High-temperature stress suppresses allene oxide cyclase 2 and causes male sterility in cotton by disrupting jasmonic acid signaling

Cotton(Gossypium spp.) yield is reduced by stress. In this study, high temperature(HT) suppressed the expression of the jasmonic acid(JA) biosynthesis gene allene oxide cyclase 2(GhAOC2), reducing JA content and causing male sterility in the cotton HT-sensitive line H05. Anther sterility was reversed by exogenous application of methyl jasmonate(MeJA) to early buds. To elucidate the role of GhAOC2 in JA biosynthesis and identify its putative contribution to the anther response to HT, we created gene knockout cotton plants using the CRISPR/Cas9 system. Ghaoc2 mutant lines showed male-sterile flowers with reduced JA content in the anthers at the tetrad stage(TS), tapetum degradation stage(TDS), and anther dehiscence stage(ADS). Exogenous application of MeJA to early mutant buds(containing TS or TDS anthers) rescued the sterile pollen and indehiscent anther phenotypes, while ROS signals were reduced in ADS anthers. We propose that HT downregulates the expression of GhAOC2 in anthers, reducing JA biosynthesis and causing excessive ROS accumulation in anthers, leading to male sterility. These findings suggest exogenous JA application as a strategy for increasing male fertility in cotton under HT.

Jasmonic acid-mediated stress responses share the molecular mechanism underlying male sterility induced by deficiency of ZmMs33 in maize

Plant male reproduction is a fine-tuned developmental process that is susceptible to stressful environments and influences crop grain yields.Phytohormone signaling functions in control of plant normal growth and development as well as in response to external stresses,but the interaction or crosstalk among phytohormone signaling,stress response,and male reproduction in plants remains poorly understood.Cross-species comparison among 514 stress-response transcriptomic libraries revealed that ms33-6038,a genic male sterile mutant deficient in the Zm Ms33/Zm GPAT6 gene,displayed an excessive drought stress-like transcriptional reprogramming in anthers triggered mainly by disturbed jasmonic acid(JA)homeostasis.An increased level of JA appeared in Zm Ms33-deficient anthers at both meiotic and postmeiotic stages and activated genes involved in JA biosynthesis and signaling as well as genes functioning in JA-mediated drought response.Excessive accumulation of JA elevated expression level of a gene encoding a WRKY transcription factor that activated the Zm Ms33 promoter.These findings reveal a feedback loop of Zm Ms33-JA-WRKY-Zm Ms33 in controlling male sterility and JA-mediated stress response in maize,shedding light on the crosstalk of stress response and male sterility mediated by phytohormone homeostasis and signaling.

Abscisic acid and jasmonic acid are involved in drought priming-induced tolerance to drought in wheat

Drought stress is a limiting factor for wheat production and food security.Drought priming has been shown to increase drought tolerance in wheat.However,the underlying mechanisms are unknown.In the present study,the genes encoding the biosynthesis and metabolism of abscisic acid(ABA)and jasmonic acid(JA),as well as genes involved in the ABA and JA signaling pathways were up-regulated by drought priming.Endogenous concentrations of JA and ABA increased following drought priming.The interplay between JA and ABA in plant responses to drought priming was further investigated using inhibitors of ABA and JA biosynthesis.Application of fluridone(FLU)or nordihydroguaiaretic acid(NDGA)to primed plants resulted in lower chlorophyll-fluorescence parameters and activities of superoxide dismutase and glutathione reductase,and higher cell membrane damage,compared to primed plants(PD)under drought stress.NDGA+ABA,but not FLU+JA,restored priming-induced tolerance,as indicated by a finding of no significant difference from PD under drought stress.Under drought priming,NDGA induced the suppression of ABA accumulation,while FLU did not affect JA accumulation.These results were consistent with the expression of genes involved in the biosynthesis of ABA and JA.They suggest that ABA and JA are required for priming-induced drought tolerance in wheat,with JA acting upstream of ABA.

The laccase gene Gh Lac1 modulates fiber initiation and elongation by coordinating jasmonic acid and flavonoid metabolism

Cotton fibers are single cells originating in the epidermis of cotton ovules,and serve as the largest natural fiber source for the textile industry.In theory,all epidermal cells have the potential to develop into fibers,but only 15%–25%of epidermis cells develop into commercially viable lint fibers.We previously showed that Gh Lac1 participates in cotton defense against biotic stress.Here we report that Gh Lac1 also has a role in cotton fiber development.Gh Lac1 RNAi lines in cotton showed increased differentiation of fiber initials from epidermis and shortened fiber length,resulting in unchanged lint percentage.Suppression of Gh Lac1 expression led to constitutively hyperaccumulated jasmonic acid(JA)and flavonoids in ovules and fiber cells.In vitro ovule culture experiments confirmed the distinct roles of JA and flavonoids in fiber initiation and elongation,and showed that fiber development is spatially regulated by these chemicals:the increased fiber initiation in Gh Lac1 RNAi lines is caused by hyperaccumulated JA and rutin content during the fiber initiation stage and shortened fiber length is caused by constitutively increased JA and naringenin content during the fiber elongation stage.

Extracellular and Intracellular Calcium both Involved in the Jasmonic Acid Induced Calcium Mobilization in Arabidopsis thaliana

The objective of this experiment is to evaluate the role of intracellular and extracellular Ca2＋ and calmodulin （CAM） in jasmonic acid （JA） signaling. The laser scanning microscopy was used to detect the changes of [Ca2＋]cyt of Arabidopsis thaliana leaf cells which pretreated with different types of calcium channel blocker. Moreover, the expression of VSP, one of JA response genes, was also investigated after pretreated with the above blocker and antagonist of CaM. The results showed that extracellular and intracellular calcium both involved in the JA-induced Ca2＋ mobilization, and then Ca2＋ exerted its functions through activating the CaM or CaM related proteins. The apoplast calcium influx and the calcium release from the calcium stores are both involved in the JA-induced calcium mobilization, then the JA-induced Ca2＋ transmited the JA signal through CaM or CaM related proteins, and regulated the JA responsive genes.

Effects of Wounding and Exogenous Jasmonic Acid on the Peroxidation of Membrane Lipid in Pea Seedlings Leaves

The changes of malondialdehyde （MDA）, H2O2, and O2^7 content, or the activities of superoxide dismutase （SOD）, catalase （CAT）, ascrobate peroxidase （APX）, peroxidase （POD）, phenylalanine ammonia lyase （PAL）, and polyphenol oxidase （PPO） in pea seedlings （Pisum sativum L.） under wounding and treatment of exogenous jasmonic acid （JA） were investigated. The results showed that the activities of both phenylalanine ammonia lyase （PAL） and polyphenol oxidase （PPO） were significantly increased by wounding and application of JA. The metabolism of reaction oxidative species （ROS） was enhanced, especially O2^7 and H2O2 appeared to rapidly increase. The activities of antioxidant enzymes such as SOD, CAT, APX and POD were also increased. Treatment of JA of 1 or 10 μmol L^-1 could effectively induce plant defense response, and thus decrease the peroxidation of cell membrane lipid. However, high concentration of JA （100 μmol L^-1） resulted in unbalance of metabolism of ROS and promoted the peroxidation of cell membrane lipid. We thus suggested that JA, under the suitable concentration, could induce defense response of pea seedlings to wounding.

Effects of Exogenous Jasmonic Acid on Concentrations of Direct-Defense Chemicals and Expression of Related Genes in Bt (Bacillus thuringiensis) Corn (Zea mays)

Bt corn is one of the top three large-scale commercialized transgenic crops around the world. It is increasingly clear that the complementary durable approaches for pest control, which combine the endogenous defense of the crop with the introduced foreign genes, are promising alternative strategies for pest resistance management and the next generation of insect-resistant transgenic crops. In the present study, we tested the inducible effects of exogenous jasmonic acid （JA） on direct-defense chemical content, Bt protein concentration, and related gene expression in the leaves of Bt corn cultivar 34B24 and non-Bt cultivar 34B23 by chemical analysis, ELISA, and RT-PCR. The results show that the expression of LOX, PR-2a, MPI, and PR-I genes in the treated leaf （the first leaf） was promoted by exogenous JA both in 34B24 and 34B23. As compared with the control, the concentration of DIMBOA in the treated leaf was significantly increased by 63 and 18% for 34B24 and 34B23, respectively. The total phenolic acid was also increased by 24 and 12% for both 34B24 and 34B23. The Bt protein content of 34B24 in the treated leaf was increased by 13% but decreased significantly by 27% in the second leaf. The induced response of 34B24 was in a systemic way and was much stronger than that of 34B23. Those findings indicated that there is a synergistic interaction between Bt gene and internally induced chemical defense system triggered by externally applied JA in Bt corn.

Trade-offs between the accumulation of cuticular wax and jasmonic acid-mediated herbivory resistance in maize

Plants have evolved complex physical and chemical defense systems that allow them to withstand herbivory infestation.Composed of a complex mixture of very-long-chain fatty acids(VLCFAs)and their derivatives,cuticular wax constitutes the first physical line of defense against herbivores.Here,we report the function of Glossy 8(ZmGL8),which encodes a 3-ketoacyl reductase belonging to the fatty acid elongase complex,in orchestrating wax production and jasmonic acid(JA)-mediated defenses against herbivores in maize(Zea mays).The mutation of GL8 enhanced chemical defenses by activating the JA-dependent pathway.We observed a trade-off between wax accumulation and JA levels across maize glossy mutants and 24 globally collected maize inbred lines.In addition,we demonstrated that mutants defective in cuticular wax biosynthesis in Arabidopsis thaliana and maize exhibit enhanced chemical defenses.Comprehensive transcriptomic and lipidomic analyses indicated that the gl8 mutant confers chemical resistance to herbivores by remodeling VLCFA-related lipid metabolism and subsequent JA biosynthesis and signaling.These results suggest that VLCFA-related lipid metabolism has a critical role in regulating the trade-offs between cuticular wax and JA-mediated chemical defenses.

MdbHLH162 connects the gibberellin and jasmonic acid signals to regulate anthocyanin biosynthesis in apple

Anthocyanins are secondary metabolites induced by environmental stimuli and developmental signals.The positive regulators of anthocyanin biosynthesis have been reported,whereas the anthocyanin repressors have been neglected.Although the signal transduction pathways of gibberellin(GA)and jasmonic acid(JA)and their regulation of anthocyanin biosynthesis have been investigated,the cross-talk between GA and JA and the antagonistic mechanism of regulating anthocyanin biosynthesis remain to be investigated.In this study,we identified the anthocyanin repressor MdbHLH162 in apple and revealed its molecular mechanism of regulating anthocyanin biosynthesis by integrating the GA and JA signals.MdbHLH162 exerted passive repression by interacting with MdbHLH3 and MdbHLH33,which are two recognized positive regulators of anthocyanin biosynthesis.MdbHLH162 negatively regulated anthocyanin biosynthesis by disrupting the formation of the anthocyanin-activated MdMYB1-MdbHLH3/33complexes and weakening transcriptional activation of the anthocyanin biosynthetic genes MdDFR and MdUF3GT by MdbHLH3 and MdbHLH33.The GA repressor MdRGL2a antagonized MdbHLH162-mediated inhibition of anthocyanins by sequestering MdbHLH162 from the MdbHLH162-MdbHLH3/33 complex.The JA repressors MdJAZ1 and MdJAZ2 interfered with the antagonistic regulation of MdbHLH162 by MdRGL2a by titrating the formation of the MdRGL2a-MdbHLH162 complex.Our findings reveal that MdbHLH162 integrates the GA and JA signals to negatively regulate anthocyanin biosynthesis.This study provides new information for discovering more anthocyanin biosynthesis repressors and explores the cross-talk between hormone signals.

Overexpression of auxin/indole-3-acetic acid gene MdIAA24 enhances Glomerella leaf spot resistance in apple(Malus domestica)

Auxin is throughout the entire life process of plants and is involved in the crosstalk with other hormones,yet its role in apple disease resistance remains unclear.In this study,we investigated the function of auxin/indole-3-acetic acid(IAA)gene Md IAA24 overexpression in enhancing apple resistance to Glomerella leaf spot(GLS)caused by Colletotrichum fructicola(Cf).Analysis revealed that,upon Cf infection,35S::Md IAA24 plants exhibited enhanced superoxide dismutase(SOD)and peroxidase(POD)activity,as well as a greater amount of glutathione(reduced form)and ascorbic acid accumulation,resulting in less H_(2)O_(2)and superoxide anion(O_(2)^(-))in apple leaves.Furthermore,35S::Md IAA24 plants produced more protocatechuic acid,proanthocyanidins B1,proanthocyanidins B2 and chlorogenic acid when infected with Cf.Following Cf infection,35S::Md IAA24 plants presented lower levels of IAA and jasmonic acid(JA),but higher levels of salicylic acid(SA),along with the expression of related genes.The overexpression of Md IAA24 was observed to enhance the activity of chitinase andβ-1,3-glucanase in Cfinfected leaves.The results indicated the ability of Md IAA24 to regulate the crosstalk between IAA,JA and SA,and to improve reactive oxygen species(ROS)scavenging and defense-related enzymes activity.This jointly contributed to GLS resistance in apple.

Induction of jasmonic acid biosynthetic genes inhibits Arabidopsis growth in response to low boron

The essential micronutrient boron(B) has key roles in cell wall integrity and B deficiency inhibits plant growth. The role of jasmonic acid(JA) in plant growth inhibition under B deficiency remains unclear. Here,we report that low B elevates JA biosynthesis in Arabidopsis thaliana by inducing the expression of JA biosynthesis genes. Treatment with JA inhibited plant growth and, a JA biosynthesis inhibitor enhanced plant growth, indicating that the JA induced by B deficiency affects plant growth. Furthermore,examination of the JA signaling mutants jasmonate resistant1, coronatine insensitive1-2, and myc2 showed that JA signaling negatively regulates plant growth under B deficiency. We identified a low-B responsive transcription factor, ERF018, and used yeast one-hybrid assays and transient activation assays in Nicotiana benthamiana leaf cells to demonstrate that ERF018 activates the expression of JA biosynthesis genes. ERF018 overexpression(OE)lines displayed stunted growth and up-regulation of JA biosynthesis genes under normal B conditions,compared to Col-0 and the difference between ERF018 OE lines and Col-0 diminished under low B.These results suggest that ERF018 enhances JA biosynthesis and thus negatively regulates plant growth. Taken together, our results highlight the importance of JA in the effect of low B on plant growth.

Suppression of Jasmonic Acid-Mediated Defense by Viral-Inducible MicroRNA319 Facilitates Virus Infection in Rice

MicroRNAs （miRNAs） are pivotal modulators of plant development and host-virus interactions. However, the roles and action modes of specific miRNAs involved in viral infection and host susceptibility remain largely unclear. In this study, we show that Rice ragged stunt virus （RRSV） infection caused increased accumulation of miR319 but decreased expression of miR319-regulated TCP （TEOSINTE BRANCHED/ CYCLOIDEA/PCF） genes, especially TCP21, in rice plants. Transgenic rice plants overexpressing miP,319 or downregulating TCP21 exhibited disease-like phenotypes and showed significantly higher susceptibility to RRSV in comparison with the wild-type plants. In contrast, only mild disease symptoms were observed in RRSV-infected lines overexpressing TCP21 and especially in the transgenic plants overexpressing miR319- resistant TCP21. Both RRSV infection and overexpression of miR319 caused the decreased endogenous jasmonic acid （JA） levels along with downregulated expression of JA biosynthesis and signaling-related genes in rice. However, treatment of rice plants with methyl jasmonate alleviated disease symptoms caused by RRSV and reduced virus accumulation. Taken together, our results suggest that the induction of miR319 by RRSV infection in rice suppresses JA-mediated defense to facilitate virus infection and symp- tom development.

Repression of the Arabidopsis thaliana Jasmonic Acid/Ethylene-Induced Defense Pathway by TGA-Interacting Glutaredoxins Depends on Their C-Terminal ALWL Motif

Glutaredoxins are small heat-stable oxidoreductases that transfer electrons from glutathione （GSH） to oxi- dized cysteine residues, thereby contributing to protein integrity and regulation. In Arabidopsis thaliana, floral glutare- doxins ROXY1 and ROXY2 and pathogen-induced ROXY19/GRX480 interact with bZIP transcription factors of the TGACG （TGA） motif-binding family. ROXY1, ROXY2, and TGA factors PERIANTHIA, TGA9, and TGA10 play essential roles in floral development. In contrast, ectopically expressed ROXY19/GRX480 negatively regulates expression of jasmonic acid （JA）/ ethylene （ET）-induced defense genes through an unknown mechanism that requires clade II transcription factors TGA2, TGA5, and/or TGA6. Here, we report that at least 17 of the 21 land plant-specific glutaredoxins encoded in the Arabidopsis genome interact with TGA2 in a yeast-two-hybrid system. To investigate their capacity to interfere with the expression of JA/ET-induced genes, we developed a transient expression system. Activation of the ORA59 （OCTADECANOID-RESPONSIVE ARABIDOPSIS AP2/ERF-domain protein 59） promoter by transcription factor EIN3 （ETHYLENE INSENSITVE 3） was sup- pressed by co-expressed ROXY19/GRX480. Suppression depended on the L＊＊LL motif in the C-terminus of ROXY19/ GRX480. This putative protein interaction domain was recently described as being essential for the TGA/ROXY interaction. Ten of the 17 tested ROXY proteins suppressed ORA59 promoter activity, which correlated with the presence of the C-terminal ALWL motif, which is essential for ROXY1 function in flower development. ROXY19/GRX480-mediated repres- sion depended on the GSH binding site, suggesting that redox modification of either TGA factors or as yet unknown target proteins is important for the suppression of ORA59 promoter activity.

Jasmonic Acid Oxidase 2 Hydroxylates Jasmonic Acid and Represses Basal Defense and Resistance Responses against Botrytis cinerea Infection

Jasmonates （JAs） orchestrate immune responses upon wound/herbivore injury or infection by necrotro- phic pathogens. Elucidation of catabolic routes has revealed new complexity in jasmonate metabolism. Two integrated pathways attenuate signaling by turning over the active hormone jasmonoyl-isoleucine （JA-Ile） through w-oxidation or deconjugation, and define an indirect route forming the derivative 12OH-JA. Here, we provide evidence for a second 12OH-JA formation pathway by direct jasmonic acid （JA） oxidation. Three jasmonic acid oxidases （JAOs） of the 2-oxoglutarate dioxygenase family catalyze spe- cific oxidation of JA to 12OH-JA, and their genes are induced by wounding or infection by the fungus Botrytis cinerea. JA02 exhibits the highest basal expression, and its deficiency in jao2 mutants strongly enhanced antifungal resistance. The resistance phenotype resulted from constitutive expression of antimi- crobial markers rather than from their higher induction in infected jao2 plants and could be reversed by ectopic expression of any of the three JAOs injao2. Elevated defense injao2 was dependent on the activity of JASMONATE RESPONSE 1 （JAR1） and CORONATINE-INSENSITIVE 1 （COI1） but was not correlated with erihanced JA-Ile accumulation. Instead, jao2 mutant lines displayed altered accumulation of several JA species in healthy and challenged plants, suggesting elevated metabolic flux through JA-Ile. Collectively, these data identify the missing enzymes hydroxylating JA and uncover an important metabolic diversion mechanism for repressing basal JA defense responses.

The Essential Role of Jasmonic Acid in Plant-Herbivore Interactions-Using the Wild Tobacco Nicotiana attenuata as a Model

The plant hormone jasmonic acid （JA） plays a central role in plant defense against herbivores. Herbivore damage elicits a rapid and transient JA burst in the wounded leaves and JA functions as a signal to mediate the accumulation of various secondary metabolites that confer resistance to herbivores. Nicotiana attenuata is a wild tobacco species that inhabits western North America. More than fifteen years of study and its unique interaction with the specialist herbivore insect Manduca sexta have made this plant one of the best models for studying plant-herbivore interactions. Here we review the recent progress in understanding the elicitation of JA accumulation by herbivore-specific elicitors, the regulation of JA biosynthesis, JA signaling, and the herbivore-defense traits in N. attenuata.

Insights into the role of jasmonic acid-mediated defenses against necrotrophic and biotrophic fungal pathogens

Jasmonic acid （JA） is a natural hormone regulator involved in development, responses against woundingand pathogen attack. Upon perception of pathogens, JA is synthesized and mediates a signaling cascade initiating various defense responses. Traditionally, necrotrophic fungi have been shown to be the primary activators of JA- dependent defenses through the JA-receptor, COIl. Conversely, plants infected with biotrophic fungi have classically been associated with suppressing JA-mediated responses. However, recent evidence has shown that certain biotrophic fungal species also trigger activation of JA-mediated responses and mutants deficient in JA signaling show an increase in susceptibility to certain biotrophic fungal pathogens. These findings suggest a new role for JA in defense against fungal biotrophs. This review will focus on recent research advancing our knowledge of JA-dependant responses involved in defense against both biotrophic and necrotrophic fungi.

An Integrative Analysis of the Effects of Auxin on Jasmonic Acid Biosynthesis in Arabidopsis thaliana

Auxin and jasmonic acid （JA） are two plant phytohormones that both participate in the regulation of many developmental processes. Jasmonic acid also plays important roles in plant stress response reactions. Although extensive investigations have been undertaken to study the biological functions of auxin and JA, little attention has been paid to the cross-talk between their regulated pathways. In the few available reports examining the effects of auxin on the expression of JA or JA-responsive genes, both synergetic and antagonistic results have been found. To further investigate the relationship between auxin and JA, we adopted an integrative method that combines microarray expression data with pathway information to study the behavior of the JA biosynthesis pathway under auxin treatment. Our results showed an overall downregulation of genes involved in JA biosynthesis, providing the first report of a relationship between auxin and the JA synthesis pathway in Arabidopsis seedlings.

Structure-guided analysis of Arabidopsis JASMONATE-INDUCED OXYGENASE(JOX)2 reveals key residues for recognition of jasmonic acid substrate by plant JOXs

The jasmonic acid(JA)signaling pathway is used by plants to control wound responses.The persistent accumulation of JA inhibits plant growth,and the hydroxylation of JA to 12-hydroxy-JA by JASMONATE-INDUCED OXYGENASEs(JOXs,also named jasmonic acid oxidases)is therefore vital for plant growth,while structural details of JA recognition by JOXs are unknown.Here,we present the 2.65Åresolution X-ray crystal structure of Arabidopsis JOX2 in complex with its substrate JA and its co-substrates 2-oxoglutarate and Fe(Ⅱ).JOX2 contains a distorted double-stranded p helix(DSBH)core flanked by a helices and loops.JA is bound in the narrow substrate pocket by hydrogen bonds with the arginine triad R225,R350,and R354 and by hydrophobic interactions mainly with the phenylalanine triad F157,F317,and F346.The most critical residues for JA binding are F157 and R225,both from the DSBH core,which interact with the cyclopentane ring of JA.The spatial distribution of critical residues for JA binding and the shape of the substrate-binding pocket together define the substrate selectivity of the JOXs.Sequence alignment shows that these critical residues are conserved among JOXs from higher plants.Collectively,our study provides insights into the mechanism by which higher plants hydroxylate the hormone JA.

Synergistic Action between Jasmonic Acid and Nitric Oxide in Inducing Matrine Accumulation of Sophora flavescens Suspension Cells

Secondary metabolites not only play important ecological roles in plants but also are important pharmaceutical and source compounds for derivative synthesis. Production of plant secondary metabolites is believed to be controlled by the endogenous signal network of plants. However, the molecular basis is still largely unknown. Here we show that matrine production of Sophora flavescens Ait. cells treated with low levels of jasmonic acid （JA） and nitric oxide （NO） is significantly increased although treatment with low concentrations of JA or NO alone has no effects on matrine production, showing that JA and NO may act synergistically in triggering matrine production. Moreover, treatment with NO triggers lipoxygenase （LOX） activity and enhances JA levels of the cells, showing that NO may activate the endogenous JA biosynthesis of S. flavescens cells. External application of JA induces nitric oxide synthase-like activities and stimulates NO generation of S. flavescens cells, which suggests that JA may trigger NO generation of the cells. Thus, the results reveal a mutually amplifying reaction between JA and NO in S. flavescens cells. Furthermore, JA and NO inhibitors suppress not only the mutually amplifying reaction between JA and NO but also the synergistic effects of NO and JA on matrine production. Therefore, the data demonstrate that the synergistic action of JA and NO in inducing matrine production might be due to the mutually amplifying reaction between JA and NO in the cells.

Silencing Brassinosteroid Receptor BRI1 Impairs Herbivory-elicited Accumulation of Jasmonic Acid-isoleucine and Diterpene Glycosides, but not Jasmonic Acid and Trypsin Proteinase Inhibitors in Nicotiana attenuata

The brassinosteroid （BR） receptor, BR insensitive 1 （BRI1）, plays a critical role in plant development, but whether BRI1-mediated BR signaling is involved in plant defense responses to herbivores was largely unknown. Here, we examined the function of BRI1 in the resistance of Nicotiana attenuata （Solanaceae） to its specialist insect herbivore Manduca sexta. Jasmonic acid （JA） and JA-isoleucine conjugate （JA-Ile） are important hormones that mediate resistance to herbivores and we found that after wounding or simulated herbivory NaBRI1 had little effect on JA levels, but was important for the induction of JA-Ile. Further experiments revealed that decreased JAR （the enzyme for JA-Ile production） activity and availability of Ile in NaBRI1-silenced plants were likely responsible for the low JA-Ile levels. Consistently, M. sexta larvae gained more weight on NaBRI1-silenced plants than on the control plants. Quantification of insect feeding-induced secondary metabolites revealed that silencing NaBRI1 resulted in decreased levels of carbon-rich defensive secondary metabolites （hydroxygeranyllinalool diterpene glycosides, chlorogenic acid, and rutin）, but had little effect on the nitrogen-rich ones （nicotine and trypsin proteinase inhibitors）. Thus, NaBRI1-mediated BR signaling is likely involved in plant defense responses to M. sexta, including maintaining JA-Ile levels and the accumulation of several carbon-rich defensive secondary metabolites.