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Exposure to (Z)-11-hexadecenal [(Z)-11-16:Ald] increases Brassica nigra susceptibility to subsequent herbivory.

ABSTRACT: It is well established that plants emit, detect and respond to volatile organic compounds; however, knowledge on the ability of plants to detect and respond to volatiles emitted by non-plant organisms is limited. Recent studies indicated that plants detect insect-emitted volatiles that induce defence responses; however, the mechanisms underlying this detection and defence priming is unknown. Therefore, we explored if exposure to a main component of Plutella xylostella female sex pheromone namely (Z)-11-hexadecenal [(Z)-11-16:Ald] induced detectable early and late stage defence-related plant responses in Brassica nigra. Exposure to biologically relevant levels of vapourised (Z)-11-16:Ald released from a loaded septum induced a change in volatile emissions of receiver plants after herbivore attack and increased the leaf area consumed by P. xylostella larvae. Further experiments examining the effects of the (Z)-11-16:Ald on several stages of plant defence-related responses showed that exposure to 100 ppm of (Z)-11-16:Ald in liquid state induced depolarisation of the transmembrane potential (Vm), an increase in cytosolic calcium concentration [Ca²⁺]_cyt, production of H₂O₂ and an increase in expression of reactive oxygen species (ROS)-mediated genes and ROS-scavenging enzyme activity. The results suggest that exposure to volatile (Z)-11-16:Ald increases the susceptibility of B. nigra to subsequent herbivory. This unexpected finding, suggest alternative ecological effects of detecting insect pheromone to those reported earlier. Experiments conducted in vitro showed that high doses of (Z)-11-16:Ald induced defence-related responses, but further experiments should assess how specific the response is to this particular aldehyde.

SUBMITTER: Brosset A

PROVIDER: S-EPMC8242006 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Insect herbivores can shift the composition of a plant community, but the mechanism underlying such shifts remains largely unexplored. A possibility is that insects alter the competitive symmetry between plant species. The effect of herbivory on competition likely depends on whether the plants are subjected to aboveground or belowground herbivory or both, and also depends on soil nitrogen levels. It is unclear how these biotic and abiotic factors interactively affect competition. In a greenhouse experiment, we measured competition between two coexisting grass species that respond differently to nitrogen deposition: Dactylis glomerata L., which is competitively favoured by nitrogen addition, and Festuca rubra L., which is competitively favoured on nitrogen-poor soils. We predicted: (1) that aboveground herbivory would reduce competitive asymmetry at high soil nitrogen by reducing the competitive advantage of D. glomerata; and (2), that belowground herbivory would relax competition at low soil nitrogen, by reducing the competitive advantage of F. rubra. Aboveground herbivory caused a 46% decrease in the competitive ability of F. rubra, and a 23% increase in that of D. glomerata, thus increasing competitive asymmetry, independently of soil nitrogen level. Belowground herbivory did not affect competitive symmetry, but the combined influence of above- and belowground herbivory was weaker than predicted from their individual effects. Belowground herbivory thus mitigated the increased competitive asymmetry caused by aboveground herbivory. D. glomerata remained competitively dominant after the cessation of aboveground herbivory, showing that the influence of herbivory continued beyond the feeding period. We showed that insect herbivory can strongly influence plant competitive interactions. In our experimental plant community, aboveground insect herbivory increased the risk of competitive exclusion of F. rubra. Belowground herbivory appeared to mitigate the influence of aboveground herbivory, and this mechanism may play a role for plant species coexistence.

Project description:Inflammasomes are cytosolic multiprotein complexes assembled by intracellular nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) and they initiate innate immune responses to invading pathogens and danger signals by activating caspase-1 (ref. 1). Caspase-1 activation leads to the maturation and release of the pro-inflammatory cytokines interleukin (IL)-1? and IL-18, as well as lytic inflammatory cell death known as pyroptosis. Recently, a new non-canonical inflammasome was described that activates caspase-11, a pro-inflammatory caspase required for lipopolysaccharide-induced lethality. This study also highlighted that previously generated caspase-1 knockout mice lack a functional allele of Casp11 (also known as Casp4), making them functionally Casp1?Casp11 double knockouts. Previous studies have shown that these mice are more susceptible to infections with microbial pathogens, including the bacterial pathogen Salmonella enterica serovar Typhimurium (S. typhimurium), but the individual contributions of caspase-1 and caspase-11 to this phenotype are not known. Here we show that non-canonical caspase-11 activation contributes to macrophage death during S. typhimurium infection. Toll-like receptor 4 (TLR4)-dependent and TIR-domain-containing adaptor-inducing interferon-? (TRIF)-dependent interferon-? production is crucial for caspase-11 activation in macrophages, but is only partially required for pro-caspase-11 expression, consistent with the existence of an interferon-inducible activator of caspase-11. Furthermore, Casp1(-/-) mice were significantly more susceptible to infection with S. typhimurium than mice lacking both pro-inflammatory caspases (Casp1(-/-)?Casp11(-/-)). This phenotype was accompanied by higher bacterial counts, the formation of extracellular bacterial microcolonies in the infected tissue and a defect in neutrophil-mediated clearance. These results indicate that caspase-11-dependent cell death is detrimental to the host in the absence of caspase-1-mediated innate immunity, resulting in extracellular replication of a facultative intracellular bacterial pathogen.

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Exposure to (Z)-11-hexadecenal [(Z)-11-16:Ald] increases Brassica nigra susceptibility to subsequent herbivory.

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