Herbicide resistance in weeds, including corn poppy (Papaver rhoeas L.), is an increasing problem compromising global crop production. The aims of this study were to evaluate the susceptibility of P. rhoeas populations in Poland to acetolactate synthase (ALS) inhibitors and elucidate their mechanisms of resistance. Between 2017 and 2020, 157 seed samples were collected nationwide and a dose-response study with various ALS-inhibiting herbicides was performed in glasshouses. This revealed 14 resistant populations with R/S ranges of 2.3–1450.2, 9.5–398.5 and 2–2.5 for tribenuron, iodosulfuron and florasulam, respectively. Eight of them were cross-resistant to both tribenuron and iodosulfuron, three and one populations were singly resistant to tribenuron and iodosulfuron, respectively, and one population had reduced susceptibility to florasulam only. In one population, cross-resistance to tribenuron, iodosulfuron and florasulam was identified. The ED50 of many populations susceptible to ALS inhibitors was close to half the recommended dose of the herbicides tested. In seven out of eight resistant P. rhoeas populations analysed, target-site resistance was identified. Six amino acid replacements were found (Ala197, Arg197, His197, Leu197, Ser197 and Thr197). In one population resistant to ALS inhibitors, no mutations in the ALS gene were detected. An efficient anti-resistance strategy is needed to reduce the development of herbicide resistance in P. rhoeas in Poland.
Tomato torrado virus (ToTV) infection manifests with burn-like symptoms on leaves, leaflets and upper stem parts of susceptible infected plants. The symptoms caused by ToTV may be considered as one of the most severe virus-induced forms of systemic necrosis, which spreads within the whole plant and leads to a lethal phenotype. However, to date there are no data revealing which viral genes encode for a specific pathogenicity determinant that triggers the plant necrotic response for any torradovirus. In this study we evaluated the influence of three coat protein subunits of ToTV: Vp23, Vp26 and Vp35, transiently expressed from a PVX-based vector, and checked their association with the induction of systemic necrosis in infected Solanum lycopersicum L. (cv. Beta Lux), a natural host of ToTV. To estimate how ToTV coat protein subunits might contribute in plant response to virus infection we over-expressed the proteins from PVX-based vector in tomato and analyzed enzymatic activities related with plant defense response. By doing protein qualitative analysis performed by mass spectrometry we indicated the PR10 in protein fraction with induced ribonuclease activity. We observed that only the Vp26 enhanced PVX pathogenicity causing severe necrosis of the infected plant. Moreover, we indicated increased RNase and oxidative activities in plants infected with PVX-Vp26 chimeras only. Importantly, we suspected that this increased RNase activity is associated with increased accumulation of PR10 mRNA and products of its translation. On the basis of the obtained results, we indicated that Vp26 acts as the elicitor of hypersensitive response-like reactions of PVX-Vp26 manifesting with enhanced pathogenicity of the recombined PVX. This might be the first described suspected necrosis determinant of torradoviruses infecting tomatoes.