Deciphering agr quorum sensing in Staphylococcus aureus: insights and therapeutic prospects.

The emergence of superbugs like methicillin-resistant Staphylococcus aureus exposed the limitations of treating microbial infections using antibiotics. At present, the discovery of novel and convincing therapeutic methods are being executed increasingly as possible substitutes to conventional antibiotic therapies. The quorum sensing helps Staphylococcus aureus become more viable through their signaling mechanisms. In recent years, targeting the prominent factors of quorum sensing has obtained remarkable attention as a futuristic approach to dealing with bacterial pathogenicity. The standard antibiotic therapy intends to inhibit the organism by targeting specific molecules and afford a chance for the evolution of antibiotic resistance. This prompts the development of novel therapeutic strategies like inhibiting quorum sensing that can limit bacterial virulence by decreasing the selective pressure, thereby restricting antibiotic resistance evolution. This review furnishes new insights into the accessory gene regulator quorum sensing in Staphylococcus aureus and its inhibition by targeting the genes that regulate the operon. Further, this review comprehensively explores the inhibitors reported up to date and their specific targets and discusses their potentially ineffective alternative therapy against methicillin-resistant Staphylococcus aureus.

C4-HSL-mediated quorum sensing regulates nitrogen removal in activated sludge process at Low temperatures.

The activated sludge process faces challenges in achieving adequate nitrification ability under low-temperature conditions. Therefore, we investigated the effects of different concentrations of exogenous N-butyryl-homoserine lactone (C4-HSL) on nitrogen removal in lab-scale sequencing batch reactors (SBRs) at 10 °C. The results revealed that both 10 and 100 µg/L of C4-HSL could improve NH4+-N removal efficiency by 26% and reduce the effluent TN concentration to below 15 mg/L. Analysis of extracellular polymeric substances (EPS) revealed that adding C4-HSL (especially 100 µg/L) reduced the protein-like substance content while increasing the humic and fulvic acid-like substance content in EPS. Protein-like substances could serve as carbon sources for denitrifiers, thus promoting denitrification. Moreover, exogenous C4-HSL increased the abundance of bacteria and genes associated with nitrification and denitrification. Further analysis of quorum sensing (QS) of microorganisms indicated that exogenous C4-HSL (especially 100 µg/L) promoted regulation, transportation, and decomposition functions in the QS process. Furthermore, CS, sdh, fum, and mdh gene expressions involved in the tricarboxylic acid (TCA) cycle were enhanced by 100 µg/L C4-HSL. Exogenous C4-HSL promoted microbial communication, microbial energy metabolism, and nitrogen metabolism, thereby improving the nitrogen removal efficiency of activated sludge systems at low temperatures. This study provides a feasible strategy for enhancing denitrogenation performance at low temperatures through exogenous C4-HSL.

Regulation and mechanism of organic selenium on quorum sensing, biofilm, and antioxidant effects of Lactobacillus paracasei.

Different organic compounds can have varying degrees of impact on the activity of Lactobacillus paracasei. The study focused on the impact and action mechanism of different organic selenium products on the bioactivity of two strains of L. paracasei. The growth, antioxidant activity, extracellular polysaccharide secretion, quorum sensing (QS), and biofilm formation of the strains before and after the addition of organic selenium crude products and three organic selenium standard were evaluated. The results showed that the addition of crude organic selenium promoted the various activities of the strain. l-selenocysteine had the strongest regulatory effect, with maximum GIM1.80 biofilm formation when it reached a critical concentration of 0.4 µg/mL; l-selenomethionine resulted in the highest activity of the signal molecule Auto inducer-2 of GDMCC1.155, when it reached a critical concentration of 0.4 µg/mL. The results of scanning electron microscopy demonstrated that the addition of organic selenium effectively improved the morphological structure of the two bacterial cells. Molecular docking revealed that the mechanism by which organic selenium regulates QS in Lactobacillus was achieved by binding two crucial receptor proteins (histidine protein kinase HKP and periplasmic binding protein LuxP) from specific sites. Furthermore, organic selenium products have a beneficial regulatory effect on the biological activity of L. paracasei. Overall, these findings provide a new alternative (organic selenium) for regulating the viability and beneficial activity of L. paracasei.

Lactate: a pearl dropped in the ocean-an overlooked signal molecule in physiology and pathology.

Lactate, once recognized as a wasty product from anaerobic glycolysis, is proved to be a pivotal signal molecule. Lactate accumulation occurs in diverse physiological and pathological settings due to the imbalance between lactate production and clearance. Under the condition with drastic changes in local microenvironment, such as tumorigenesis, inflammation, and microbial infection, the glycolysis turns to be active in surrounding cells leading to increased lactate release. Meanwhile, lactate can be utilized by these cells as an energy substrate and acts as a signal molecule to regulate cell functions through receptor-dependent or independent pathways. In this review, we tended to tease out the contribution of lactate in tumor progression and immunomodulation. And we also discussed the accessory role of lactate, beyond as the energy source only, in the growth of invading pathogens.

Plant Disease Resistance-Related Signaling Pathways: Recent Progress and Future Prospects.

Plant-pathogen interactions induce a signal transmission series that stimulates the plant's host defense system against pathogens and this, in turn, leads to disease resistance responses. Plant innate immunity mainly includes two lines of the defense system, called pathogen-associated molecular pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). There is extensive signal exchange and recognition in the process of triggering the plant immune signaling network. Plant messenger signaling molecules, such as calcium ions, reactive oxygen species, and nitric oxide, and plant hormone signaling molecules, such as salicylic acid, jasmonic acid, and ethylene, play key roles in inducing plant defense responses. In addition, heterotrimeric G proteins, the mitogen-activated protein kinase cascade, and non-coding RNAs (ncRNAs) play important roles in regulating disease resistance and the defense signal transduction network. This paper summarizes the status and progress in plant disease resistance and disease resistance signal transduction pathway research in recent years; discusses the complexities of, and interactions among, defense signal pathways; and forecasts future research prospects to provide new ideas for the prevention and control of plant diseases.

Stabilizing AqdC, a Pseudomonas Quinolone Signal-Cleaving Dioxygenase from Mycobacteria, by FRESCO-Based Protein Engineering.

The mycobacterial PQS dioxygenase AqdC, a cofactor-less protein with an α/ß-hydrolase fold, inactivates the virulence-associated quorum-sensing signal molecule 2-heptyl-3-hydroxy-4(1H)-quinolone (PQS) produced by the opportunistic pathogen Pseudomonas aeruginosa and is therefore a potential anti-virulence tool. We have used computational library design to predict stabilizing amino acid replacements in AqdC. While 57 out of 91 tested single substitutions throughout the protein led to stabilization, as judged by increases in Tappm of >2 °C, they all impaired catalytic activity. Combining substitutions, the proteins AqdC-G40K-A134L-G220D-Y238W and AqdC-G40K-G220D-Y238W showed extended half-lives and the best trade-off between stability and activity, with increases in Tappm of 11.8 and 6.1 °C and relative activities of 22 and 72 %, respectively, compared to AqdC. Molecular dynamics simulations and principal component analysis suggested that stabilized proteins are less flexible than AqdC, and the loss of catalytic activity likely correlates with an inability to effectively open the entrance to the active site.

Histamine: A Bacterial Signal Molecule.

Bacteria have evolved sophisticated signaling mechanisms to coordinate interactions with organisms of other domains, such as plants, animals and human hosts. Several important signal molecules have been identified that are synthesized by members of different domains and that play important roles in inter-domain communication. In this article, we review recent data supporting that histamine is a signal molecule that may play an important role in inter-domain and inter-species communication. Histamine is a key signal molecule in humans, with multiple functions, such as being a neurotransmitter or modulator of immune responses. More recent studies have shown that bacteria have evolved different mechanisms to sense histamine or histamine metabolites. Histamine sensing in the human pathogen Pseudomonas aeruginosa was found to trigger chemoattraction to histamine and to regulate the expression of many virulence-related genes. Further studies have shown that many bacteria are able to synthesize and secrete histamine. The release of histamine by bacteria in the human gut was found to modulate the host immune responses and, at higher doses, to result in host pathologies. The elucidation of the role of histamine as an inter-domain signaling molecule is an emerging field of research and future investigation is required to assess its potential general nature.

Atmospheric H2S exposure does not affect stomatal aperture in maize.

MAIN CONCLUSION: Stomatal aperture in maize is not affected by exposure to a subtoxic concentration of atmospheric H2S. At least in maize, H2S, thus, is not a gaseous signal molecule that controls stomatal aperture. Sulfur is an indispensable element for the physiological functioning of plants with hydrogen sulfide (H2S) potentially acting as gasotransmitter in the regulation of stomatal aperture. It is often assumed that H2S is metabolized into cysteine to stimulate stomatal closure. To study the significance of H2S for the regulation of stomatal closure, maize was exposed to a subtoxic atmospheric H2S level in the presence or absence of a sulfate supply to the root. Similar to other plants, maize could use H2S as a sulfur source for growth. Whereas sulfate-deprived plants had a lower biomass than sulfate-sufficient plants, exposure to H2S alleviated this growth reduction. Shoot sulfate, glutathione, and cysteine levels were significantly higher in H2S-fumigated plants compared to non-fumigated plants. Nevertheless, this was not associated with changes in the leaf area, stomatal density, stomatal resistance, and transpiration rate of plants, meaning that H2S exposure did not affect the transpiration rate per stoma. Hence, it did not affect stomatal aperture, indicating that, at least in maize, H2S is not a gaseous signal molecule controlling this aperture.

Advances in research on signal molecules regulating biofilms.

Bacterial biofilms (BFs) are membrane-like structures formed by the secretion of extracellular polymeric substances (EPS) by bacteria. The formation of BFs contributes to bacterial survival and drug resistance. When bacteria proliferate, they produce secondary metabolites that act as signaling molecules in bacterial communities that regulate intracellular and cell-to-cell communication. This communication can directly affect the physiological behavior of bacteria, including the production and emission of light (bioluminescence), the expression of virulence factors, the resistance to antibiotics, and the shift between planktonic and biofilm lifestyles. We review the major signaling molecules that regulate BF formation, with a focus on quorum-sensing systems (QS), cyclic diguanylate (c-di-GMP), two-component systems (TCS), and small RNA (sRNA). Understanding these processes will lead to new approaches for treating chronic diseases and preventing bacterial resistance.

[Quantitative detection and clinical value of CD44 in patients with nonalcoholic fatty liver disease].

Objective: To quantitatively detect CD44 expression in patients with nonalcoholic fatty liver disease (NAFLD) for comparative analysis. Methods: Patients with chronic liver diseases accompanied with or without NAFLD, including chronic hepatitis B, cirrhosis and hepatocellular carcinoma after chronic hepatitis B, and healthy blood donors as normal controls who admitted to the Affiliated Hospital of Nantong University from May to October 2018 were selected. The proportion of CD44 positive cells was analyzed by flow cytometry. CD44 level was quantified by an enzyme-linked immunosorbent assay, and the biochemical indicators such as serum aspartate aminotransferase, alanine aminotransferase activity, total cholesterol and triglyceride were routinely analyzed. The cancerous and adjacent cancerous tissues of patients accompanied with or without NAFLD were collected by self-matching method and analyzed by immunoblotting and histochemistry and compared by CD44 integrated optical density. Image-Pro Plus version 6.0, Image J, GraphPad Prism 5.0, Photoshop, Microsoft Excel and IBM SPSS statistics 23 were used to analyze and draw pictures. An independent sample t-test was used to compare the differences between groups. Results: Patients accompanied with NAFLD had hepatocyte injury and dyslipidemia. NAFLD and chronic liver disease patients had significantly elevated serum CD44 levels than normal control group (P < 0.01). CD44 positive lymphocyte ratio was 78.19 % ± 16.33 % in NAFLD patients and 68.47% ± 20.91% in chronic hepatitis B group, which was higher than the control group (46.51% ± 20.52%). Chronic hepatitis B group with steatosis had significantly higher CD44 concentration (181.42 ± 49.36) ng/ml than chronic hepatitis B group (142.52 ± 53.87) ng/ml and normal control group (99.47 ± 15.23) ng/ml. CD44/GAPDH ratio in the liver cancer group (1.306 ± 0.614) was significantly higher than paracancerous group (0.477 ± 0.291) and the difference between the two groups was statistically significant (t = 3.451, P = 0.004). The integrated optical density of CD44 in the NAFLD-related liver cancer and paracancerous group were 25.721 ± 5.881 and 14.155 ± 4.001 and the difference between the groups was statistically significant (t = 14.544, P < 0.001). The pathological features of high expression of CD44 in patients with hepatocellular carcinoma were significantly correlated with HBV infection, tumor size, single/multi-center, and lymph node metastasis, degree of differentiation, TNM grade, Child-Pugh score, portal vein tumor thrombus and extrahepatic metastasis. HCC patients with NAFLD had significantly higher serum CD44 (234.62 ± 69.40) ng/ml than patients without NAFLD (186.49 ± 58.89) ng/ml (t = -3.191, P = 0.002), but there was no statistically significant difference in the clinicopathological characteristics between the high/low CD44 groups of HCC patients with NAFLD. Conclusion: The results suggest that CD44 is abnormally activated and its mechanism may play an important role in the progression of NAFLD.

Disparate response to microoxia and nitrogen oxides of the Bradyrhizobium japonicum napEDABC, nirK and norCBQD denitrification genes.

Expression of the Bradyrhizobium japonicum napEDABC, nirK and norCBQD denitrification genes requires low oxygen (O2) tension and nitrate (NO3-), through a regulatory network comprised of two coordinated cascades, FixLJ-FixK2-NnrR and RegSR-NifA. To precisely understand how these signals are integrated in the FixLJ-FixK2-NnrR circuit, we analyzed ß-Galactosidase activities from napE-lacZ, nirK-lacZ and norC-lacZ fusions, and performed analyses of NapC and NorC levels as well as periplasmic nitrate reductase (Nap) activity, in B. japonicum wildtype and fixK2 and nnrR mutant backgrounds. While microoxic conditions (2% O2 at headspace) were sufficient to induce expression of napEDABC and nirK genes and this control depends on FixK2, norCBQD expression requires, in addition to microoxia, nitric oxide gas (NO) and both FixK2 and NnrR transcription factors. Purified FixK2 protein directly interacted and activated transcription in collaboration with B. japonicum RNA polymerase (RNAP) from the napEDABC and nirK promoters, but not from the norCBQD promoter. Further, recombinant NnrR protein bound exclusively to the norCBQD promoter in an O2-sensitive manner. Our work suggest a disparate regulation of B. japonicum denitrifying genes expression with regard to their dependency to microoxia, nitrogen oxides (NOx), and the regulatory proteins FixK2 and NnrR. In this control, expression of napEDABC and nirK genes requires microoxic conditions and directly depends on FixK2, while expression of norCBQD genes relies on NO, being NnrR the candidate which directly interacts with the norCBQD promoter.

Trimethylamine-The Extracorporeal Envoy.

One of the most widespread and efficient mechanisms that has evolved to enable communication between discrete and spatially separate living organisms is the use of specific chemical messengers. The organoleptic properties of certain molecules, even at concentrations that do not necessarily evoke a conscious response, have been exploited to transmit information across relatively large distances. The trimethylated derivative of ammonia is one such molecule that is ideally suited to this function and several species are known to respond to its presence. This review uniquely collects together and integrates widely dispersed data to show that trimethylamine also may serve a communicatory role in man, with its influence extending outside of the body.

Enhanced poly(γ-glutamic acid) production by H2 O2 -induced reactive oxygen species in the fermentation of Bacillus subtilis NX-2.

Effects of reactive oxygen species (ROS) on cell growth and poly(γ-glutamic acid) (γ-PGA) synthesis were studied by adding hydrogen peroxide to a medium of Bacillus subtilis NX-2. After optimizing the addition concentration and time of H2 O2 , a maximum concentration of 33.9 g/L γ-PGA was obtained by adding 100 µM H2 O2 to the medium after 24 H. This concentration was 20.6% higher than that of the control. The addition of diphenyleneiodonium chloride (ROS inhibitor) can interdict the effect of H2 O2 -induced ROS. Transcriptional levels of the cofactors and relevant genes were also determined under ROS stress to illustrate the possible metabolic mechanism contributing to the improve γ-PGA production. The transcriptional levels of genes belonging to the tricarboxylic acid cycle and electron transfer chain system were significantly increased by ROS, which decreased the NADH/NAD+ ratio and increased the ATP levels, thereby providing more reducing power and energy for γ-PGA biosynthesis. The enhanced γ-PGA synthetic genes also directly promoted the formation of γ-PGA. This study was the first to use the ROS control strategy for γ-PGA fermentation and provided valuable information on the possible mechanism by which ROS regulated γ-PGA biosynthesis in B. subtilis NX-2.

Traveling waves in response to a diffusing quorum sensing signal in spatially-extended bacterial colonies.

In the behavior known as quorum sensing (QS), bacteria release diffusible signal molecules known as autoinducers, which by accumulating in the environment induce population-wide changes in gene expression. Although QS has been extensively studied in well-mixed systems, the ability of diffusing QS signals to synchronize gene expression in spatially extended colonies is not well understood. Here we investigate the one-dimensional spatial propagation of QS-circuit activation in a simple, analytically tractable reaction-diffusion model for the LuxR-LuxI circuit, which regulates bioluminescence of the marine bacterium Aliivibrio fischeri. The quorum activation loop is modeled by a Hill function with a cooperativity exponent (m=2.2). The model is parameterized from laboratory data and captures the major empirical properties of the LuxR-LuxI system and its QS regulation of A. fischeri bioluminescence. Our simulations of the model show propagating waves of activation or deactivation of the QS circuit in a spatially extended colony. We further prove analytically that the model equations possess a traveling wave solution. This mathematical proof yields the rate of autoinducer degradation that is compatible with a traveling wave of gene expression as well as the critical degradation rate at which the nature of the wave switches from activation to deactivation. Our results can be used to predict the direction and activating or deactivating nature of a wave of gene expression in experimentally controlled bacterial populations subject to a diffusing autoinducer signal.

Role of PLC-PIP2 and cAMP-PKA signal pathways in radiation-induced immune-suppressing effect.

OBJECTIVE: The purpose of the present study was to observe the changes in CD4+CD25+Nrp1+Treg cells after irradiation with different doses and explore the possible molecular mechanisms involved. METHODS: ICR mice and mouse lymphoma cell line (EL-4 cells) was used. The expressions of CD4, CD25, Nrp1, calcineurin and PKC-α were detected by flow cytometry. The expressions of TGF-ß1, IL-10, PKA and cAMP were estimated with ELISA. RESULTS: At 12 h after irradiation, the expression of Nrp1 increased significantly in 4.0 Gy group, compared with sham-irradiation group (P<0.05) in the spleen and thymus, respectively, when ICR mice received whole-body irradiation (WBI). Meanwhile the synthesis of Interleukin 10 (IL-10) and transforming growth factor-ß1 (TGF-ß1) increased significantly after high dose irradiation (HDR) (> or = 1.0 Gy). In addition, the expression of cAMP and PKA protein increased, while PKC-α, calcineurin decreased at 12h in thymus cells after 4.0 Gy X-irradiation. While TGF-ß1 was clearly inhibited when the PLC-PIP2 signal pathway was stimulated or the cAMP-PKA signal pathway was blocked after 4.0 Gy X-irradiation, this did not limit the up-regulation of CD4+CD25+Nrp1+Treg cells after ionizing radiation. CONCLUSION: These results indicated that HDR might induce CD4+CD25+Nrp1+Treg cells production and stimulate TGF-ß1 secretion by regulating signal molecules in mice.

Friend or foe: Lactate in neurodegenerative diseases.

Lactate, a byproduct of glycolysis, was considered as a metabolic waste until identified by studies on the Warburg effect. Increasing evidence elucidates that lactate functions as energy fuel, signaling molecule, and donor for protein lactylation. Altered lactate utilization is a common metabolic feature of the onset and progression of neurodegenerative diseases, such as Alzheimer's disease, multiple sclerosis, amyotrophic lateral sclerosis, Parkinson's disease and Huntington's disease. This review offers an overview of lactate metabolism from the perspective of production, transportation and clearance, and the role of lactate in neurodegenerative progression, as well as a summary of protein lactylation and the signaling function of lactate in neurodegenerative diseases. Besides, this review delves into the dual roles of changed lactate metabolism during neurodegeneration and explores prospective therapeutic methods targeting lactate. We propose that elucidating the correlation between lactate and neurodegeneration is pivotal for exploring innovative therapeutic interventions for neurodegenerative diseases.

Two-way role of iron-carbon in biochemical reactions: Microelectrolysis and enhanced activity of aerobic granular sludge for efficient refractory wastewater treatment.

Industrial wastewater contained a large amount of refractory organics, and single treatment processes had limitations. This study investigated the mechanism of refractory organics removal using iron-carbon built-in coupled activated sludge (ICAS) and explored the role and function of iron-carbon (IC) within the ICAS system. The aerobic granular sludge (AGS) cultivated with IC exhibited a loose surface and a tight interior structure. Iron in the AGS concentrated near the outer layer to form a crust, which protected the inner microorganisms. IC promoted EPS secretion and regulated the abundance of positive and negative signaling molecules to maintain AGS stability. Experiments using quinoline as a model refractory organic showed that both physical adsorption by IC and biological adsorption by sludge rapidly fixed a large amount of pollutants, providing a buffer capacity for the system. The iron mineral crust on the AGS surface enhanced quinoline adsorption. Hydroxylation was the first step in quinoline degradation, with IC upregulating the genes iorA/B, qorB, and wrbA involved in this process, and the relative abundances of quinoline-degrading bacteria. Both pyridine ring opening and benzene ring cleavage occurred in the single IC system, and the microelectrolysis process produced •OH and [H], which made degradation pathway for quinoline through IC more complex than microbial degradation. Although the IC-mediated pathway accounted for only a small part of overall quinoline removal in the ICAS system, the ICAS system not only preserved the microelectrolysis process but also enhanced microbial metabolic activity. This work provided insights into the synergistic removal of pollutants and maintenance of AGS stability by the ICAS process, ensuring efficient treatment of refractory organic wastewater.

Efficient and sustained inhibition of ammonia nitrogen release from sediment in water by microbial self-aggregation zeolite layer.

Despite global efforts to manage water eutrophication, the continual release of ammonia nitrogen from sediments maintains the eutrophic state of water bodies, presenting serious challenges to the management. In order to find an efficient method for sediment remediation, the experiment of using signal molecules to enhance the adhesion of microorganisms on zeolite was carried out. Five different zeolitic ammonium adsorptions were examined using two different signal molecules, N-(3-oxohexanoyl)-L-homoserine lactone (OHHL) and N-(ß-ketocaproyl)-DL-homoserine lactone (C6), to enhance microbial attachment on two types of zeolites. The results showed that the modified microbial attached Z1 zeolite reinforced with signal molecule C6 had the best effect. The effect was better in the case of high ammonium adsorption, and the TN removal could reach 7.99 mg·L-1 with an inhibition rate of 90.08%. The ammonia nitrogen removal reached 4.75 mg·L-1 with an inhibition rate of 87.64%, and the ammonia nitrogen and total nitrogen of the overlying water reached the surface III water quality standard. In addition, the addition of the signal molecule increased the zeta potential on the surface of the bacterial colloid. In addition, the amount of protein I in the dissolved organic matter (DOM) fraction increased, improving microbial adhesion ability and facilitating their attachment to the zeolite surface. The signal molecule C6 could increase the zeta potential of microbial surface and promote the production of protein I, thus strengthening the attachment of zeolite biofilm and improving the water quality.

Nitric oxide and brassinosteroids mediated fungal endophyte-induced volatile oil production through protein phosphorylation pathways in Atractylodes lancea plantlets.

Fungal endophytes have been isolated from almost every plant, infecting their hosts without causing visible disease symptoms, and yet have still proved to be involved in plant secondary metabolites accumulation. To decipher the possible physiological mechanisms of the endophytic fungus-host interaction, the role of protein phosphorylation and the relationship between endophytic fungus-induced kinase activity and nitric oxide (NO) and brassinolide (BL) in endophyte-enhanced volatile oil accumulation in Atractylodes lancea plantlets were investigated using pharmacological and biochemical approaches. Inoculation with the endophytic fungus Gilmaniella sp. AL12 enhanced the activities of total protein phosphorylation, Ca²âº-dependent protein kinase, and volatile oil accumulation in A. lancea plantlets. The upregulation of protein kinase activity could be blocked by the BL inhibitor brassinazole. Furthermore, pretreatments with the NO-specific scavenger cPTIO significantly reduced the increased activities of protein kinases in A. lancea plantlets inoculated with endophytic fungus. Pretreatments with different protein kinase inhibitors also reduced fungus-induced NO production and volatile oil accumulation, but had barely no effect on the BL level. These data suggest that protein phosphorylation is required for endophyte-induced volatile oil production in A. lancea plantlets, and that crosstalk between protein phosphorylation and the NO pathway may occur and act as a downstream signaling event of the BL pathway.

Pathogen virulence of Phytophthora infestans: from gene to functional genomics.

The oomycete, Phytophthora infestans, is one of the most important plant pathogens worldwide. Much of the pathogenic success of P. infestans, the potato late blight agent, relies on its ability to generate large amounts of sporangia from mycelia, which release zoospores that encyst and form infection structures. Until recently, little was known about the molecular basis of oomycete pathogenicity by the avirulence molecules that are perceived by host defenses. To understand the molecular mechanisms interplay in the pathogen and host interactions, knowledge of the genome structure was most important, which is available now after genome sequencing. The mechanism of biotrophic interaction between potato and P. infestans could be determined by understanding the effector biology of the pathogen, which is until now poorly understood. The recent availability of oomycete genome will help in understanding of the signal transduction pathways followed by apoplastic and cytoplasmic effectors for translocation into host cell. Finally based on genomics, novel strategies could be developed for effective management of the crop losses due to the late blight disease.