Plants have the ability to acquire an enhanced level of resistance to pathogen attack after being exposed to specific biotic stimuli. In Arabidopsis, nonpathogenic, root-colonizing Pseudomonas fluorescens bacteria trigger an induced systemic resistance (ISR) response against infection by the bacterial leaf pathogen P. syringae pv tomato. In contrast to classic, pathogen-induced systemic acquired resistance (SAR), this rhizobacteria-mediated ISR response is independent of salicylic acid accumulation and pathogenesis-related gene activation. Using the jasmonate response mutant jar1 , the ethylene response mutant etr1 , and the SAR regulatory mutant npr1 , we demonstrate that signal transduction leading to P. fluorescens WCS417r-mediated ISR requires responsiveness to jasmonate and ethylene and is dependent on NPR1. Similar to P. fluorescens WCS417r, methyl jasmonate and the ethylene precursor 1-aminocyclopropane-1-carboxylate were effective in inducing resistance against P. s. tomato in salicylic acid-nonaccumulating NahG plants. Moreover, methyl jasmonate-induced protection was blocked in jar1 , etr1 , and npr1 plants, whereas 1-aminocyclopropane-1-carboxylate-induced protection was affected in etr1 and npr1 plants but not in jar1 plants. Hence, we postulate that rhizobacteria-mediated ISR follows a novel signaling pathway in which components from the jasmonate and ethylene response are engaged successively to trigger a defense reaction that, like SAR, is regulated by NPR1. We provide evidence that the processes downstream of NPR1 in the ISR pathway are divergent from those in the SAR pathway, indicating that NPR1 differentially regulates defense responses, depending on the signals that are elicited during induction of resistance. INTRODUCTIONPlants of which the roots have been colonized by selected strains of nonpathogenic fluorescent Pseudomonas spp develop an enhanced level of protection against pathogen attack (reviewed in van Loon et al., 1998). Strain WCS417r of P. fluorescens is a biological control strain that has been shown to trigger an induced systemic resistance (ISR) response in several plant species, including carnation (van Peer et al., 1991), radish (Leeman et al., 1995), tomato (Duijff et al., 1996), and Arabidopsis (Pieterse et al., 1996). In Arabidopsis, P. fluorescens WCS417r-mediated ISR has been demonstrated against the bacterial leaf pathogen P. syringae pv tomato , the fungal root pathogen Fusarium oxysporum f sp raphani (Pieterse et al., 1996;van Wees et al., 1997), and the fungal leaf pathogen Peronospora parasitica (J. Ton and C.M.J. Pieterse, unpublished data), indicating that this type of biologically induced resistance is effective against different types of pathogens.ISR-inducing rhizobacteria show host specificity in regard to eliciting resistance (Leeman et al., 1995;van Wees et al., 1997), which indicates that specific recognition between protective bacteria and the plant is a prerequisite for the activation of the signaling cascade leading to ISR. The downstream signaling event...

Plants have the ability to acquire an enhanced level of resistance to pathogen attack after being exposed to specific biotic stimuli. In Arabidopsis, nonpathogenic, root-colonizing Pseudomonas fluorescens bacteria trigger an induced systemic resistance (ISR) response against infection by the bacterial leaf pathogen P. syringae pv tomato. In contrast to classic, pathogen-induced systemic acquired resistance (SAR), this rhizobacteria-mediated ISR response is independent of salicylic acid accumulation and pathogenesis-related gene activation. Using the jasmonate response mutant jar1 , the ethylene response mutant etr1 , and the SAR regulatory mutant npr1 , we demonstrate that signal transduction leading to P. fluorescens WCS417r-mediated ISR requires responsiveness to jasmonate and ethylene and is dependent on NPR1. Similar to P. fluorescens WCS417r, methyl jasmonate and the ethylene precursor 1-aminocyclopropane-1-carboxylate were effective in inducing resistance against P. s. tomato in salicylic acid-nonaccumulating NahG plants. Moreover, methyl jasmonate-induced protection was blocked in jar1 , etr1 , and npr1 plants, whereas 1-aminocyclopropane-1-carboxylate-induced protection was affected in etr1 and npr1 plants but not in jar1 plants. Hence, we postulate that rhizobacteria-mediated ISR follows a novel signaling pathway in which components from the jasmonate and ethylene response are engaged successively to trigger a defense reaction that, like SAR, is regulated by NPR1. We provide evidence that the processes downstream of NPR1 in the ISR pathway are divergent from those in the SAR pathway, indicating that NPR1 differentially regulates defense responses, depending on the signals that are elicited during induction of resistance. INTRODUCTIONPlants of which the roots have been colonized by selected strains of nonpathogenic fluorescent Pseudomonas spp develop an enhanced level of protection against pathogen attack (reviewed in van Loon et al., 1998). Strain WCS417r of P. fluorescens is a biological control strain that has been shown to trigger an induced systemic resistance (ISR) response in several plant species, including carnation (van Peer et al., 1991), radish (Leeman et al., 1995), tomato (Duijff et al., 1996), and Arabidopsis (Pieterse et al., 1996). In Arabidopsis, P. fluorescens WCS417r-mediated ISR has been demonstrated against the bacterial leaf pathogen P. syringae pv tomato , the fungal root pathogen Fusarium oxysporum f sp raphani (Pieterse et al., 1996;van Wees et al., 1997), and the fungal leaf pathogen Peronospora parasitica (J. Ton and C.M.J. Pieterse, unpublished data), indicating that this type of biologically induced resistance is effective against different types of pathogens.ISR-inducing rhizobacteria show host specificity in regard to eliciting resistance (Leeman et al., 1995;van Wees et al., 1997), which indicates that specific recognition between protective bacteria and the plant is a prerequisite for the activation of the signaling cascade leading to ISR. The downstream signaling event...

In developing seeds, the permeability of the plasma membrane of seed coat parenchyma cells is crucial for the supply of nutrients to the embryo. Here, we report characteristics of the transport of the organic cation choline and the basic amino acid l-histidine (His; cation at pH 5, electroneutral at pH 7) into isolated seed coats of pea (Pisum sativum). Supplied at sub-micromolar concentrations, choline ϩ accumulated in the seed coat tissue 5.1 Ϯ 0.8-fold, His ϩ 2.4 Ϯ 0.3-fold, and His 0 1.3 Ϯ 0.2-fold. Taking into consideration that at pH 5 His influxes as a cation but effluxes as a neutral molecule, these accumulations are in reasonable agreement with (electro) diffusional uptake at the prevailing membrane potential of Ϫ55 Ϯ 3 mV. At a concentration of 100 mm, choline ϩ and His ϩ , but not His 0 , depolarized the membrane of the parenchyma cells and neither of the substrates was accumulated. At this concentration, the relative influx (the ratio of influx and external concentration, a measure for membrane permeability) of choline and His was approximately 10 mol g Ϫ1 fresh weight min Ϫ1 m Ϫ1 , similar to that found for neutral amino acids, sucrose, glucose, and mannitol. At lower concentrations, the relative influx of choline ϩ and His ϩ increased because of increasingly more negative membrane potentials, giving rise to apparent saturation kinetics. It is suggested that transport of organic cations can proceed by a general, poorly selective pore in the plasma membrane of seed coat parenchyma cells. This pore is thought to be responsible for the unloading of a range of solutes that serve as nutrients for the embryo.During the development of the pea (Pisum sativum) seed, the embryo receives its nutrients from the surrounding maternal seed coat. These nutrients arrive in the seed coat mainly through the phloem of three vascular bundles and are then distributed by cell-tocell transport over the seed coat parenchyma (Grusak and Minchin, 1988; Patrick et al., 1995; Tegeder et al., 1999). Because embryo and seed coat are symplasmically isolated from each other, the nutrients have to be unloaded into the apoplast. This implies the transport of the nutrients across the plasma membrane of the seed coat parenchyma cells. The mechanism by which the various nutrients (Suc, amino acids, and inorganic ions) are released from the parenchyma cells is still incompletely understood.The release of sugars and amino acids from the pea seed coat is biphasic, consisting of a fast and a slow component (De Jong and Wolswinkel, 1995). It is most likely that the fast component represents the efflux across the plasma membrane of seed coat parenchyma cells. The rate constant for the fast component in the release of Suc and amino acids amounts to approximately 1.4 h Ϫ1 , corresponding to a half-life time of approximately 0.5 h. For a spherical cell, the permeability coefficient (P) is related to the half-life time (t 1/2 ) and the cell radius (r) by P ϭ ln2 ϫ r/3t 1/2