Molecular interactions between quinoa, the biocontrol agent Trichoderma and the pathogen Peronospora variabilis

Plants have developed complex molecular mechanisms to recognize and respond to the different microorganisms present in their surroundings. The most studied response mechanisms are plant defense responses. These defense response mechanisms share many similar components with the plant response mechanisms to beneficial microbes. Therefore, studying the defense response mechanisms against pathogens can contribute to the understanding of compatible and incompatible interactions with beneficial microbes.In this work, the molecular interactions of quinoa with the pathogen Peronospora variabilis, causal agent of the downy mildew disease, and the interactions of quinoa with the beneficial biocontrol fungi Trichoderma harzianum were studied. Experimental systems for interaction experiments were developed and used, followed by morphological, biochemical and transcriptomic analysis. We describe the response of two quinoa cultivars to the infection of P. variabilis under controlled conditions. The quinoa cultivar Kurmi was more tolerant to P. variabilis infection than the Real cultivar, despite the lack of hypersensitive response. The defense response observed in the Kurmi cultivar might be mediated by the jasmonic acid signaling pathway. Cultivars that can trigger hypersensitive response are more resistant to P. variabilis than Kurmi and therefore a better selection for agriculture.Quinoa in the presence of Trichoderma had variable outcomes depending on the growth conditions. We observed that quinoa growth was promoted in regular soil experiments or by interaction with Trichoderma volatile compounds in axenic co-culture. However, the growth of two quinoa cultivars was significantly inhibited by T. harzianum in axenic co-culture and in steamed soil experiments. The transcriptomic data of the quinoa growth inhibition by Trichoderma suggests activation of molecular signaling very similar to the signaling observed during defense response against pathogens. Further, we observed a specific group of quinoa plant defensins to be more rapidly induced by Trichoderma in a resistant cultivar but not in a susceptible one. These plant defensins showed a recent evolutionary expansion and could play a major role in providing pathogen resistance to certain quinoa cultivars.In order to protect quinoa from P. variabilis infections by Trichoderma application and enhance the quinoa yields in agricultural systems might be necessary to perform compatibility tests between the Trichoderma biocontrol agents and the quinoa cultivars. These compatibility tests should be performed in regular soil

Trichoderma harzianum T-22 and BOL-12QD inhibits lateral root development of Chenopodium quinoa in axenic co-culture

To investigate the symbiotic interaction of Trichoderma harzianum Rifaion Chenopodium quinoa Willd. in isolation, we studied axenic co-culture of the T. harzianum isolates T-22 and BOL-12QD and the C. quinoa cultivars Kurmi andManiqueña real. Neither T-22 nor BOL-12QD affected seedling growth during two days of co-culture in the early growth phase of rapid primary root extension.However, after longer axenic co-culture, T-22 and BOL-12 were found to significantly inhibit the overall growth of C. quinoa cv. Kurmi and Real, affecting also vitality parameters as seen for chlorophyll and betalains. Lateral root development was strongly inhibited in all plant−fungal combinations, leaving stunted lateral roots. These results suggest that T. harzianum has a general capacity to inhibit the growth of C. quinoa plants with a main effect on the lateral root development

Apoptins : selective anticancer agents

•Apoptins are viral proteins that trigger cell death.•Apoptins show cancer-selective toxicity.•Potential delivery methods are being assayed for future apoptin clinical trials.Therapies that selectively target cancer cells for death have been the center of intense research recently. One potential therapy may involve apoptin proteins, which are able to induce apoptosis in cancer cells leaving normal cells unharmed. Apoptin was originally discovered in the Chicken anemia virus (CAV); however, human gyroviruses (HGyV) have recently been found that also harbor apoptin-like proteins. Although the cancer cell specific activity of these apoptins appears to be well conserved, the precise functions and mechanisms of action are yet to be fully elucidated. Strategies for both delivering apoptin to treat tumors and disseminating the protein inside the tumor body are now being developed, and have shown promise in preclinical animal studies

Pre-administration of turmeric prevents methotrexate-induced liver toxicity and oxidative stress

Background: Methotrexate (MTX) is an antimetabolite broadly used in treatment of cancer and autoimmune diseases. MTX-induced hepatotoxicity limits its application. We investigated hepatoprotective effects of turmeric in MTX-induced liver toxicity. Methods: All experiments were performed on male Wistar albino rats that were randomly divided into six groups. Group one received saline orally for 30 days (control group), groups two and three received turmeric extract (100, 200 mg/kg respectively) orally for 30 days, group four received single dose, of MTX IP at day 30, groups five and six received turmeric extract 100 and 200 mg/kg orally respectively for 30 days and single dose of methoterxate IP (20 mg/kg) at day 30. Four days after MTX injection animals were sacrificed and evaluated. Blood ALT and AST (indicators of hepatocyte injury), ALP and bilirubin (markers of biliary function), albumin (reflect liver synthetic function) as well as the plasma TAS concentration (antioxidant defenses) were determined. The cellular antioxidant defense activities were examined in liver tissue samples using SOD, CAT, and GSH-Px for the oxidative stress, and MDA for lipid peroxidation. In addition, liver damage was evaluated histopathologically. Results: MTX significantly induced liver damage (P less than 0.05) and decreased its antioxidant capacity, while turmeric was hepatoprotective. Liver tissue microscopic evaluation showed that MTX treatment induced severe centrilobular and periportal degeneration, hyperemia of portal vein, increased artery inflammatory cells infiltration and necrosis, while all of histopathological changes were attenuated by turmeric (200 mg/kg). Conclusion: Turmeric extract can successfully attenuate MTX-hepatotoxicity. The effect is partly mediated through extracts antinflammatory activity.Funding Agencies|University of Manitoba start-up fund; Linkoping University; IGEN; Cancerfonden [2013/391]; VR-NanoVision [K2012-99X-22325-01-5]</p