Adaptive plant responses to specific abiotic stresses or biotic agents are fine-tuned by a network of hormonal signaling cascades, including abscisic acid (ABA), ethylene, jasmonic acid (JA) and salicylic acid. Moreover, hormonal cross-talk modulates plant responses to abiotic stresses and defenses against insect herbivores when they occur simultaneously. How such interactions affect plant responses under multiple stresses, however, is less understood, even though this may frequently occur in natural environments. Here, we review our current knowledge on how hormonal signaling regulates abiotic stress responses and defenses against insects, and discuss the few recent studies that attempted to dissect hormonal interactions occurring under simultaneous abiotic stress and herbivory. Based on this we hypothesize that drought stress enhances insect resistance due to synergistic interactions between JA and ABA signaling. Responses to flooding or waterlogging involve ethylene signaling, which likely reduces plant resistance to chewing herbivores due to its negative cross-talk with JA. However, the outcome of interactions between biotic and abiotic stress signaling is often plant and/or insect species-dependent and cannot simply be predicted based on general knowledge on the involvement of signaling pathways in single stress responses. More experimental data on non-model plant and insect species are needed to reveal general patterns and better understand the molecular mechanisms allowing plants to optimize their responses in complex environments.

In the field, biotic and abiotic stresses frequently co-occur. As a consequence, common molecular signalling pathways governing adaptive responses to individual stresses can interact, resulting in compromised phenotypes. How plant signalling pathways interact under combined stresses is poorly understood. To assess this, we studied the consequence of drought and soil flooding on resistance of Solanum dulcamara to Spodoptera exigua and their effects on hormonal and transcriptomic profiles. The results showed that S. exigua larvae performed less well on drought-stressed plants than on well-watered and flooded plants. Both drought and insect feeding increased abscisic acid and jasmonic acid (JA) levels, whereas flooding did not induce JA accumulation. RNA sequencing analyses corroborated this pattern: drought and herbivory induced many biological processes that were repressed by flooding. When applied in combination, drought and herbivory had an additive effect on specific processes involved in secondary metabolism and defence responses, including protease inhibitor activity. In conclusion, drought and flooding have distinct effects on herbivore-induced responses and resistance. Especially, the interaction between abscisic acid and JA signalling may be important to optimize plant responses to combined drought and insect herbivory, making drought-stressed plants more resistant to insects than well-watered and flooded plants.

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Regulation of the positive transcription elongation factor, P-TEFb, plays a major role in controlling mammalian transcription and this is accomplished in part by controlled release of P-TEFb from the 7SK snRNP that sequesters the kinase in an inactive state. We demonstrate here that a similar P-TEFb control system exists in Drosophila. We show that an RNA previously suggested to be a 7SK homolog is, in fact, associated with P-TEFb, through the action of a homolog of the human HEXIM1/2 proteins (dHEXIM). In addition, a Drosophila La related protein (now called dLARP7) is shown to be the functional homolog of human LARP7. The Drosophila 7SK snRNP (d7SK snRNP) responded to treatment of cells with P-TEFb inhibitors and to nuclease treatment of cell lysates by releasing P-TEFb. Supporting a critical role for the d7SK snRNP in Drosophila development, dLARP7 and dHEXIM were found to be ubiquitously expressed throughout embryos and tissues at all stages. Importantly, knockdown of dHEXIM was embryonic lethal, and reduction of dHEXIM in specific tissues led to serious developmental defects. Our results suggest that regulation of P-TEFb by the d7SK snRNP is essential for the growth and differentiation of tissues required during Drosophila development.

Plants are attacked by diverse herbivores and respond with manifold defence responses. To study transcriptional and other early regulation events of these plant responses, herbivory is often simulated to standardize the temporal and spatial dynamics that vary tremendously for natural herbivory. Yet, to what extent such simulations of herbivory are able to elicit the same plant response as real herbivory remains largely undetermined. We examined the transcriptional response of a wild model plant to herbivory by lepidopteran larvae and to a commonly used herbivory simulation by applying the larvae's oral secretions to standardized wounds. We designed a microarray for Solanum dulcamara and showed that the transcriptional responses to real and to simulated herbivory by Spodoptera exigua overlapped moderately by about 40%. Interestingly, certain responses were mimicked better than others; 60% of the genes upregulated but not even a quarter of the genes downregulated by herbivory were similarly affected by application of oral secretions to wounds. While the regulation of genes involved in signalling, defence and water stress was mimicked well by the simulated herbivory, most of the genes related to photosynthesis, carbohydrate-and lipid metabolism were exclusively regulated by real herbivory. Thus, wounding and application of oral secretions decently mimics herbivory-induced defence responses but likely not the reallocation of primary metabolites induced by real herbivory.caterpillar oral secretions, elicitation, induced plant defence, microarray, photosynthesis, phytohormone signalling, plant-insect interactions, simulated herbivory

In nature, plants are frequently subjected to multiple biotic and abiotic stresses, resulting in a convergence of adaptive responses. We hypothesised that hormonal signalling regulating defences to different herbivores may interact with drought responses, causing distinct resistance phenotypes. To test this, we studied the hormonal and transcriptomic responses of Solanum dulcamara subjected to drought and herbivory by the generalist Spodoptera exigua (beet armyworm; BAW) or the specialist Leptinotarsa decemlineata (Colorado potato beetle; CPB). Bioassays showed that the performance of BAW, but not CPB, decreased on plants under drought compared to controls. While drought did not alter BAW-induced hormonal responses, it enhanced the CPB-induced accumulation of jasmonic acid and salicylic acid (SA), and suppressed ethylene (ET) emission. Microarray analyses showed that under drought, BAW herbivory enhanced several herbivore-induced responses, including cell-wall remodelling and the metabolism of carbohydrates, lipids, and secondary metabolites. In contrast, CPB herbivory enhanced several photosynthesis-related and pathogen responses in drought-stressed plants. This may divert resources away from defence production and increase leaf nutritive value. In conclusion, while BAW suffers from the drought-enhanced defences, CPB may benefit from the effects of enhanced SA and reduced ET signalling. This suggests that the fine-tuned interaction between the plant and its specialist herbivore is sustained under drought.

controls the pathogenicity of interactions with arthropod hosts via the activity of the CrbS/R two component system. This signaling pathway regulates the consumption of acetate, which in turn, alters the relative virulence of interactions with arthropods, including CrbS is a histidine kinase that links a transporter-like domain to its signaling apparatus via putative STAC and PAS domains. CrbS and its cognate response regulator are required for expression of acetyl-CoA synthetase (), which converts acetate to acetyl-CoA. We demonstrate that the STAC domain of CrbS is required for signaling in culture; without it, transcription is reduced in LB medium, and cannot grow on acetate minimal media. However, the strain remains virulent towards and expresses similarly to wild-type during infection. This suggests that there exists a unique signal or environmental variable that modulates CrbS in the gastrointestinal tract of Secondly, we present evidence in support of CrbR, the response regulator that interacts with CrbS, binding directly to the promoter, and we identify a region of the promoter that CrbR may target. We further demonstrate that nutrient signals, together with the CRP-cAMP system, control transcription, but regulation may occur indirectly, as CRP-cAMP activates expression of the and genes. Lastly, we define the role of the Pta-AckA system in and identify redundancy built into acetate excretion pathways in this pathogen. CrbS is a member of a unique family of sensor histidine kinases, as its structure suggests that it may link signaling to transport of a molecule. However, mechanisms through which CrbS senses and communicates information about the outside world are unknown. In the , orthologs of CrbS regulate acetate metabolism, which can, in turn, affect interactions with host organisms. Here, we situate CrbS within a larger regulatory framework, demonstrating that is regulated by nutrient sensing systems. Furthermore, CrbS domains may play varying roles in signaling during infection and growth in culture, suggesting a unique mechanism of host recognition. Lastly, we define the roles of additional pathways in acetate flux, as a foundation for further studies of this metabolic nexus point.

Acetylation is a broadly conserved mechanism of covalently modifying the proteome to precisely control protein activity. In bacteria, central metabolic enzymes and regulatory proteins, including those involved in virulence, can be targeted for acetylation. In this study, we directly link a putative acetylation system to metabolite-dependent virulence in the pathogen We demonstrate that the and genes, which encode homologs of a deacetylase and an acetyltransferase, respectively, modulate metabolism of acetate, a bacterially derived short-chain fatty acid with important physiological roles in a diversity of host organisms. In , a model arthropod host for infection, the pathogen consumes acetate within the gastrointestinal tract, which contributes to fly mortality. We show that deletion of impairs growth on acetate minimal medium, delays the consumption of acetate from rich medium, and reduces virulence of toward These impacts can be reversed by complementing or by introducing a deletion of into the Δ background. We further show that controls the accumulation of triglycerides in the midgut, which suggests that directly modulates metabolite levels In K-12, is upregulated by cAMP-cAMP receptor protein (CRP), and we identified a similar pattern of regulation in , arguing that the system is activated in response to similar environmental cues. In summary, we demonstrate that proteins likely involved in acetylation can modulate the outcome of infection by regulating metabolite exchange between pathogens and their colonized hosts. The bacterium causes severe disease in humans, and strains can persist in the environment in association with a wide diversity of host species. By investigating the molecular mechanisms that underlie these interactions, we can better understand constraints affecting the ecology and evolution of this global pathogen. The model of infection has revealed that bacterial regulation of acetate and other small metabolites from within the fly gastrointestinal tract is crucial for its virulence. Here, we demonstrate that genes that may modify the proteome of affect virulence toward , most likely by modulating central metabolic pathways that control the consumption of acetate as well as other small molecules. These findings further highlight the many layers of regulation that tune bacterial metabolism to alter the trajectory of interactions between bacteria and their hosts.