The plant-growth-promoting rhizobacterium Paenibacillus polymyxa induces changes in Arabidopsis thaliana gene expression: a possible connection between biotic and abiotic stress responses.

This paper addresses changes in plant gene expression induced by inoculation with plant-growth-promoting rhizobacteria (PGPR). A gnotobiotic system was established with Arabidopsis thaliana as model plant, and isolates of Paenibacillus polymyxa as PGPR. Subsequent challenge by either the pathogen Erwinia carotovora (biotic stress) or induction of drought (abiotic stress) indicated that inoculated plants were more resistant than control plants. With RNA differential display on parallel RNA preparations from P. polymyxa-treated or untreated plants, changes in gene expression were investigated. From a small number of candidate sequences obtained by this approach, one mRNA segment showed a strong inoculation-dependent increase in abundance. The corresponding gene was identified as ERD15, previously identified to be drought stress responsive. Quantification of mRNA levels of several stress-responsive genes indicated that P. polymyxa induced mild biotic stress. This suggests that genes and/or gene classes associated with plant defenses against abiotic and biotic stress may be co-regulated. Implications of the effects of PGPR on the induction of plant defense pathways are discussed.     

Signalling in Rhizobacteria-Induced Systemic Resistance in Arabidopsis thaliana

Abstract: To protect themselves from disease, plants have evolved sophisticated defence mechanisms in which the signal molecules salicylic acid, jasmonic acid and ethylene often play crucial roles. Elucidation of signalling pathways controlling disease resistance is a major objective in research on plant-pathogen interactions. The capacity of a plant to develop a broad spectrum, systemic acquired resistance (SAR) after primary infection with a necrotizing pathogen is well-known and its signal transduction pathway extensively studied. Plants of which the roots have been colonized by specific strains of non-pathogenic fluorescent Pseudomonas spp. develop a phenotypically similar form of protection that is called rhizobacteria-mediated induced systemic resistance (ISR). In contrast to pathogen-induced SAR, which is regulated by salicylic acid, rhizobacteria-mediated ISR is controlled by a signalling pathway in which jasmonic acid and ethylene play key roles. In the past eight years, the model plant species Arabidopsis thaliana was explored to study the molecular basis of rhizobacteria-mediated ISR. Here we review current knowledge of the signal transduction steps involved in the ISR pathway that leads from recognition of the rhizobacteria in the roots to systemic expression of broad-spectrum disease resistance in aboveground foliar tissues.     

Induced systemic resistance (ISR) in plants: mechanism of action

Plants possess a range of active defense apparatuses that can be actively expressed in response to biotic stresses (pathogens and parasites) of various scales (ranging from microscopic viruses to phytophagous insect). The timing of this defense response is critical and reflects on the difference between coping and succumbing to such biotic challenge of necrotizing pathogens/parasites. If defense mechanisms are triggered by a stimulus prior to infection by a plant pathogen, disease can be reduced. Induced resistance is a state of enhanced defensive capacity developed by a plant when appropriately stimulated. Systemic acquired resistance (SAR) and induced systemic resistance (ISR) are two forms of induced resistance wherein plant defenses are preconditioned by prior infection or treatment that results in resistance against subsequent challenge by a pathogen or parasite. Selected strains of plant growth-promoting rhizobacteria (PGPR) suppress diseases by antagonism between the bacteria and soil-borne pathogens as well as by inducing a systemic resistance in plant against both root and foliar pathogens. Rhizobacteria mediated ISR resembles that of pathogen induced SAR in that both types of induced resistance render uninfected plant parts more resistant towards a broad spectrum of plant pathogens. Several rhizobacteria trigger the salicylic acid (SA)-dependent SAR pathway by producing SA at the root surface whereas other rhizobacteria trigger different signaling pathway independent of SA. The existence of SA-independent ISR pathway has been studied in Arabidopsis thaliana, which is dependent on jasmonic acid (JA) and ethylene signaling. Specific Pseudomonas strains induce systemic resistance in viz., carnation, cucumber, radish, tobacco, and Arabidopsis, as evidenced by an enhanced defensive capacity upon challenge inoculation. Combination of ISR and SAR can increase protection against pathogens that are resisted through both pathways besides extended protection to a broader spectrum of pathogens than ISR/SAR alone. Beside Pseudomonas strains, ISR is conducted by Bacillus spp. wherein published results show that several specific strains of species B. amyloliquifaciens, B. subtilis, B. pasteurii, B. cereus, B. pumilus, B. mycoides, and B.sphaericus elicit significant reduction in the incidence or severity of various diseases on a diversity of hosts.     

Comparative analysis of defence responses induced by the endophytic plant growth-promoting rhizobacterium Burkholderia phytofirmans strain PsJN and the non-host bacterium Pseudomonas syringae pv. pisi in grapevine cell suspensions

Plant growth-promoting rhizobacteria (PGPR) are beneficial microorganisms that colonize the rhizosphere of many plant species and confer beneficial effects, such as an increase in plant growth. PGPR are also well known as inducers of systemic resistance to pathogens in plants. However, the molecular mechanisms involved locally after direct perception of these bacteria by plant cells still remain largely unknown. Burkholderia phytofirmans strain PsJN is an endophytic PGPR that colonizes grapevine and protects the plant against the grey mould disease caused by Botrytis cinerea. This report focuses on local defence events induced by B. phytofirmans PsJN after perception by the grapevine cells. It is demonstrated that, after addition to cell suspension cultures, the bacteria were tightly attaching to plant cells in a way similar to the grapevine non-host bacteria Pseudomonas syringae pv. pisi. B. phytofirmans PsJN perception led to a transient and monophasic extracellular alkalinization but no accumulation of reactive oxygen species or cell death were detected. By contrast, challenge with P. syringae pv. pisi induced a sustained and biphasic extracellular alkalinization, a two phases oxidative burst, and a HR-like response. Perception of the PGPR also led to the production of salicylic acid (SA) and the expression of a battery of defence genes that was, however, weaker in intensity compared with defence gene expression triggered by the non-host bacteria. Some defence genes up-regulated after B. phytofirmans PsJN challenge are specifically induced by exogenous treatment with SA or jasmonic acid, suggesting that both signalling pathways are activated by the PGPR in grapevine.     

Influence of Methyl Bromide Fumigation on Microbe-induced Resistance in Cucumber

Field experiments were conducted to evaluate growth promotion and induced systemic disease resistance (ISR) in cucumber mediated by plant growth-promoting rhizobacteria (PGPR) with and without methyl bromide soil fumigation. In both fumigated and nonfumigated plots, numbers of cucumber beetles, Acalymma vittata (F.), and the incidence of bacterial wilt disease, caused by the beetle-transmitted pathogen Erwinia tracheiphila , were significantly lower with PGPR treatment compared with the nonbacterized control. However, in PGPR-treated plots, the incidence of bacterial wilt was more than 2-fold lower in the nonfumigated treatments compared with fumigated treatments, indicating that the level of PGPR-mediated ISR was greater without methyl bromide fumigation than with methyl bromide. Cucumber plant growth at 21 days after planting was greater in fumigated plots than in nonfumigated plots; however, plant height values in the nonfumigated, PGPR treatments and the fumigated, PGPR treatments were equivalent. This suggests that PGPR treatment compensated for delayed plant growth that often occurs in nonfumigated soil. These results indicate that, in cucumber production systems, withdrawal of methyl bromide will not negatively impact PGPRmediated ISR, and also that PGPR may have potential as an alternative to methyl bromide fumigation.     

The elicitation of a systemic resistance by Pseudomonas putida BTP1 in tomato involves the stimulation of two lipoxygenase isoforms

Background  

Some non-pathogenic rhizobacteria called Plant Growth Promoting Rhizobacteria (PGPR) possess the capacity to induce in plant defense mechanisms effective against pathogens. Precedent studies showed the ability of Pseudomonas putida BTP1 to induce PGPR-mediated resistance, termed ISR (Induced Systemic Resistance), in different plant species. Despite extensive works, molecular defense mechanisms involved in ISR are less well understood that in the case of pathogen induced systemic acquired resistance.     

Systemic resistance and lipoxygenase-related defence response induced in tomato by <Emphasis Type="Italic">Pseudomonas putida</Emphasis>strain BTP1

Background  

Previous studies showed the ability of Pseudomonas putida strain BTP1 to promote induced systemic resistance (ISR) in different host plants. Since ISR is long-lasting and not conducive for development of resistance of the targeted pathogen, this phenomenon can take part of disease control strategies. However, in spite of the numerous examples of ISR induced by PGPR in plants, only a few biochemical studies have associated the protective effect with specific host metabolic changes.     

The Arabidopsis ISR1 Locus is Required for Rhizobacteria-Mediated Induced Systemic Resistance Against Different Pathogens

Abstract: In Arabidopsis thaliana, non-pathogenic, root-colonizing Pseudomonas fluorescens WCS417r bacteria trigger an induced systemic resistance (ISR) that is phenotypically similar to pathogen-induced systemic acquired resistance (SAR). In contrast to SAR, WCS417r-mediated ISR is controlled by a salicylic acid (SA)-independent signalling pathway that requires an intact response to the plant hormones jasmonic acid (JA) and ethylene (ET). Arabidopsis accessions RLD1 and Ws-0 fail to express ISR against Pseudomonas syringae pv. tomato and show enhanced disease susceptibility to this pathogen. Genetic analysis of progeny from crosses between WCS417r-responsive and non-responsive accessions demonstrated that ISR inducibility and basal resistance against P. syringae pv. tomato are controlled by a single dominant locus (ISR1) on chromosome III (Ton et al., 1999^[294]). Here, we investigated the role of the ISR1 locus in ISR, SAR and basal resistance against three additional pathogens: Xanthomonas campestris pv. armoraciae, Peronospora parasitica and turnip crinkle virus (TCV), using accessions Col-0 (ISR1), RLD1 (isr1) and Ws-0 (isr1) as host plants.     

Differential inducible defense mechanisms against bacterial speck pathogen in Arabidopsis thaliana by plant-growth-promoting-fungus Penicillium sp. GP16-2 and its cell free filtrate

Although a wealth of information is available regarding resistance induced by plant growth-promoting rhizobacteria (PGPR), not much is known about plant growth-promoting fungi (PGPF). Hence, the goal of the present research was to provide more information on this matter. In Arabidopsis thaliana L., root colonizing PGPF Penicillium sp. GP16-2 or its cell free filtrate (CF) elicited an induced systemic resistance (ISR) against infection by Pseudomonas syringae pv. tomato DC3000 (Pst), leading to a restriction of pathogen growth and disease development. We demonstrate that signal transduction leading to GP16-2-mediated ISR requires responsiveness to JA and ET in a NPR1-dependent manner, while CF-mediated ISR shows dispensability of SA, JA, ET and NPR1-dependent signaling (at least individually). In addition, root colonization by GP16-2 is not associated with a direct effect on expression of known defense-related genes, but potentiates the activation of JA/ET-inducible ChitB, which only becomes apparent after infection by Pst. However, CF-mediated ISR was partly associated with the direct activation of marker genes responsive to both SA and JA/ET signaling pathways and partly associated with priming, leading to activation of JA-/ET-inducible ChitB and Hel genes. These suggest that CF may contain one or more elicitors that induce resistance by way where at least SA, JA and ET may play a role in defense signaling in Arabidopsis. Therefore, defense gene changes and underlying signaling pathways induced by Penicillium sp. GP16-2 root colonization and its CF application are not the same and only partially overlap.     

HISTONE DEACETYLASE19 is involved in jasmonic acid and ethylene signaling of pathogen response in Arabidopsis

Histone acetylation is modulated through the action of histone acetyltransferases and deacetylases, which play key roles in the regulation of eukaryotic gene expression. Previously, we have identified a yeast histone deacetylase REDUCED POTASSIUM DEPENDENCY3 (RPD3) homolog, HISTONE DEACETYLASE19 (HDA19) (AtRPD3A), in Arabidopsis thaliana. Here, we report further study of the expression and function of HDA19. Analysis of Arabidopsis plants containing the HDA19:beta-glucuronidase fusion gene revealed that HDA19 was expressed throughout the life of the plant and in most plant organs examined. In addition, the expression of HDA19 was induced by wounding, the pathogen Alternaria brassicicola, and the plant hormones jasmonic acid and ethylene. Using green fluorescent protein fusion, we demonstrated that HDA19 accumulated in the nuclei of Arabidopsis cells. Overexpression of HDA19 in 35S:HDA19 plants decreased histone acetylation levels, whereas downregulation of HDA19 in HDA19-RNA interference (RNAi) plants increased histone acetylation levels. In comparison with wild-type plants, 35S:HDA19 transgenic plants had increased expression of ETHYLENE RESPONSE FACTOR1 and were more resistant to the pathogen A. brassicicola. The expression of jasmonic acid and ethylene regulated PATHOGENESIS-RELATED genes, Basic Chitinase and beta-1,3-Glucanase, was upregulated in 35S:HDA19 plants but downregulated in HDA19-RNAi plants. Our studies provide evidence that HDA19 may regulate gene expression involved in jasmonic acid and ethylene signaling of pathogen response in Arabidopsis.     

One shot-two pathogens blocked: Exposure of Arabidopsis to hexadecane,a long chain volatile organic compound,confers induced resistance against both Pectobacterium carotovorum and Pseudomonas syringae

Bacteria and plant derived volatile organic compounds have been reported as the chemical triggers that elicit induced resistance in plants. Previously, volatile organic compounds (VOCs), including acetoin and 2,3-butanediol, were found to be emitted from plant growth-promoting rhizobacteria (PGPR) Bacillus subtilis GB03, which had been shown to elicit ISR and plant growth promotion. More recently, we reported data that stronger induced resistance could be elicited against Pseudomonas syringae pv maculicola ES4326 in plants exposed to C13 VOC from another PGPR Paenibacillus polymyxa E681 compared with that of strain GB03. Here, we assessed whether another long hydrocarbon C16 hexadecane (HD) conferred protection to Arabidopsis from infection of a biotrophic pathogen, P. syringae pv maculicola and a necrotrophic pathogen, Pectobacterium carotovorum subsp carotovorum. Collectively, long-chain VOCs can be linked to a plant resistance activator for protecting plants against both biotrophic and necrotrophic pathogens at the same time.