Relationships between Plant Defense Inducer Activities and Molecular Structure of Gallomolecules.

Plant defense inducers (PDIs) are booming and attractive protection agents designed to immunostimulate the plant to reduce subsequent pathogen colonization. The structure-PDI activity relationships of four flavan-3-ols: Epicatechin (EC), Epigallocatechin (EGC), Epicatechin gallate (ECG), Epigallocatechin gallate (EGCG) and Gallotannic acid (GTA) were investigated in both whole plant and suspension cell systems. ECG, EGCG, and GTA displayed elicitor activities. Their infiltration into tobacco leaves induced hypersensitive reaction-like lesions with topical scopoletin and PR-target transcript accumulations. On the contrary, EC and EGC infiltrations fail to trigger the biochemical changes in tobacco tissues. The tobacco BY-2 cells challenged with ECG, EGCG, or GTA led to alkalinization of the BY-2 extracellular medium while EC and EGC did not trigger any pH variation. This work provides evidence that the esterified gallate pattern is as an essential flavonoid entity to induce plant defense reactions in tobacco. The phytoprotective properties of the esterified gallate-free EC and the esterified gallate-rich GTA were evaluated on the tobacco/Phytophthora parasitica var. nicotianae (Ppn) pathosystem. Tobacco treatment with EC did not induce significant protection against Ppn compared to GTA which shows antimicrobial properties on Ppn and decreases the infection on GTA-infiltrated and -sprayed wild-type leaves. GTA protection was impaired in the transgenic NahG tobacco plants, suggesting that protection was mediated by salicylic acid.

Honeybee gut microbiota dysbiosis in pesticide/parasite co-exposures is mainly induced by Nosema ceranae.

Honeybees ensure a key ecosystem service by pollinating many agricultural crops and wild plants. However, in the past few decades, managed bee colonies have been declining in Europe and North America. Researchers have emphasized both parasites and pesticides as the most important factors. Infection by the parasite Nosema ceranae and exposure to pesticides can contribute to gut dysbiosis, impacting the honeybee physiology. Here, we examined and quantified the effects of N. ceranae, the neonicotinoid thiamethoxam, the phenylpyrazole fipronil and the carboxamide boscalid, alone and in combination, on the honeybee gut microbiota. Chronic exposures to fipronil and thiamethoxam alone or combined with N. ceranae infection significantly decreased honeybee survival whereas the fungicide boscalid had no effect on uninfected bees. Interestingly, increased mortality was observed in N. ceranae-infected bees after exposure to boscalid, with synergistic negative effects. Regarding gut microbiota composition, co-exposure to the parasite and each pesticide led to decreased abundance of Alphaproteobacteria, and increased abundance of Gammaproteobacteria. The parasite also induced an increase of bacterial alpha-diversity (species richness). Our findings demonstrated that exposure of honeybees to N. ceranae and/or pesticides play a significant role in colony health and is associated with the establishment of a dysbiotic gut microbiota.

A Pediococcus strain to rescue honeybees by decreasing Nosema ceranae- and pesticide-induced adverse effects.

Honeybees ensure a key ecosystemic service by pollinating many agricultural crops and wild plants. However, since few decades, managed bee colonies have declined worldwide. This phenomenon is considered to be multifactorial, with a strong emphasis on both parasites and pesticides. Infection by the parasite Nosema ceranae and exposure to pesticides can contribute to adverse effects, resulting in a perturbation of the honeybee physiology. We thus hypothesized that probiotic treatment could be promising to treat or prevent these disturbances. The aim of this study was to evaluate the effects of probiotics on N. ceranae-infected and intoxicated honeybees (by the insecticide thiamethoxam and the fungicide boscalid). For this purpose, experiments were conducted with five probiotics. Among them, Pediococcus acidilactici (PA) showed the best protective effect against the parasite and pesticides. PA significantly improved the infected honeybee lifespan as prophylactic and curative treatments (respectively 2.3 fold and 1.7 fold). Furthermore, the exposure to pesticides induced an increase of honeybee mortality compared with the control group (p < .001) that was restored by the PA treatment. Despite its beneficial effect on honeybee lifespan, the PA administration did not induce changes in the gut bacterial communities (neither in abundance or diversity). N. ceranae and the pesticides were shown to deregulate genes involved in honeybee development (vitellogenin), immunity (serine protease 40, defensin) and detoxification system (glutathione peroxidase-like 2, catalase), and these effects were corrected by the PA treatment. This study highlights the promising use of PA to protect honeybees from both pathogens and pesticides.