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

Abstract

Programmed cell death (PCD) pathways caused by Turnip mosaic virus (TuMV) infection before symptom appearance were studied by light microscopy and electrolyte leakage following sap inoculation of Brassica carinata (Ethiopian mustard) TZ‐SMN‐44‐6 plants. Leaf responses to inoculation with avirulent (TuMV‐avir) and virulent (TuMV‐vir) isolates, and mock‐inoculation, were compared at 2, 20 and 52 h after inoculation (hai). The phenotypes induced were localized resistance (TuMV‐avir) and systemic susceptibility (TuMV‐vir). No visible TuMV symptoms were recorded in any inoculated plants during the 2–52 hai sampling period, but appeared as chlorotic spots in inoculated leaves at 5 days after inoculation. With TuMV‐vir alone, they were followed by systemic infection (mosaic). Dead cell number, deformation, percentage area and percentage integrated intensity, and conductivity of electrolyte leakage data, were analysed to examine their possible roles in stimulating cell death pathways. At 2 hai, dead cell number and percentage area were significantly greater for TuMV‐avir than TuMV‐vir infection or mock‐inoculation. Overall, isolate TuMV‐vir caused significantly greater cell deformation than TuMV‐avir, whereas wounding by mock‐inoculation had negligible effects. By 52 hai, isolate TuMV‐avir caused significantly greater electrolyte leakage than isolate TuMV‐vir or mock‐inoculation. This suggests both isolates triggered morphological changes consistent with apoptotic‐like PCD and necrosis‐like PCD that depended upon isolate virulence and stage of infection, respectively. These findings highlight how quantification of dead cell deformation and electrolyte leakage offer a new understanding of compatible and incompatible plant responses to early virus infection in plants.

Virus Diseases of Cereal and Oilseed Crops in Australia: Current Position and Future Challenges

“…When early TuMV infection before appearance of phenotype R symptoms (chlorotic spot local lesions) was investigated in Ethiopian mustard TZ-SMN using light microscopy and electrolyte leakage, it was shown to have initiated morphological changes associated with apoptotic-like programmed cell death and necrosis-like programmed cell death. Their development depended upon TuMV pathotype and the stage of infection reached [271]. Similar studies to these are lacking with LHR (phenotype R N ).…”

The apparent non‐host resistance of Ethiopian mustard to a radish‐infecting strain of Turnip mosaic virus is largely determined by the C‐terminal region of the P3 viral protein

“…Unfortunately, none of these reports provided details of the strain characterization of the infecting TuMV isolates. Work on TuMV and Ethiopian mustard has also been carried out in Australia (Nyalugwe et al ., ). None of the TuMV isolates reported as infecting crops or weeds in Australia belonged to the viral strain represented by isolate JPN 1 (Sánchez et al ., ; Tomimura et al ., ); therefore, although isolates were tested on Ethiopian mustard (Nyalugwe et al ., ), we could not establish direct comparisons.…”

Study on Italian Onion Cultivars/Ecotypes towards Onion Yellow Dwarf Virus (OYDV) Infection

“…Most commonly, it is widely believed that virus infections are harmful to the host or havea negative acceptation, but little is known about the biology of plant viruses and their host in a natural system, regarding synergic or more complex interaction networking. Physiological and morphological responses to virus infection in plant depends by host species, virus-host recognition, virus species and/or strain [31]. OYDV is known to induce severe symptoms in Allium spp.…”