A new resistance-breaking strain of Turnip mosaic virus (TuMV) overcomes TuMV resistance genes that currently suppress spread of this virus in Brassica napus crops in the Liverpool Plains region of eastern Australia. Isolates 12.1 and 12.5 of this strain and three other isolates in TuMV pathotypes 1 (NSW-2), 7 (NSW-1), and 8 (WA-Ap1) were inoculated to plants of 19 B. napus cultivars and one breeding line. All plants of these cultivars and the breeding line proved susceptible to 12.1 and 12.5 but developed only resistance phenotypes with WA-Ap1 or mostly resistance phenotypes with NSW-1 and NSW-2. Five different TuMV resistance phenotypes occurred either alone or segregating in different combinations. When these five isolates were inoculated to plants of nine other crop or wild Brassicaceae spp. and four indicator hosts in other families, 12.1 and 12.5 resembled the other three in inducing TuMV resistance phenotypes in some Brassicaceae spp. but not others, and by inducing extreme resistance phenotypes in all inoculated plants of B. oleracea var. botrytis and Raphanus sativus. Therefore, the overall resistance-breaking properties of 12.1 and 12.5 were restricted to B. napus. When isolates 12.1, 12.5, and WA-Ap1 and additional Australian isolate WA-EP1 were sequenced and complete genomes of each compared, 12.1 and 12.5 grouped separately from the other 2 and from all 23 Australian isolates with complete genomes sequenced previously. In addition, there was evidence for at least six separate TuMV introductions to Australia. Spread of this B. napus resistance-breaking strain poses a significant threat to the B. napus oilseed industry. Breeding B. napus cultivars with resistance to this strain constitutes a critical priority for B. napus breeding programs in Australia and elsewhere.

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Turnip mosaic virus (TuMV) causes crop losses worldwide. Eight Australian TuMV isolates originally obtained from five different species in two plant families were inoculated to 14 plant species belonging to four families to compare their host reactions. They differed considerably in virulence in Brassicaceae crop species and virus indicator hosts belonging to three other families. The isolates infected most Brassica species inoculated, but not Raphanus sativus, usually causing systemic mosaic symptoms, so they resembled TuMV biological host type [B]. Whole genome sequences of seven of the Australian isolates were obtained and had lengths of 9834 nucleotides (nt). When they were compared with 37 non-recombinant TuMV genomes from other continents and another whole genome from Australia, six of them formed an Australian group within the overall world-B phylogenetic grouping, while the remaining new genome sequence and the additional whole genome from Australia were part of the basal-B grouping. When the seven new Australian genomes and the additional whole genome from Australia were subjected to recombination analysis, six different recombination events were found. Six genomes contained one or two recombination events each, but one was non-recombinant. The non-recombinant isolate was in the Australian grouping within the overall world-B group while the remaining recombinant isolates were in the basal-B and world-B phylogenetic groups.

Systemic hypersensitive resistance (SHR) caused by Turnip mosaic virus (TuMV) was studied by light microscopy and histochemical analysis in stem cross sections of Brassica juncea (Indian mustard) plants. Ten TuMV isolates were inoculated to leaves of susceptible line JM 06006, cv. Oasis CI, which carries TuMV systemic hypersensitivity gene TuRBJU 01, and F3 progeny plants obtained from a cross between them. Systemic mosaic (SM) symptoms were induced by all 10 isolates in plants of JM 06006, and by resistance-breaking isolate NSW-3 in all cv. Oasis CI and F3 plants. With the other nine isolates, cv. Oasis CI plants developed SHR while F3 progeny plants segregated for both phenotypes; mock-inoculated control plants never became infected. Presence of SHR did not delay systemic invasion as this commenced within 2 hours after inoculation (hai) and was almost complete by 72 hai regardless of whether plants subsequently developed SHR or SM. When stem cross sections sampled 9 to 12 days after inoculation were examined for the plant defense responses, phloem necrosis, hydrogen peroxide accumulation, and additional lignin deposition, sections from plants with SHR demonstrated all of these characteristics, but sections from plants with SM or mock-inoculation did not. Based on consolidated data from all isolates except NSW-3, stems developing SHR had significantly more occluded xylem vessels (P < 0.001) compared with stems from plants developing SM or mock-inoculated plants. Both light microscopy and histochemical tests with phloroglucinol-HCl and toluidine blue O indicated that the xylem occlusions could be gels. Thus, phloem necrosis, xylem occlusion, lignification, and hydrogen peroxide accumulation were all associated with the SHR in B. juncea plants carrying TuMV hypersensitivity gene TuRBJU 01. In addition, virus inclusion bodies were fewer in sections from plants with SHR. Phloem necrosis was apparently acting as the primary cause of SHR and xylem occlusion as an important secondary cause.