Endure and call for help : Strategies of black mustard plants to deal with a specialized caterpillar

Plants have evolved inducible resistance and tolerance mechanisms against insect herbivores. Resistance mechanisms that affect herbivorous insects directly can be effective against generalist herbivores, but will not deter specialist herbivores from attacking the plant. Tolerance mechanisms and indirect plant resistance are more likely effective strategies used by plants when dealing with specialist herbivores. However, inducible indirect resistance and tolerance mechanisms have rarely been investigated within the same study system. We studied multiple tolerance mechanisms and the role of natural enemies in reducing fitness loss of Brassica nigra plants incurred by feeding by the specialist herbivore Pieris brassicae. For this, we measured the changes in carbon and nitrogen triggered by herbivore attack and quantified plant biomass and seed production under field conditions, in the presence or absence of natural enemies of the herbivores. We also assessed whether B. nigra increased selfing rates when exposed to herbivore infestation, and investigated whether infestation by P. brassicae rendered B. nigra plants more attractive to night-active pollinators than control plants. We found that B. nigra flowers are rarely visited by insects during the night, and exposure to herbivores did not influence selfing rates. Brassica nigra plants compensated for herbivory in terms of vegetative biomass. Seed set was negatively affected by herbivory in the absence of natural enemies, but not in the presence of natural enemies. Plants responded to herbivory with drastic changes in nitrogen contents of leaves and flowers, whereas no changes in carbon concentrations were detected. The investment in reproduction or re-growth of vegetative tissues is not sufficient to sustain plant fitness. Reproductive output of flowering mustard plants is only sustained when interactions with the natural enemies of the herbivores are preserved. We conclude that natural enemies of herbivorous insects play an important role as component of the plant's defence strategy. This study reveals that both tolerance and indirect resistance are strategies of this plant species to sustain fitness

Plant phenotypic and transcriptional changes induced by volatiles from the fungal root pathogen Rhizoctonia solani

Beneficial soil microorganisms can affect plant growth and resistance by the production of volatile organic compounds (VOCs). Yet, little is known on how VOCs from soil-borne plant pathogens affect plant growth and resistance. Here we show that VOCs released from mycelium and sclerotia of the fungal root pathogen Rhizoctonia solani enhance growth and accelerate development of Arabidopsis thaliana. Seedlings briefly exposed to the fungal VOCs showed similar phenotypes, suggesting that enhanced biomass and accelerated development are primed already at early developmental stages. Fungal VOCs did not affect plant resistance to infection by the VOC-producing pathogen itself but reduced aboveground resistance to the herbivore Mamestra brassicae. Transcriptomics of A. thaliana revealed that genes involved in auxin signaling were up-regulated, whereas ethylene and jasmonic acid signaling pathways were down-regulated by fungal VOCs. Mutants disrupted in these pathways showed similar VOC-mediated growth responses as the wild-type A. thaliana, suggesting that other yet unknown pathways play a more prominent role. We postulate that R. solani uses VOCs to predispose plants for infection from a distance by altering root architecture and enhancing root biomass. Alternatively, plants may use enhanced root growth upon fungal VOC perception to sacrifice part of the root biomass and accelerate development and reproduction to survive infection.</p

Evaluation of a quality improvement intervention to reduce anastomotic leak following right colectomy (EAGLE): pragmatic, batched stepped-wedge, cluster-randomized trial in 64 countries

Background Anastomotic leak affects 8 per cent of patients after right colectomy with a 10-fold increased risk of postoperative death. The EAGLE study aimed to develop and test whether an international, standardized quality improvement intervention could reduce anastomotic leaks. Methods The internationally intended protocol, iteratively co-developed by a multistage Delphi process, comprised an online educational module introducing risk stratification, an intraoperative checklist, and harmonized surgical techniques. Clusters (hospital teams) were randomized to one of three arms with varied sequences of intervention/data collection by a derived stepped-wedge batch design (at least 18 hospital teams per batch). Patients were blinded to the study allocation. Low- and middle-income country enrolment was encouraged. The primary outcome (assessed by intention to treat) was anastomotic leak rate, and subgroup analyses by module completion (at least 80 per cent of surgeons, high engagement; less than 50 per cent, low engagement) were preplanned. Results A total 355 hospital teams registered, with 332 from 64 countries (39.2 per cent low and middle income) included in the final analysis. The online modules were completed by half of the surgeons (2143 of 4411). The primary analysis included 3039 of the 3268 patients recruited (206 patients had no anastomosis and 23 were lost to follow-up), with anastomotic leaks arising before and after the intervention in 10.1 and 9.6 per cent respectively (adjusted OR 0.87, 95 per cent c.i. 0.59 to 1.30; P = 0.498). The proportion of surgeons completing the educational modules was an influence: the leak rate decreased from 12.2 per cent (61 of 500) before intervention to 5.1 per cent (24 of 473) after intervention in high-engagement centres (adjusted OR 0.36, 0.20 to 0.64; P &lt; 0.001), but this was not observed in low-engagement hospitals (8.3 per cent (59 of 714) and 13.8 per cent (61 of 443) respectively; adjusted OR 2.09, 1.31 to 3.31). Conclusion Completion of globally available digital training by engaged teams can alter anastomotic leak rates. Registration number: NCT04270721 (http://www.clinicaltrials.gov)