BABA-induced Resistance Research Articles

Potato β-aminobutyric acid receptor IBI1 manipulates VOZ1 and VOZ2 transcription factor activity to promote disease resistance.

Upon infection with non-pathogenic microorganisms or treatment with natural or synthetic compounds, plants exhibit a more rapid and potent response to both biotic and abiotic stresses. However, the molecular mechanisms behind this phenomenon, known as defense priming, are poorly understood. β-aminobutyric acid (BABA) is an endogenous stress metabolite that enhances plant tolerance to various abiotic stresses and primes plant defense responses, providing the ability to resist a variety of pathogens (broad-spectrum resistance). In this study, we identified an aspartyl-tRNA synthetase (AspRS), StIBI1 (named after Arabidopsis IMPAIRED IN BABA-INDUCED IMMUNITY 1; IBI1), as a BABA receptor in Solanum tuberosum. We elucidated the regulatory mechanisms by which StIBI1 interacts with two NAC (NAM, ATAF1, 2, and CUC2) transcription factors (TFs), StVOZ1 and StVOZ2 (VASCULAR PLANT ONE ZINC FINGER, VOZ), to activate BABA-induced resistance (BABA-IR). StVOZ1 represses, whereas StVOZ2 promotes, immunity to the late blight pathogen Phytophthora infestans. Interestingly, BABA and StIBI1 influence StVOZ1- and StVOZ2-mediated immunity. StIBI1 interacts with StVOZ1 and StVOZ2 in the cytoplasm, reducing the nuclear accumulation of StVOZ1 and promoting the nuclear accumulation of StVOZ2. Our findings indicate that StVOZ1 and StVOZ2 finely regulate potato resistance to late blight through distinct signaling pathways. In summary, our study provides insights into the interaction between the potato BABA receptor StIBI1 and the TFs StVOZ1 and StVOZ2, which affects StVOZ1 and StVOZ2stability and nuclear accumulation to regulate late blight resistance during BABA-IR. This research advances our understanding of the primary mechanisms of BABA-IR in potato and contributes to a theoretical basis for the prevention and control of potato late blight using BABA-IR.

BABA-induced pathogen resistance: a multi-omics analysis of the tomato response reveals a hyper-receptive status involving ethylene.

Prior exposure to microbial-associated molecular patterns or specific chemical compounds can promote plants into a primed state with stronger defence responses. β-aminobutyric acid (BABA) is an endogenous stress metabolite that induces resistance protecting various plants towards diverse stresses. In this study, by integrating BABA-induced changes in selected metabolites with transcriptome and proteome data, we generated a global map of the molecular processes operating in BABA-induced resistance (BABA-IR) in tomato. BABA significantly restricts the growth of the pathogens Oidium neolycopersici and Phytophthora parasitica but not Botrytis cinerea. A cluster analysis of the upregulated processes showed that BABA acts mainly as a stress factor in tomato. The main factor distinguishing BABA-IR from other stress conditions was the extensive induction of signaling and perception machinery playing a key role in effective resistance against pathogens. Interestingly, the signalling processes and immune response activated during BABA-IR in tomato differed from those in Arabidopsis with substantial enrichment of genes associated with jasmonic acid (JA) and ethylene (ET) signalling and no change in Asp levels. Our results revealed key differences between the effect of BABA on tomato and other model plants studied until now. Surprisingly, salicylic acid (SA) is not involved in BABA downstream signalization whereas ET and JA play a crucial role.

β-Aminobutyric acid induced phytotoxicity and effectiveness against nematode is stereomer-specific and dose-dependent in tomato.

β-Aminobutyric acid (BABA) induces resistance to a/biotic stress but is associated with phytotoxicity in some plant species. There are two enantiomers of BABA, the R and S enantiomers. We evaluated the phytotoxicity caused by the RS BABA (racemic mixture of R and S BABA), evaluating the dose-response effect and different modes of application on tomato. Results show that RS BABA-induced phytotoxicity in tomato is dose-dependent and stronger with foliar applications than with soil drench. We further evaluated the phytotoxicity of the two enantiomers separately and observed that BABA-induced phytotoxicity is stereomer-specific. In comparison with less phytotoxic effects induced by S BABA, R BABA induces dose-dependent and systemic phytotoxic symptoms. To investigate the possible physiological causes of this phytotoxicity, we measured levels of oxidative stress and anthocyanins and validated the findings with gene expression analyses. Our results show that high doses of RS and R BABA induce hydrogen peroxide, lipid peroxidation, and anthocyanin accumulation in tomato leaves, while this response is milder and more transient upon S BABA application. Next, we evaluated BABA induced resistance against root-knot nematode Meloidogyne incognita in tomato. BABA-induced resistance was found to be stereomer-specific and dependent on dose and mode of application. R or RS BABA multiple soil drench application at low doses induces resistance to nematodes with less phytotoxic effects. Taken together, our data provide useful knowledge on how BABA can be applied in crop production by enhancing stress tolerance and limiting phytotoxicity.

L-Aspartate and L-Glutamine Inhibit Beta-Aminobutyric Acid-Induced Resistance in Tomatoes.

Plant diseases caused by pathogens lead to economic and agricultural losses, while plant resistance is defined by robustness and timing of defence response. Exposure to microbial-associated molecular patterns or specific chemical compounds can promote plants into a primed state with more robust defence responses. β-aminobutyric acid (BABA) is an endogenous stress metabolite that induces resistance, thereby protecting various plants' diverse stresses by induction of non-canonical activity after binding into aspartyl-tRNA synthetase (AspRS). In this study, by integrating BABA-induced changes in selected metabolites and transcript data, we describe the molecular processes involved in BABA-induced resistance (BABA-IR) in tomatoes. BABA significantly restricted the growth of the pathogens P. syringae pv. tomato DC3000 and was related to the accumulation of transcripts for pathogenesis-related proteins and jasmonic acid signalling but not salicylic acid signalling in Arabidopsis. The resistance was considerably reduced by applying amino acids L-Asp and L-Gln when L-Gln prevents general amino acid inhibition in plants. Analysis of amino acid changes suggests that BABA-IR inhibition by L-Asp is due to its rapid metabolisation to L-Gln and not its competition with BABA for the aspartyl-tRNA synthetase (AspRS) binding site. Our results showed differences between the effect of BABA on tomatoes and other model plants. They highlighted the importance of comparative studies between plants of agronomic interest subjected to treatment with BABA.

MADS2 regulates priming defence in postharvest peach through combined salicylic acid and abscisic acid signaling.

MADS-box genes play well-documented roles in plant development, but relatively little is known regarding their involvement in defence responses. In this study, pre-treatment of peach (Prunus persica) fruit with β-aminobutyric acid (BABA) activated resistance against Rhizopus stolonifer, leading to a significant delay in the symptomatic appearance of disease. This was associated with an integrated defence response that included a H2O2 burst, ABA accumulation, and callose deposition. cDNA library screening identified nucleus-localized MADS2 as an interacting partner with NPR1, and this was further confirmed by yeast two-hybrid, luciferase complementation imaging, and co-immunoprecipitation assays. The DNA-binding activity of NPR1 conferred by the NPR1-MADS2 complex was required for the transcription of SA-dependent pathogenesis-related (PR) and ABA-inducible CalS genes in order to gain the BABA-induced resistance, in which MAPK1-induced post-translational modification of MADS2 was also involved. In accordance with this, overexpression of PpMADS2 in Arabidopsis potentiated the transcription of a group of PR genes and conferred fungal resistance in the transgenic plants. Conversely, Arabidopsis mads2-knockout lines showed high sensitivity to the fungal pathogen. Our results indicate that MADS2 positively participates in BABA-elicited defence in peach through a combination of SA-dependent NPR1 activation and ABA signaling-induced callose accumulation, and that this defence is also related to the post-translational modification of MADS2 by MAPK1 for signal amplification.

Heat Shock Protein HSP24 Is Involved in the BABA-Induced Resistance to Fungal Pathogen in Postharvest Grapes Underlying an NPR1-Dependent Manner.

Although heat shock proteins (HSPs), a family of ubiquitous molecular chaperones, are well characterized in heat stress-related responses, their function in plant defense remains largely unclear. Here, we report the role of VvHSP24, a class B HSP from Vitis vinifera, in β-aminobutyric acid (BABA)-induced priming defense against the necrotrophic fungus Botrytis cinerea in grapes. Grapes treated with 10 mmol L–1 BABA exhibited transiently increased transcript levels of VvNPR1 and several SA-inducible genes, including PR1, PR2, and PR5. Additionally, phytoalexins accumulated upon inoculation with the gray mold fungus B. cinerea, which coincided with the action of a priming mode implicated in pathogen-driven resistance. Intriguingly, electrophoretic mobility shift (EMSA), yeast two-hybrid (Y2H) and His pull-down assays demonstrated that the nuclear chaperone VvHSP24 cannot modulate the transcript of PR genes but does directly interact with VvNPR1 in vivo or in vitro. Furthermore, we found that VvHSP24 overexpression enhanced the transcript levels of NPR1 and SA-responsive genes (PR1, PR2, and PR5) and increased the resistance of transgenic Arabidopsis thaliana to B. cinerea compared with wildtype Col-0. An opposite trend between CRISPR mutants of AtHSFB1 (the orthologous gene of VvHSP24 in Arabidopsis) and wildtype plants was observed. Hence, our results suggest that VvHSP24 has a potential role in NPR1-dependent plant resistance to fungal pathogen. BABA-induced priming defense in grapes may require posttranslational modification of the chaperone VvHSP24 to activate VvNPR1 transcript, leading to PR gene expressions and resistance phenotypes.

Redox status regulates subcelluar localization of PpTGA1 associated with a BABA-induced priming defence againstRhizopus rot in peach fruit.

This study attempted to characterize the involvement of a change in the redox status and subcellular localization in the BABA-induced priming resistance of peach fruit against Rhizopus rot. Specifically, 50mM BABA primed the peaches for the enhanced disease resistance against R. stolonifer, as demonstrated by suppression of the disease development upon pathogen challenge accompanied by the clearly elevated level of TGA transcription factor (PpTGA1) and NPR1 gene (PpNPR1). In addition, the BABA elicitation enhanced the activities of a series of critical enzymes in the PPP and AsA-GSH cycle, and eventually promoted the NADPH and GSH pools, which altered the intracellular redox state towards a highly reductive condition. Additionally, PpTGA1-GFP was localized in the cytoplasm in the absence of BABA treatment or R. stolonifer inoculation, while BABA elicitation plus R. stolonifer inoculation caused PpTGA1-GFP to specifically translocate to the nucleus, where it interacted with PpNPR1 and regulated the positive expression of PR genes. Therefore, the observations implied that BABA could promote the reduction of the redox state, resulting in the translocation of PpTGA1 to the nucleus, which was a prerequisite for the induction of a priming defence against Rhizopus rot in peach.

The IBI1 Receptor of β-Aminobutyric Acid Interacts with VOZ Transcription Factors to Regulate Abscisic Acid Signaling and Callose-Associated Defense

External and internal signals can prime the plant immune system for a faster and/or stronger response to pathogen attack. β-aminobutyric acid (BABA) is an endogenous stress metabolite that induces broad-spectrum disease resistance in plants. BABA perception in Arabidopsis is mediated by the aspartyl tRNA synthetase IBI1, which activates priming of multiple immune responses, including callose-associated cell wall defenses that are under control by abscisic acid (ABA). However, the immediate signaling components after BABA perception by IBI1, as well as the regulatory role of ABA therein, remain unknown. Here, we have studied the early signaling events controlling IBI1-dependent BABA-induced resistance (BABA-IR), using untargeted transcriptome and protein interaction analyses. Transcriptome analysis revealed that IBI1-dependent expression of BABA-IR against the biotrophic oomycete Hyaloperonospora arabidopsidis is associated with suppression of ABA-inducible abiotic stress genes. Protein interaction studies identified the VOZ1 and VOZ2 transcription factors (TFs) as IBI1-interacting partners, which are transcriptionally induced by ABA but suppress pathogen-induced expression of ABA-dependent genes. Furthermore, we show that VOZ TFs require nuclear localization for their contribution to BABA-IR by mediating augmented expression of callose-associated defense. Collectively, our study indicates that the IBI1-VOZ signaling module channels pathogen-induced ABA signaling toward cell wall defense while simultaneously suppressing abiotic stress-responsive genes.

Nitric Oxide Plays an Important Role in β-Aminobutyric Acid-Induced Resistance to Botrytis cinerea in Tomato Plants.

β-Aminobutyric acid (BABA) has consistently been reported to enhance plant immunity. However, the specific mechanisms and downstream components that mediate this resistance are not yet agreed upon. Nitric oxide (NO) is an important signal molecule involved in a diverse range of physiological processes, and whether NO is involved in BABA-induced resistance is interesting. In this study, treatment with BABA significantly increased NO accumulation and reduced the sensitivity to Botrytis cinerea in tomato plants. BABA treatment reduced physical signs of infection and increased both the transcription of key defense marker genes and the activity of defensive enzymes. Interestingly, compared to treatment with BABA alone, treatment with BABA plus cPTIO (NO specific scavenger) not only significantly reduced NO accumulation, but also increased disease incidence and lesion area. These results suggest that NO accumulation plays an important role in BABA-induced resistance against B. cinerea in tomato plants.

β-Aminobutyric Acid Priming Acquisition and Defense Response of Mango Fruit to Colletotrichum gloeosporioides Infection Based on Quantitative Proteomics.

β-aminobutyric acid (BABA) is a new environmentally friendly agent to induce disease resistance by priming of defense in plants. However, molecular mechanisms underlying BABA-induced priming defense are not fully understood. Here, comprehensive analysis of priming mechanism of BABA-induced resistance was investigated based on mango-Colletotrichum gloeosporioides interaction system using iTRAQ-based proteome approach. Results showed that BABA treatments effectively inhibited the expansion of anthracnose caused by C. gleosporioides in mango fruit. Proteomic results revealed that stronger response to pathogen in BABA-primed mango fruit after C. gleosporioides inoculation might be attributed to differentially accumulated proteins involved in secondary metabolism, defense signaling and response, transcriptional regulation, protein post-translational modification, etc. Additionally, we testified the involvement of non-specific lipid-transfer protein (nsLTP) in the priming acquisition at early priming stage and memory in BABA-primed mango fruit. Meanwhile, spring effect was found in the primed mango fruit, indicated by inhibition of defense-related proteins at priming phase but stronger activation of defense response when exposure to pathogen compared with non-primed fruit. As an energy-saving strategy, BABA-induced priming might also alter sugar metabolism to provide more backbone for secondary metabolites biosynthesis. In sum, this study provided new clues to elucidate the mechanism of BABA-induced priming defense in harvested fruit.

Starch degradation, abscisic acid and vesicular trafficking are important elements in callose priming by indole-3-carboxylic acid in response to Plectosphaerella cucumerina infection.

A fast callose accumulation has been shown to mediate defence priming in certain plant-pathogen interactions, but the events upstream of callose assembly following chemical priming are poorly understood, mainly because those steps comprise sugar transfer to the infection site. β-Amino butyric acid (BABA)-induced resistance in Arabidopsis against Plectosphaerella cucumerina is known to be mediated by callose priming. Indole-3-carboxylic acid (ICOOH, also known as I3CA) mediates BABA-induced resistance in Arabidopsis against P.cucumerina. This indolic compound is found in a common fingerprint of primed metabolites following treatments with various priming stimuli. In the present study, we show that I3CA induces resistance in Arabidopsis against P.cucumerina and primes enhancement of callose accumulation. I3CA treatment increased abscisic acid (ABA) levels before infection with P.cucumerina. An intact ABA synthesis pathway is needed to activate a starch amylase (BAM1) to trigger augmented callose deposition against P.cucumerina during I3CA-IR. To verify the relevance of the BAM1 amylase in I3CA-IR, knockdown mutants and overexpressors of the BAM1 gene were tested. The mutant bam1 was impaired to express I3CA-IR, but complemented 35S::BAM1-YFP lines in the background of bam1 restored an intact I3CA-IR and callose priming. Therefore, a more active starch metabolism is a committed step for I3CA-IR, inducing callose priming in adult plants. Additionally, I3CA treatments induced expression of the ubiquitin ligase ATL31 and syntaxin SYP131, suggesting that vesicular trafficking is relevant for callose priming. As a final element in the callose priming, an intact Powdery Mildew resistant4 (PMR4) gene is also essential to fully express I3CA-IR.

When the story proceeds backward: The discovery of endogenous β-aminobutyric acid as the missing link for a potential new plant hormone

ABSTRACTThe capacity of β-aminobutyric acid (BABA) to induce resistance in plants against biotic and abiotic stresses has been known for more than 50 y. In the beginning reports were mainly descriptive of the phenomenon, but it became clear with the discovery of BABA insensitive mutants in Arabidopsis that there was definitely a genetic basis underlying BABA-induced resistance. The study of these mutants, along with the use of regular hormone mutants, allowed establishing the defense pathways activated upon defense induction. To date it is clear that BABA potentiates the defense pathway more appropriate to counteract the upcoming stress situation, through a phenomenon termed priming. Interestingly, plants possess a receptor for BABA, but up to recently there was a general consensus on the fact that BABA was a xenobiotic molecule. The development of an accurate non-destructive assay for measuring aminobutyric acid isomers in planta and the finding of plant-produced BABA, thus seems to represent the missing link for the discovery of a novel plant hormone. Differences and similarities with some of the classical plant hormones are presented here.

Induction of resistance in pepper against Xanthomonas euvesicatoria by β-aminobutyric acid

Xanthomonas euvesicatoria is one of the most destructive pathogens of pepper that results in serious yield loss worldwide. Previous studies confirmed that β-aminobutyric acid (BABA) induces resistance in plants against a variety of pathogens. A promoted resistance of pepper induced by BABA to X. euvesicatoria was demonstrated in this study. Additionally, induction of catalase and pathogenesis-related gene 1 during the BABA-induced resistance was confirmed. Our data provides useful information for the development of disease management programs.

Diverse responses of wild and cultivated tomato to BABA, oligandrin and Oidium neolycopersici infection.

Current strategies for increased crop protection of susceptible tomato plants against pathogen infections include treatment with synthetic chemicals, application of natural pathogen-derived compounds or transfer of resistance genes from wild tomato species within breeding programmes. In this study, a series of 45 genes potentially involved in defence mechanisms was retrieved from the genome sequence of inbred reference tomato cultivar Solanum lycopersicum 'Heinz 1706'. The aim of the study was to analyse expression of these selected genes in wild and cultivated tomato plants contrasting in resistance to the biotrophic pathogen Oidium neolycopersici , the causative agent of powdery mildew. Plants were treated either solely with potential resistance inducers or by inducers together with the pathogen. The resistance against O. neolycopersici infection as well as RT-PCR-based analysis of gene expression in response to the oomycete elicitor oligandrin and chemical agent β-aminobutyric acid (BABA) were investigated in the highly susceptible domesticated inbred genotype Solanum lycopersicum 'Amateur' and resistant wild genotype Solanum habrochaites . Differences in basal expression levels of defensins, germins, β-1,3-glucanases, heveins, chitinases, osmotins and PR1 proteins in non-infected and non-elicited plants were observed between the highly resistant and susceptible genotypes. Moreover, these defence genes showed an extensive up-regulation following O. neolycopersici infection in both genotypes. Application of BABA and elicitin induced expression of multiple defence-related transcripts and, through different mechanisms, enhanced resistance against powdery mildew in the susceptible tomato genotype. The results indicate that non-specific resistance in the resistant genotype S. habrochaites resulted from high basal levels of transcripts with proven roles in defence processes. In the susceptible genotype S. lycopersicum 'Amateur', oligandrin- and BABA-induced resistance involved different signalling pathways, with BABA-treated leaves displaying direct activation of the ethylene-dependent signalling pathway, in contrast to previously reported jasmonic acid-mediated signalling for elicitins.

BABA-induced resistance: milestones along a 55-year journey

β-aminobutyric acid (BABA) has been known as an inducer of disease-resistance since 1963, however, only in the recent two decades an increasing number of reports have been published shedding light on its spectrum of activity, physiological impacts, and mode of action. BABA has been shown to protect about 40 plant species against about 80 pathogens and pests, including a virus, protista, bacteria, oomycetes, fungi, nematodes and arthropods. Interestingly, it is also active against abiotic stress and enhances salt, heat and drought tolerance in several plant species. Although generally regarded as a xenobiotic, there are a few reports that mention its occurrence in plants. BABA-treated plants react faster and in a more robust manner to a stress situation, a phenomenon that has been termed priming. 14C BABA is highly systemic, readily taken up by roots and leaves, and translocate both acropetally and basipetally. No metabolites of BABA are known. BABA is effective as a foliar spray, soil drench and seed treatment. Seeds derived from treated plants may produce primed progeny, making BABA the first agent with transgenerational efficacy. BABA induces numerous biochemical changes in treated plants. Among them are the induction of reactive oxygen species (ROS) and glycolate oxidase (GO) that are tightly linked to defense. ROS scavengers may alleviate the activity of BABA. Interestingly, only the R but not the S enantiomer of BABA primes for resistance. Unfortunately, BABA can also impose growth stress (and phytotoxicity) in some treated plants therefore BABA analogs with reduced stress effects are highly desirable for agricultural use.

Induction of Direct or Priming Resistance against Botrytis cinerea in Strawberries by β-Aminobutyric Acid and Their Effects on Sucrose Metabolism.

The specific forms of disease resistance induced by β-aminobutyric acid (BABA) and their impacts on sucrose metabolism of postharvest strawberries were determined in the present research. Treatment with 10-500 mmol L(-1) BABA inhibited the Botrytis cinerea infection, possibly directly by suppressing the fungus growth and indirectly by triggering disease resistance. Moreover, BABA-induced resistance against B. cinerea infection in strawberries was associated with either one of two mechanisms, depending upon the concentration used: BABA at concentrations higher than 100 mmol L(-1) directly induced the defense response, including a H2O2 burst, modulation of the expression of PR genes, including FaPR1, FaChi3, Faβglu, and FaPAL, and increased activities of chitinase, β-1,3-glucanase, and PAL, whereas BABA at 10 mmol L(-1) activated a priming response because the BABA-treated fruits exhibited an increased capacity to express molecular defense only when the fruits were inoculated with B. cinerea. Activation of the priming defense appeared almost as effective against B. cinerea as inducing direct defense. However, the primed strawberries maintained higher activities of SS synthesis and SPS and SPP enzymes) and lower level of SS cleavage during the incubation; these activities contributed to higher sucrose, fructose, and glucose contents, sweetness index, and sensory scores compared to fruits exhibiting the direct defense. Thus, it is plausible that the priming defense, which can be activated by BABA at relatively low concentrations, represents an optimal strategy for combining the advantages of enhanced disease protection and soluble sugar accumulation.

The Arabidopsis Malectin-Like/LRR-RLK IOS1 Is Critical for BAK1-Dependent and BAK1-Independent Pattern-Triggered Immunity.

Plasma membrane-localized pattern recognition receptors (PRRs) such as FLAGELLIN SENSING2 (FLS2), EF-TU RECEPTOR (EFR), and CHITIN ELICITOR RECEPTOR KINASE1 (CERK1) recognize microbe-associated molecular patterns (MAMPs) to activate pattern-triggered immunity (PTI). A reverse genetics approach on genes responsive to the priming agent β-aminobutyric acid (BABA) revealed IMPAIRED OOMYCETE SUSCEPTIBILITY1 (IOS1) as a critical PTI player. Arabidopsis thaliana ios1 mutants were hypersusceptible to Pseudomonas syringae bacteria. Accordingly, ios1 mutants showed defective PTI responses, notably delayed upregulation of the PTI marker gene FLG22-INDUCED RECEPTOR-LIKE KINASE1, reduced callose deposition, and mitogen-activated protein kinase activation upon MAMP treatment. Moreover, Arabidopsis lines overexpressing IOS1 were more resistant to bacteria and showed a primed PTI response. In vitro pull-down, bimolecular fluorescence complementation, coimmunoprecipitation, and mass spectrometry analyses supported the existence of complexes between the membrane-localized IOS1 and BRASSINOSTEROID INSENSITIVE1-ASSOCIATED KINASE1 (BAK1)-dependent PRRs FLS2 and EFR, as well as with the BAK1-independent PRR CERK1. IOS1 also associated with BAK1 in a ligand-independent manner and positively regulated FLS2-BAK1 complex formation upon MAMP treatment. In addition, IOS1 was critical for chitin-mediated PTI. Finally, ios1 mutants were defective in BABA-induced resistance and priming. This work reveals IOS1 as a novel regulatory protein of FLS2-, EFR-, and CERK1-mediated signaling pathways that primes PTI activation.

BTH and BABA induce resistance in pea against rust (Uromyces pisi) involving differential phytoalexin accumulation.

Systemic acquired resistance elicitors, BTH and BABA, reduce rust penetration in pea through phytoalexins pathway but differing in their mode of action. It has been previously shown that rust (Uromyces pisi) infection can be reduced in pea (Pisum sativum) by exogenous applications of systemic acquired resistance elicitors such as BTH and BABA. This protection is known to be related with the induction of the phenolic pathway but the particular metabolites involved have not been determined yet. In this work, we tackled the changes induced in phytoalexin content by BTH and BABA treatments in the context of the resistance responses to pea rust. Detailed analysis through high-performance liquid chromatography (HPLC) showed qualitative and quantitative differences in the content, as well as in the distribution of phytoalexins. Thus, following BTH treatment, we observed an increase in scopoletin, pisatin and medicarpin contents in all, excreted, soluble and cell wall-bound fraction. This suggests fungal growth impairment by both direct toxic effect as well as plant cell wall reinforcement. The response mediated by BTH was genotype-dependent, since coumarin accumulation was observed only in the resistant genotype whereas treatment by BABA primed phytoalexin accumulation in both genotypes equally. Exogenous application to the leaves of scopoletin, medicarpin and pisatin lead to a reduction of the different fungal growth stages, confirming a role for these phytoalexins in BTH- and BABA-induced resistance against U. pisi hampering pre- and postpenetration fungal stages.

β-Aminobutyric Acid-Induced Resistance Against Root-Knot Nematodes in Rice Is Based on Increased Basal Defense.

The nonprotein amino acid β-aminobutyric acid (BABA) is known to protect plants against various pathogens. The mode of action is relatively diverse and specific in different plant-pathogen systems. To extend the analysis of the mode of action of BABA to plant-parasitic nematodes in monocot plants, we evaluated the effect of BABA against the root-knot nematode (RKN) Meloidogyne graminicola in rice. BABA treatment of rice plants inhibited nematode penetration and resulted in delayed nematode and giant cell development. BABA-induced resistance (BABA-IR) was still functional in mutants or transgenics defective in salicylic acid biosynthesis and response or abscisic acid (ABA) response. Pharmacological inhibition of jasmonic acid (JA) and ethylene (ET) biosynthesis indicated that BABA-IR against rice RKN likely occurs independent of JA and ET. However, histochemical and biochemical quantification in combination with quantitative real-time reverse transcription-polymerase chain reaction data suggest that BABA protects rice against RKN through the activation of basal defense mechanisms of the plant, such as reactive oxygen species accumulation, lignin formation, and callose deposition.

B-Amino Butyric Acid ? Resistance Inducing Agent in Pearl Millet

β-amino butyric acid (BABA), applied as inducer of resistance to the seeds of susceptible cultivar of pearl millet [Pennisetum glaucum (L) R Br] against downy mildew [Sclerospora graminicola (Sacc) Schroet]. Infection offered protection to the host operative through vegetative and reproductive growth. Biochemical studies identified a close association between BABA-treatment and accumulation of defence-related proteins like phenylalanine ammonia lyase, peroxidise and β-1,3-glucanase. Studies on phenotypic host defence identified modifications in host cell wall leading to papillae formation with hydroxyproline-rich glycoproteins (HRGPs) as its major constituent. The HRGPs were identified as extensions by use of MAC 265 monoclonal antibodies. PgMPK4 (mitogen-activated protein kinase) was identified as the crucial signal transduction module signalling of pathogen cues. This increased accumulation of PgMPK4 mRNA and kinase activity in BABA-treated samples and further kinase inhibitor treatments providing critical evidence of PgMPK4 involvement in the JA- and SA mediated expression of defence genes, it may be assumed that BABA-induced resistance could be a JA/SA mediated phenomenon.