Growth-defense Tradeoffs Research Articles

GhCNGC13 and 32 Act as Critical Links between Growth and Immunity in Cotton.

Cyclic nucleotide-gated ion channels (CNGCs) remain poorly studied in crop plants, most of which are polyploid. In allotetraploid Upland cotton (Gossypium hirsutum), silencing GhCNGC13 and 32 impaired plant growth and shoot apical meristem (SAM) development, while triggering plant autoimmunity. Both growth hormones (indole-3-acetic acid and gibberellin) and stress hormones (abscisic acid, salicylic acid, and jasmonate) increased, while leaf photosynthesis decreased. The silenced plants exhibited an enhanced resistance to Botrytis cinerea; however, Verticillium wilt resistance was weakened, which was associated with LIPOXYGENASE2 (LOX2) downregulation. Transcriptomic analysis of silenced plants revealed 4835 differentially expressed genes (DEGs) with functional enrichment in immunity and photosynthesis. These DEGs included a set of transcription factors with significant over-representation in the HSF, NAC, and WRKY families. Moreover, numerous members of the GhCNGC family were identified among the DEGs, which may indicate a coordinated action. Collectively, our results suggested that GhCNGC13 and 32 functionally link to photosynthesis, plant growth, and plant immunity. We proposed that GhCNGC13 and 32 play a critical role in the "growth-defense tradeoff" widely observed in crops.

PSKR1 balances the plant growth-defence trade-off in the rhizosphere microbiome.

Microbiota benefit their hosts by improving nutrient uptake and pathogen protection. How host immunity restricts microbiota while avoiding autoimmunity is poorly understood. Here we show that the Arabidopsis phytosulfokine receptor 1 (pskr1) mutant displays autoimmunity (plant stunting, defence-gene expression and reduced rhizosphere bacterial growth) in response to growth-promoting Pseudomonas fluorescens. Microbiome profiling and microbiota colonization showed that PSKR1-mediated reduction in bacterial growth and stunting is largely specific to Pseudomonas. Transcriptional profiling demonstrated that PSKR1 regulates the growth-defence trade-off during Pseudomonas colonization: PSKR1 upregulates plant photosynthesis and root growth but suppresses salicylic-acid-mediated defences. Genetic epistasis experiments showed that pskr1 stunting and restriction of bacterial growth are salicylic acid dependent. Finally, we showed that Pseudomonas, but not other bacteria, induces PSKR1 expression in roots, suggesting that Pseudomonas might manipulate plant signalling to promote its colonization. Our data demonstrate a genetic mechanism to coordinate beneficial functions of the microbiome while preventing autoimmunity.

Immunity priming uncouples the growth-defense trade-off in tomato.

Plants have developed an array of mechanisms to protect themselves against pathogen invasion. The deployment of defense mechanisms is imperative for plant survival, but can come at the expense of plant growth, leading to the 'growth-defense trade-off' phenomenon. Following pathogen exposure, plants can develop resistance to further attack. This is known as induced resistance, or priming. Here, we investigated the growth-defense trade-off, examining how defense priming via systemic acquired resistance (SAR), or induced systemic resistance (ISR), affects tomato development and growth. We found that defense priming can promote, rather than inhibit, plant development, and that defense priming and growth trade-offs can be uncoupled. Cytokinin response was activated during induced resistance, and found to be required for the observed growth and disease resistance resulting from ISR activation. ISR was found to have a stronger effect than SAR on plant development. Our results suggest that growth promotion and induced resistance can be co-dependent, and that, in certain cases, defense priming can drive developmental processes and promote plant yield.

The rice peroxisomal receptor PEX5 negatively regulates resistance to rice blast fungus Magnaporthe oryzae

The receptor protein PEX5, an important component of peroxisomes, regulates growth, development, and immunity in yeast and mammals. PEX5 also influences growth and development in plants, but whether it participates in plant immunity has remained unclear. Here, we report that knockdown of OsPEX5 enhances resistance to the rice blast fungus Magnaporthe oryzae. We demonstrate that OsPEX5 interacts with the E3 ubiquitin ligase APIP6, a positive regulator of plant immunity. APIP6 ubiquitinates OsPEX5 invitro and promotes its degradation invivo via the 26S proteasome pathway. In addition, OsPEX5 interacts with the aldehyde dehydrogenase OsALDH2B1, which functions in growth-defense trade-offs in rice. OsPEX5 stabilizes OsALDH2B1 to enhance its repression of the defense-related gene OsAOS2. Our study thus uncovers a previously unrecognized hierarchical regulatory mechanism in which an E3 ubiquitin ligase targets a peroxisome receptor protein that negatively regulates immunity in rice by stabilizing an aldehyde dehydrogenase that suppresses defense gene expression.

Metabolic priming in G6PDH isoenzyme-replaced tobacco lines improves stress tolerance and seed yields via altering assimilate partitioning.

We investigated the basis for better performance of transgenic Nicotiana tabacum plants with G6PDH-isoenzyme replacement in the cytosol (Xanthi::cP2::cytRNAi, Scharte etal., 2009). After six generations of selfing, infiltration of Phytophthora nicotianae zoospores into source leaves confirmed that defence responses (ROS, callose) are accelerated, showing as fast cell death of the infected tissue. Yet, stress-related hormone profiles resembled susceptible Xanthi and not resistant cultivar SNN, hinting at mainly metabolic adjustments in the transgenic lines. Leaves of non-stressed plants contained twofold elevated fructose-2,6-bisphosphate (F2,6P2 ) levels, leading to partial sugar retention (soluble sugars, starch) and elevated hexose-to-sucrose ratios, but also more lipids. Above-ground biomass lay in between susceptible Xanthi and resistant SNN, with photo-assimilates preferentially allocated to inflorescences. Seeds were heavier with higher lipid-to-carbohydrate ratios, resulting in increased harvest yields - also under water limitation. Abiotic stress tolerance (salt, drought) was improved during germination, and in floated leaf disks of non-stressed plants. In leaves of salt-watered plants, proline accumulated to higher levels during illumination, concomitant with efficient NADP(H) use and recycling. Non-stressed plants showed enhanced PSII-induction kinetics (upon dark-light transition) with little differences at the stationary phase. Leaf exudates contained 10% less sucrose, similar amino acids, but more fatty acids - especially in the light. Export of specific fatty acids via the phloem may contribute to both, earlier flowering and higher seed yields of the Xanthi-cP2 lines. Apparently, metabolic priming by F2,6P2 -combined with sustained NADP(H) turnover-bypasses the genetically fixed growth-defence trade-off, rendering tobacco plants more stress-resilient and productive.

Jasmonates Coordinate Secondary with Primary Metabolism.

Jasmonates (JAs), including jasmonic acid (JA), its precursor 12-oxo-phytodienoic acid (OPDA) and its derivatives jasmonoyl-isoleucine (JA-Ile), methyl jasmonate (MeJA), cis-jasmone (CJ) and other oxylipins, are important in the regulation of a range of ecological interactions of plants with their abiotic and particularly their biotic environments. Plant secondary/specialized metabolites play critical roles in implementing these ecological functions of JAs. Pathway and transcriptional regulation analyses have established a central role of JA-Ile-mediated core signaling in promoting the biosynthesis of a great diversity of secondary metabolites. Here, we summarized the advances in JAs-induced secondary metabolites, particularly in secondary metabolites induced by OPDA and volatile organic compounds (VOCs) induced by CJ through signaling independent of JA-Ile. The roles of JAs in integrating and coordinating the primary and secondary metabolism, thereby orchestrating plant growth-defense tradeoffs, were highlighted and discussed. Finally, we provided perspectives on the improvement of the adaptability and resilience of plants to changing environments and the production of valuable phytochemicals by exploiting JAs-regulated secondary metabolites.

Comparative constraint-based modelling of fruit development across species highlights nitrogen metabolism in the growth-defence trade-off.

Although primary metabolism is well conserved across species, it is useful to explore the specificity of its network to assess the extent to which some pathways may contribute to particular outcomes. Constraint-based metabolic modelling is an established framework for predicting metabolic fluxes and phenotypes and helps to explore how the plant metabolic network delivers specific outcomes from temporal series. After describing the main physiological traits during fruit development, we confirmed the correlations between fruit relative growth rate (RGR), protein content and time to maturity. Then a constraint-based method is applied to a panel of eight fruit species with a knowledge-based metabolic model of heterotrophic cells describing a generic metabolic network of primary metabolism. The metabolic fluxes are estimated by constraining the model using a large set of metabolites and compounds quantified throughout fruit development. Multivariate analyses showed a clear common pattern of flux distribution during fruit development with differences between fast- and slow-growing fruits. Only the latter fruits mobilise the tricarboxylic acid cycle in addition to glycolysis, leading to a higher rate of respiration. More surprisingly, to balance nitrogen, the model suggests, on the one hand, nitrogen uptake by nitrate reductase to support a high RGR at early stages of cucumber and, on the other hand, the accumulation of alkaloids during ripening of pepper and eggplant. Finally, building virtual fruits by combining 12 biomass compounds shows that the growth-defence trade-off is supported mainly by cell wall synthesis for fast-growing fruits and by total polyphenols accumulation for slow-growing fruits.

Growth-defense tradeoff in rice: The role of gibberellic acid catabolism.

Growth-defense tradeoff in rice: The role of gibberellic acid catabolism.

Arabidopsis subtilases promote defense-related pectin methylesterase activity and robust immune responses to botrytis infection

Plants involve a fine modulation of pectin methylesterase (PME) activity against microbes. PME activity can promote the cell wall stiffening and the production of damage signals able to induce defense responses and plant resistance to pathogens. However, the molecular mechanisms underlying PME activation during disease remain largely unknown. In this study, we explored the role of subtilases (SBTs) as PME activators in Arabidopsis immunity. By using biochemical and reverse genetic approaches, we found that the expression of SBT3.3 and SBT3.5 influences the induction of defense-related PME activity and resistance to the fungus Botrytis cinerea. Arabidopsis sbt3.3 and sbt3.5 knockout mutants showed decreased induction of PME activity and increased susceptibility to the fungus. SBT3.3 expression was stimulated by oligogalacturonides. Overexpression of SBT3.3 overactivated PME activity during fungal infection and enhanced resistance to B. cinerea. A negative correlation was observed between SBT3.3 expression and cell wall methyl ester content in the genotypes analyzed after B. cinerea infection. Increased expression of defense-related genes, including PAD3, CYP81F2 and WAK2, was also revealed in SBT3.3 overexpressing lines. We also demonstrated that SBT3.3 and pro-PME17 are both secreted into the cell wall using distinct protein secretion pathways and different kinetics. Our results propose SBT3.3 and SBT3.5 as modulators of PME activity in Arabidopsis against Botrytis to promptly boost immunity limiting the growth-defense trade-off.

Back to the drawing board: re‐thinking growth–defense tradeoffs

Well‐established ecological equations such as logistic growth may carry implicit assumptions that are not immediately obvious. When such equations are adapted for a different context, missing awareness of their hidden assumptions can confound our conclusions. We demonstrate how this has happened in predator–prey models with rapid adaptation of prey defense to variable predation risk, where costs of defense typically manifest as a growth‐defense tradeoff. Assuming logistic prey growth, this tradeoff is often implemented as a reduced intrinsic growth rate, while the carrying capacity is unaffected. We show that this assumption is not only extremely ecologically unrealistic, but also results in highly problematic model behavior and destroys any potential for eco‐evolutionary or biomass‐trait feedbacks. To reconcile the problematic results of this assumption with its ubiquity in existing models with rapid adaptation, we conducted a literature survey of models on prey adaptation or predator–prey co‐adaptation. This reveals that many models, despite describing a tradeoff affecting only the intrinsic growth rate, do incorporate an additional cost affecting the carrying capacity, but in a way that is implicit and not acknowledged. It is this cost that drives the famous feedbacks between defense adaptation and predator–prey dynamics. Finally, we discuss the implications for existing theory on eco‐evolutionary dynamics, and provide guidelines for implementing growth‐defense tradeoffs in a more realistic way.

NIGT1 represses plant growth and mitigates phosphate starvation signaling to balance the growth response tradeoff in rice.

Inorganic phosphate (Pi) availability is an important factor that affects the growth and yield of crops, thus an appropriate and effective response to Pi-fluctuation is critical. However, how crops orchestrate Pi-signaling and growth under Pi-starvation conditions to optimize the growth defense tradeoff remains unclear. Here we show that a Pi-starvation induced transcription factor NIGT1 (NITRATE-INDUCIBLE GARP-TYPE TRANSCRIPTIONAL REPRESSOR 1) controls plant growth and prevents a hyperresponse to Pi-starvation by directly repressing the expression of growth-related and Pi-signaling genes to achieve a balance between growth and response under a varying Pi environment. NIGT1 directly binds to the promoters of Pi-starvation signaling marker genes, like IPS1, miR827 and SPX2, under Pi-deficient conditions to mitigate the Pi-starvation responsive (PSR). It also directly represses the expression of vacuolar Pi efflux transporter genes VPE1/2 to regulate plant Pi-homeostasis. We further demonstrate that NIGT1 constrains shoot growth by repressing the expression of growth-related regulatory genes, including brassinolide signal transduction master regulator BZR1, cell division regulator CYCB1;1, and DNA replication regulator PSF3. Our findings reveal the function of NIGT1 in orchestrating plant growth and Pi-starvation signaling, and also provide evidence that NIGT1 acts as a safeguard to avoid hyperresponse during Pi-starvation stress in rice. This article is protected by copyright. All rights reserved.

Modifications in steroid and triterpenoid metabolism in Calendula officinalis plants and hairy root culture in response to chitosan treatment

BackgroundChitosan, a deacetylated derivative of chitin, is one of the most preferred biopolymers for use as biostimulants and biofertilizers in organic agriculture and as elicitors to enhance the productivity of plant in vitro cultures. Valued as a non-toxic, biodegradable, and environment-friendly agent, it is widely applied to improve plant growth and yield, the content of bioactive specialized metabolites, and resistance to stress conditions and pathogens. However, the influence of chitosan on the growth-defense trade-off, particularly the interplay between steroid and triterpenoid metabolism, has not been extensively investigated.ResultsIn this study, Calendula officinalis pot plants and hairy root cultures exposed to chitosan treatment displayed reduced biomass and altered steroid and triterpenoid metabolism. Biosynthesis and accumulation of free forms of sterols (particularly stigmasterol) were inhibited, while the content of sterol esters increased remarkably. The content of some triterpenoids (mainly free triterpenoid acids) was slightly enhanced; however, the biosynthesis of triterpenoid saponins was negatively affected.ConclusionsThese results indicate that in certain plants, chitosan treatment might not positively influence the growth and metabolite production. Therefore, to avoid unexpected effects, initial studies of the conditions of chitosan treatment are recommended, including the dose and the number of chitosan applications, the type of treatment (e.g., foliar or soil), and the vegetative stage of the treated plants.

The energy-water limitation threshold explains divergent drought responses in tree growth, needle length, and stable isotope ratios.

Predicted increases in extreme droughts will likely cause major shifts in carbon sequestration and forest composition. Although growth declines during drought are widely documented, an increasing number of studies have reported both positive and negative responses to the same drought. These divergent growth patterns may reflect thresholds (i.e., nonlinear responses) promoted by changes in the dominant climatic constraints on tree growth. Here we tested whether stemwood growth exhibited linear or nonlinear responses to temperature and precipitation and whether stemwood growth thresholds co-occurred with multiple thresholds in source and sink processes that limit tree growth. We extracted 772 tree cores, 1398 needle length records, and 1075 stable isotope samples from 27 sites across whitebark pine's (Pinus albicaulis Engelm.) climatic niche in the Sierra Nevada. Our results indicated that a temperature threshold in stemwood growth occurred at 8.4°C (7.12-9.51°C; estimated using fall-spring maximum temperature). This threshold was significantly correlated with thresholds in foliar growth, as well as carbon (δ13 C) and nitrogen (δ15 N) stable isotope ratios, that emerged during drought. These co-occurring thresholds reflected the transition between energy- and water-limited tree growth (i.e., the E-W limitation threshold). This transition likely mediated carbon and nutrient cycling, as well as important differences in growth-defense trade-offs and drought adaptations. Furthermore, whitebark pine growing in energy-limited regions may continue to experience elevated growth in response to climate change. The positive effect of warming, however, may be offset by growth declines in water-limited regions, threatening the long-term sustainability of the recently listed whitebark pine species in the Sierra Nevada.

Effect of interfering TOR signaling pathway on the biosynthesis of terpenoids in Salvia miltiorrhiza Bge

ABSTRACT The TOR (Target of Rapamycin) signaling pathway, which takes TOR kinase as the core, regulates the absorption, distribution, and recycling of nutrients by integrating metabolic network and other signaling pathways, thus participating in the plant growth-defense trade-off. While terpenoids play an important role in plant growth, development, stress response, and signal transduction. The effect of the TOR signaling pathway on terpenoid biosynthesis in plants has yet to be studied in detail. In this study, the tissue culture seedlings of Salvia miltiorrhiza were treated with the TOR inhibitor AZD8055. The results show that the roots of the control group had begun to grow on the 8th day, while the seedlings treated with AZD8055 had no rooting signs. Combined with the expression changes of genes related to the TOR signaling pathway in the first 8 days, samples on the 3rd, 6th, and 8th days were selected for RNA-Seq analysis. Through RNA-Seq analysis, a total of 50,689 unigenes were obtained from the samples of these three periods, of which 4088 unigenes showed differential expression. The function enrichment and time-series analysis of differentially expressed genes (DEGs) showed that the main influence of the TOR signal pathway on plant growth-related processes was gradually transmitted with treatment time after TOR was inhibited. Pathway enrichment analysis of DEGs showed that the genes in the biosynthesis of terpenoids, such as diterpenoid and carotenoid biosynthetic pathways, could be regulated. Compared with other stages, DEGs related to terpenoid biosynthesis were mainly regulated in the S2 stage. In addition, the genes involved in terpenoid skeleton biosynthesis was also considerably enriched in the S2 stage, according to the results of gene set enrichment analysis (GSEA) of unigenes. Inhibition of the TOR signaling pathway may affect the biosynthesis of terpenoid signaling molecules, inhibit gibberellin’s biosynthesis, and promote abscisic acid’s biosynthesis. This study has discussed the effect of interfering with the TOR pathway on terpenoid biosynthesis in S. miltiorrhiza from the perspective of omics and provides new insight into the interaction between the terpenoid biosynthesis pathway and the growth-defense trade-off of medicinal plants.

Tomato defence against Meloidogyne incognita by jasmonic acid-mediated fine-tuning of kaempferol homeostasis.

Jasmonic acid (JA) is involved in the modulation of defence and growth activities in plants. The best-characterized growth-defence trade-offs stem from antagonistic crosstalk among hormones. In this study, we first confirmed that JA negatively regulates root-knot nematode (RKN) susceptibility via the root exudates (REs) of tomato plants. Omics and toxicological analyses implied that kaempferol, a type of flavonol, from REs has a negative effect on RKN infection. We demonstrated that SlMYB57 negatively regulated kaempferol contents in tomato roots, whereas SlMYB108/112 had the opposite effect. We revealed that JA fine-tuned the homeostasis of kaempferol via SlMYB-mediated transcriptional regulation and the interaction between SlJAZs and SlMYBs, thus ensuring a balance between lateral root (LR) development and RKN susceptibility. Overall, this work provides novel insights into JA-modulated LR development and RKN susceptibility mechanisms and elucidates a trade-off model mediated by JA in plants encountering stress.

Biotinylated Tn5 transposase-mediated CUT&Tag efficiently profiles transcription factor-DNA interactions in plants.

In contrast to CUT&Tag approaches for profiling bulk histone modifications, current CUT&Tag methods for analysing specific transcription factor (TF)-DNA interactions remain technically challenging due to TFs having relatively low abundance. Moreover, an efficient CUT&Tag strategy for plant TFs is not yet available. Here, we first applied biotinylated Tn5 transposase-mediated CUT&Tag (B-CUT&Tag) to produce high-quality libraries for interrogating TF-DNA interactions. B-CUT&Tag combines streptavidin-biotin-based DNA purification with routine CUT&Tag, optimizing the removal of large amounts of intact chromatin not targeted by specific TFs. The biotinylated chromatin fragments are then purified for construction of deep sequencing libraries or qPCR analysis. We applied B-CUT&Tag to probe genome-wide DNA targets of Squamosa promoter-binding-like protein 9 (SPL9), a well-established TF in Arabidopsis; the resulting profiles were efficient and consistent in demonstrating its well-established target genes in juvenile-adult transition/flowering, trichome development, flavonoid biosynthesis, wax synthesis and branching. Interestingly, our results indicate functions of AtSPL9 in modulating growth-defence trade-offs. In addition, we established a method for applying qPCR after CUT&Tag (B-CUT&Tag-qPCR) and successfully validated the binding of SPL9 in Arabidopsis and PHR2 in rice. Our study thus provides a convenient and highly efficient CUT&Tag strategy for profiling TF-chromatin interactions that is widely applicable to the annotation of cis-regulatory elements for crop improvement.

Growth-defence trade-off in rice: fast-growing and acquisitive genotypes have lower expression of genes involved in immunity.

Plant ecologists and molecular biologists have long considered the hypothesis of a trade-off between plant growth and defence separately. In particular, how genes thought to control the growth-defence trade-off at the molecular level relate to trait-based frameworks in functional ecology, such as the slow-fast plant economics spectrum, is unknown. We grew 49 phenotypically diverse rice genotypes in pots under optimal conditions and measured growth-related functional traits and the constitutive expression of 11 genes involved in plant defence. We also quantified the concentration of silicon (Si) in leaves to estimate silica-based defences. Rice genotypes were aligned along a slow-fast continuum, with slow-growing, late-flowering genotypes versus fast-growing, early-flowering genotypes. Leaf dry matter content and leaf Si concentrations were not aligned with this axis and negatively correlated with each other. Live-fast genotypes exhibited greater expression of OsNPR1, a regulator of the salicylic acid pathway that promotes plant defence while suppressing plant growth. These genotypes also exhibited greater expression of SPL7 and GH3.2, which are also involved in both stress resistance and growth. Our results do not support the hypothesis of a growth-defence trade-off when leaf Si and leaf dry matter content are considered, but they do when hormonal pathway genes are considered. We demonstrate the benefits of combining ecological and molecular approaches to elucidate the growth-defence trade-off, opening new avenues for plant breeding and crop science.

Tuning the Wavelength: Manipulation of Light Signaling to Control Plant Defense.

The growth-defense trade-off in plants is a phenomenon whereby plants must balance the allocation of their resources between developmental growth and defense against attack by pests and pathogens. Consequently, there are a series of points where growth signaling can negatively regulate defenses and where defense signaling can inhibit growth. Light perception by various photoreceptors has a major role in the control of growth and thus many points where it can influence defense. Plant pathogens secrete effector proteins to manipulate defense signaling in their hosts. Evidence is emerging that some of these effectors target light signaling pathways. Several effectors from different kingdoms of life have converged on key chloroplast processes to take advantage of regulatory crosstalk. Moreover, plant pathogens also perceive and react to light in complex ways to regulate their own growth, development, and virulence. Recent work has shown that varying light wavelengths may provide a novel way of controlling or preventing disease outbreaks in plants.

Nutrient enrichment promotes invasion success of alien plants via increased growth and suppression of chemical defenses.

In support of the prediction of the enemy release hypothesis regarding a growth-defense trade-off, invasive alien plants often exhibit greater growth and lower anti-herbivory defenses than native plants. However, it remains unclear how nutrient enrichment of invaded habitats may influence competitive interactions between invasive alien and co-occurring native plants, as well as production of anti-herbivore defense compounds, growth-promoting hormones, and defense-regulating hormones by the two groups of plants. Here, we tested whether: (i) nutrient enrichment causes invasive alien plants to produce greater biomass and lower concentrations of the defense compounds flavonoids and tannins than native plants; and (ii) invasive alien plants produce lower concentrations of a defense-regulating hormone jasmonic acid (JA) and higher concentrations of a growth-promoting hormone gibberellic acid (GA3). In a greenhouse experiment, we grew five congeneric pairs of invasive alien and native plant species under two levels each of nutrient enrichment (low vs. high), simulated herbivory (leaf clipping vs. no-clipping), and competition (alone vs. competition) in 2.5-L pots. In the absence of competition, high-nutrient treatment induced a greater increase in total biomass of invasive alien species than that of native species, whereas the reverse was true under competition as native species benefitted more from nutrient enrichment than invasive alien species. Moreover, high-nutrient treatment caused a greater increase in total biomass of invasive alien species than that of native species in the presence of simulated herbivory. Competition induced higher production of flavonoids and tannins. Simulated herbivory induced higher flavonoid expression in invasive alien plants under low-nutrient than high-nutrient treatments. However, flavonoid concentrations of native plants did not change under nutrient enrichment and simulated herbivory treatments. Invasive alien plants produced higher concentrations of GA3 than native plants. Taken together, these results suggest that impact of nutrient enrichment on growth of invasive alien and co-occurring native plants may depend on the level of competition that they experience. Moreover, invasive alien plants might adjust their flavonoid-based defense more efficiently than native plants in response to variation in soil nutrient availability and herbivory pressure. Our findings suggest that large-scale efforts to reduce nutrient enrichment of invaded habitats may help to control future invasiveness of target alien plant species.

The effect of warming on seagrass wasting disease depends on host genotypic identity and diversity.

Temperature increases due to climate change have affected the distribution and severity of diseases in natural systems, causing outbreaks that can destroy host populations. Host identity, diversity, and the associated microbiome can affect host responses to both infection and temperature, but little is known about how they could function as important mediators of disease in altered thermal environments. We conducted an 8-week warming experiment to test the independent and interactive effects of warming, host genotypic identity, and host genotypic diversity on the prevalence and intensity of infections of seagrass (Zostera marina) by the wasting disease parasite (Labyrinthula zosterae). At elevated temperatures, we found that genotypically diverse host assemblages had reduced infection intensity, but not reduced prevalence, relative to less diverse assemblages. This dilution effect on parasite intensity was the result of both host composition effects as well as emergent properties of biodiversity. In contrast with the benefits of genotypic diversity under warming, diversity actually increased parasite intensity slightly in ambient temperatures. We found mixed support for the hypothesis that a growth-defense trade-off contributed to elevated disease intensity under warming. Changes in the abundance (but not composition) of a few taxa in the host microbiome were correlated with genotype-specific responses to wasting disease infections under warming, consistent with the emerging evidence linking changes in the host microbiome to the outcome of host-parasite interactions. This work emphasizes the context dependence of biodiversity-disease relationships and highlights the potential importance of interactions among biodiversity loss, climate change, and disease outbreaks in a key foundation species.