Systemic Hypersensitive Resistance to Turnip mosaic virus in Brassica juncea is Associated With Multiple Defense Responses, Especially Phloem Necrosis and Xylem Occlusion

Abstract

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.

NtTPN1: a RPP8‐like R gene required for Potato virus Y‐induced veinal necrosis in tobacco

“…This suggests that ClYVV‐induced systemic cell death is regulated by an R ‐gene‐mediated pathway, and that Cyn1 may represent a weak resistance gene to ClYVV, or that ClYVV expresses weak elicitor molecules (Ravelo et al ., ). R genes have also been associated with HR and systemic HR (SHR) phenotypes in TuMV‐infected Brassica species, including TuRBJU 01 in Brassica juncea (Nyalugwe et al ., ,b).…”

Comparative Transcriptome Analysis Provides Molecular Insights into the Interaction of Beet necrotic yellow vein virus and Beet soil-borne mosaic virus with Their Host Sugar Beet

“…The transcriptome analysis revealed a strong defence response of sugar beet towards BNYVV and BSBMV infection since DEGs belonging to the GO term "response to stress" were significantly enriched in both datasets. One important defence mechanism is inducible barriers made of lignin, preventing systemic spread of pathogens within the vascular tissues [92,93]. Lignin production in plants is nearly exclusively based on the phenylpropanoid pathway [94].…”

Programmed cell death pathways induced by early plant‐virus infection are determined by isolate virulence and stage of infection

“…TuMV isolates WA‐Ap1 (= TMV‐avir) from Raphanus raphanistrum (wild radish) growing at Applecross, Perth, Western Australia (Coutts et al ., ) and 12.5 (= TMV‐vir) from B. napus growing in the Liverpool Plains, New South Wales, Australia (Nyalugwe et al ., ,b) were used. Virus cultures were maintained by serial subculture using sap inoculation to plants of B. juncea (Indian mustard) JM 06006, which developed a susceptible (mosaic) phenotype.…”

“…Use of virus‐resistant cultivars, when available, can provide an important approach to managing TuMV spread in Brassica crops (Walsh & Jenner, , ). A range of TuMV resistance phenotypes occur in vegetable and oilseed Brassica species, including extreme resistance, HR, SHR and localization associated with chlorotic lesions (Jenner & Walsh, ; Walsh & Jenner, , ; Coutts et al ., ; Nyalugwe et al ., , , ,b). R genes have been associated with extreme resistance, HR and SHR phenotypes in Brassica species (Walsh & Jenner, ; Nyalugwe et al ., , ), but not as yet with virus localization associated with chlorotic lesions.…”