 ratio (systemic necrosis: susceptibility) at an early stage of TuMV infection, and a 1:2:1 ratio at a late stage of infection +ND: +N: +. These findings show that a single incompletely dominant resistance gene, designated here as TuRBJU 01 (TuMV resistance in B rassica ju ncea 01), was responsible for systemic necrosis phenotypes +ND (homozygous) and +N (heterozygous) in B. juncea. B. juncea resistance gene TuRBJU 01, along with lines of B. oleracea and R. sativus that developed phenotype O uniformly, and of C. sativa that developed phenotype +ND uniformly are potentially valuable in breeding TuMV-resistant cultivars of these three species.