Christine Rustérucci

Université de Picardie Jules Verne, Amiens, Picardie, France

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Publications (22)107.35 Total impact

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    ABSTRACT: Understanding the changes affecting the plant cell wall is a key element in addressing its functional role in plant growth and in the response to stress. Pectins, which are the main constituents of the primary cell wall in dicot species, play a central role in the control of cellular adhesion and thereby of the rheological properties of the wall. This is likely to be a major determinant of plant growth. How the discrete changes in pectin structure are mediated is thus a key issue in our understanding of plant development and plant responses to changes in the environment. In particular, understanding the remodelling of homogalacturonan (HG), the most abundant pectic polymer, by specific enzymes is a current challenge in addressing its fundamental role. HG, a polymer that can be methylesterified or acetylated, can be modified by HGMEs (HG-modifying enzymes) which all belong to large multigenic families in all species sequenced to date. In particular, both the degrees of substitution (methylesterification and/or acetylation) and polymerization can be controlled by specific enzymes such as pectin methylesterases (PMEs), pectin acetylesterases (PAEs), polygalacturonases (PGs), or pectate lyases-like (PLLs). Major advances in the biochemical and functional characterization of these enzymes have been made over the last 10 years. This review aims to provide a comprehensive, up to date summary of the recent data concerning the structure, regulation, and function of these fascinating enzymes in plant development and in response to biotic stresses.
    Journal of Experimental Botany 07/2014; · 5.24 Impact Factor
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    ABSTRACT: • Here, we focused on the biochemical characterization of the Arabidopsis thaliana pectin methylesterase 3 gene (AtPME3; At3g14310) and its role in plant development. • A combination of biochemical, gene expression, Fourier transform-infrared (FT-IR) microspectroscopy and reverse genetics approaches were used. • We showed that AtPME3 is ubiquitously expressed in A. thaliana, particularly in vascular tissues. In cell wall-enriched fractions, only the mature part of the protein was identified, suggesting that it is processed before targeting the cell wall. In all the organs tested, PME activity was reduced in the atpme3-1 mutant compared with the wild type. This was related to the disappearance of an activity band corresponding to a pI of 9.6 revealed by a zymogram. Analysis of the cell wall composition showed that the degree of methylesterification (DM) of galacturonic acids was affected in the atpme3-1 mutant. A change in the number of adventitious roots was found in the mutant, which correlated with the expression of the gene in adventitious root primordia. • Our results enable the characterization of AtPME3 as a major basic PME isoform in A. thaliana and highlight its role in adventitious rooting.
    New Phytologist 06/2011; 192(1):114-26. · 6.74 Impact Factor
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    ABSTRACT: Fruit development is a highly complex process, which involves major changes in plant metabolism leading to cell growth and differentiation. Changes in cell wall composition and structure play a major role in modulating cell growth. We investigated the changes in cell wall composition and the activities of associated enzymes during the dry fruit development of the model plant Arabidopsis thaliana. Silique development is characterized by several specific phases leading to fruit dehiscence and seed dispersal. We showed that early phases of silique growth were characterized by specific changes in non-cellulosic sugar content (rhamnose, arabinose, xylose, galactose and galacturonic acid). Xyloglucan oligosaccharide mass profiling further showed a strong increase in O-acetylated xyloglucans over the course of silique development, which could suggest a decreased capacity of xyloglucans to be associated with each other or to cellulose. The degree of methylesterification, mediated by the activity of pectin methylesterases (PMEs), decreased over the course of silique growth and dehiscence. The major changes in cell wall composition revealed by our analysis suggest that it could be major determinants in modulating cell wall rheology leading to growth or growth arrest.
    Phytochemistry 11/2010; 72(1):59-67. · 3.05 Impact Factor
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    ABSTRACT: To access phloem sap, aphids have developed a furtive strategy, their stylets progressing towards sieve tubes mainly through the apoplasmic compartment. Aphid feeding requires that they overcome a number of plant responses, ranging from sieve tube occlusion and activation of phytohormone-signalling pathways to expression of anti-insect molecules. In addition to bypassing plant defences, aphids have been shown to affect plant primary metabolism, which could be a strategy to improve phloem sap composition in nutrients required for their growth. During compatible interactions, leading to successful feeding and reproduction, aphids cause alterations in their host plant, including morphological changes, modified resource allocation and various local as well as systemic symptoms. Repeated salivary secretions injected from the first probe in the epidermal tissue up to ingestion of sieve-tube sap may play a crucial role in the compatibility between the aphid and the plant.
    Comptes rendus biologies 01/2010; 333(6-7):516-23. · 1.71 Impact Factor
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    ABSTRACT: Reverse transcription-polymerase chain reaction (RT-PCR) approaches have been used in a large proportion of transcriptome analyses published to date. The accuracy of the results obtained by this method strongly depends on accurate transcript normalization using stably expressed genes, known as references. Statistical algorithms have been developed recently to help validate reference genes, and most studies of gene expression in mammals, yeast and bacteria now include such validation. Surprisingly, this important approach is under-utilized in plant studies, where putative housekeeping genes tend to be used as references without any appropriate validation. Using quantitative RT-PCR, the expression stability of several genes commonly used as references was tested in various tissues of Arabidopsis thaliana and hybrid aspen (Populus tremula x Populus tremuloides). It was found that the expression of most of these genes was unstable, indicating that their use as references is inappropriate. The major impact of the use of such inappropriate references on the results obtained by RT-PCR is demonstrated in this study. Using aspen as a model, evidence is presented indicating that no gene can act as a universal reference, implying the need for a systematic validation of reference genes. For the first time, the extent to which the lack of a systematic validation of reference genes is a stumbling block to the reliability of results obtained by RT-PCR in plants is clearly shown.
    Plant Biotechnology Journal 05/2008; 6(6):609-18. · 6.28 Impact Factor
  • Jérôme Pelloux, Christine Rustérucci, Ewa J Mellerowicz
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    ABSTRACT: In bacteria, fungi and plants, pectin methylesterases are ubiquitous enzymes that modify the degree of methylesterification of pectins, which are major components of plant cell walls. Such changes in pectin structure are associated with changes in cellular adhesion, plasticity, pH and ionic contents of the cell wall and influence plant development and stress responses. In plants, pectin methylesterases belong to large multigene families, are regulated in a highly specific manner, and are involved in vegetative and reproductive processes, including wood and pollen formation, in addition to plant-pathogen interactions. Although, overall, protein structures are highly conserved between isoforms, recent data indicate that structural variations might be associated with the targeting and functions of specific pectin methylesterases.
    Trends in Plant Science 07/2007; 12(6):267-77. · 11.81 Impact Factor
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    ABSTRACT: Nitric oxide and S-nitrosothiols (SNOs) are widespread signaling molecules that regulate immunity in animals and plants. Levels of SNOs in vivo are controlled by nitric oxide synthesis (which in plants is achieved by different routes) and by S-nitrosoglutathione turnover, which is mainly performed by the S-nitrosoglutathione reductase (GSNOR). GSNOR is encoded by a single-copy gene in Arabidopsis (Arabidopsis thaliana; Martínez et al., 1996; Sakamoto et al., 2002). We report here that transgenic plants with decreased amounts of GSNOR (using antisense strategy) show enhanced basal resistance against Peronospora parasitica Noco2 (oomycete), which correlates with higher levels of intracellular SNOs and constitutive activation of the pathogenesis-related gene, PR-1. Moreover, systemic acquired resistance is impaired in plants overexpressing GSNOR and enhanced in the antisense plants, and this correlates with changes in the SNO content both in local and systemic leaves. We also show that GSNOR is localized in the phloem and, thus, could regulate systemic acquired resistance signal transport through the vascular system. Our data corroborate the data from other authors that GSNOR controls SNO in vivo levels, and shows that SNO content positively influences plant basal resistance and resistance-gene-mediated resistance as well. These data highlight GSNOR as an important and widely utilized component of resistance protein signaling networks conserved in animals and plants.
    Plant physiology 04/2007; 143(3):1282-92. · 6.56 Impact Factor
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    ABSTRACT: We initially compared lipid peroxidation profiles in tobacco (Nicotiana tabacum) leaves during different cell death events. An upstream oxylipin assay was used to discriminate reactive oxygen species (ROS)-mediated lipid peroxidation from 9- and 13-lipoxygenase (LOX)-dependent lipid peroxidation. Free radical-mediated membrane peroxidation was measured during H(2)O(2)-dependent cell death in leaves of catalase-deficient plants. Taking advantage of these transgenic plants, we demonstrate that, under light conditions, H(2)O(2) plays an essential role in the execution of cell death triggered by an elicitor, cryptogein, which provokes a similar ROS-mediated lipid peroxidation. Under dark conditions, however, cell death induction by cryptogein was independent of H(2)O(2) and accompanied by products of the 9-LOX pathway. In the hypersensitive response induced by the avirulent pathogen Pseudomonas syringae pv syringae, both 9-LOX and oxidative processes operated concurrently, with ROS-mediated lipid peroxidation prevailing in the light. Our results demonstrate, therefore, the tight interplay between H(2)O(2) and lipid hydroperoxides and underscore the importance of light during the hypersensitive response.
    Plant physiology 08/2005; 138(3):1516-26. · 6.56 Impact Factor
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    ABSTRACT: As plants mature it has been observed that some become more resistant to normally virulent pathogens. The ability to manifest the Age-Related Resistance (ARR) response in Arabidopsis to Pseudomonas syringae pathovars tomato (Pst) coincided with the transition to flowering in plants both delayed and accelerated in the transition to flowering. ARR was also associated with a change in PR-1 gene expression, such that young plants expressed PR-1 abundantly at 3 days post inoculation (dpi) while mature plants expressed much less. The Arabidopsis ARR response requires SA accumulation via isochorismate synthase (ICS1) [24]. ICS1 was expressed one dpi with virulent and avirulent Pst in both young and mature plants. The ARR response was also effective versus avirulent Pst providing an additional 4-fold limitation in bacterial growth. Arabidopsis ARR was found to be ineffective against two necrotrophs, Erwinia carotovora subspecies carotovora (bacterium) and Botrytis cinerea (fungus) and one obligate biotroph, Erysiphe cichoracearum (fungus). However, mature wild type, SA-deficient sid2 and NahG plants supported little growth of the obligate biotrophic oomycete, Peronospora parasitica. Therefore ARR to P. parasitica appears to be SA-independent, however the level of ARR resistance was somewhat reduced in these mutants in some experiments. Thus, there may be numerous defence pathways that contribute to adult plant resistance in Arabidopsis.
    Physiological and Molecular Plant Pathology. 01/2005;
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    ABSTRACT: The lsd1 mutant of Arabidopsis fails to limit the boundaries of hypersensitive cell death response during avirulent pathogen infection and initiates unchecked lesions in long day photoperiod giving rise to the runaway cell death (rcd) phenotype. We link here the initiation and propagation of rcd to the activity of photosystem II, stomatal conductance and ultimately to photorespiratory H(2)O(2). A cross of lsd1 with the chlorophyll a/b binding harvesting-organelle specific (designated cao) mutant, which has a reduced photosystem II antenna, led to reduced lesion formation in the lsd1/cao double mutant. This lsd1 mutant also had reduced stomatal conductance and catalase activity in short-day permissive conditions and induced H(2)O(2) accumulation followed by rcd when stomatal gas exchange was further impeded. All of these traits depended on the defense regulators EDS1 and PAD4. Furthermore, nonphotorespiratory conditions retarded propagation of lesions in lsd1. These data suggest that lsd1 failed to acclimate to light conditions that promote excess excitation energy (EEE) and that LSD1 function was required for optimal catalase activity. Through this regulation LSD1 can influence the effectiveness of photorespiration in dissipating EEE and consequently may be a key determinant of acclimatory processes. Salicylic acid, which induces stomatal closure, inhibits catalase activity and triggers the rcd phenotype in lsd1, also impaired acclimation of wild-type plants to conditions that promote EEE. We propose that the roles of LSD1 in light acclimation and in restricting pathogen-induced cell death are functionally linked.
    Plant physiology 10/2004; 136(1):2818-30. · 6.56 Impact Factor
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    ABSTRACT: LSD1 was defined as a negative regulator of plant cell death and basal disease resistance based on its null mutant phenotypes. We addressed the relationship between lsd1-mediated runaway cell death and signaling components required for systemic acquired resistance (SAR), namely salicylic acid (SA) accumulation and NIM1/NPR1. We present two important findings. First, SA accumulation and NIM1/NPR1 are required for lsd1-mediated runaway cell death following pathogen infection or application of chemicals that mimic SA action. This implies that lsd1-dependent cell death occurs 'downstream' of the accumulation of SA. As SA application triggers runaway cell death in lsd1 but not wild-type plants, we infer that LSD1 negatively regulates an SA-dependent signal leading to cell death. Thus SA is both a trigger and a required mediator of lsd1 runaway cell death. Second, neither SA accumulation nor NIM1/NPR1 function is required for the basal resistance operating in lsd1. Therefore LSD1 negatively regulates a basal defense pathway that can act upstream or independently of both NIM1/NPR1 function and SA accumulation following avirulent or virulent pathogen challenge. Our data, together with results from other studies, point to the existence of an SA-dependent 'signal potentiation loop' controlling HR. Continued escalation of signaling in the absence of LSD1 leads to runaway cell death. We propose that LSD1 is a key negative regulator of this signal potentiation.
    The Plant Journal 03/2002; 29(3):381-91. · 6.58 Impact Factor
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    ABSTRACT: SummaryLSD1 was defined as a negative regulator of plant cell death and basal disease resistance based on its null mutant phenotypes. We addressed the relationship between lsd1-mediated runaway cell death and signaling components required for systemic acquired resistance (SAR), namely salicylic acid (SA) accumulation and NIM1/NPR1. We present two important findings. First, SA accumulation and NIM1/NPR1 are required for lsd1-mediated runaway cell death following pathogen infection or application of chemicals that mimic SA action. This implies that lsd1-dependent cell death occurs ‘downstream’ of the accumulation of SA. As SA application triggers runaway cell death in lsd1 but not wild-type plants, we infer that LSD1 negatively regulates an SA-dependent signal leading to cell death. Thus SA is both a trigger and a required mediator of lsd1 runaway cell death. Second, neither SA accumulation nor NIM1/NPR1 function is required for the basal resistance operating in lsd1. Therefore LSD1 negatively regulates a basal defense pathway that can act upstream or independently of both NIM1/NPR1 function and SA accumulation following avirulent or virulent pathogen challenge. Our data, together with results from other studies, point to the existence of an SA-dependent ‘signal potentiation loop’ controlling HR. Continued escalation of signaling in the absence of LSD1 leads to runaway cell death. We propose that LSD1 is a key negative regulator of this signal potentiation.
    The Plant Journal 01/2002; 29(3):381 - 391. · 6.58 Impact Factor
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    ABSTRACT: SummaryLSD1 was defined as a negative regulator of plant cell death and basal disease resistance based on its null mutant phenotypes. We addressed the relationship between lsd1-mediated runaway cell death and signaling components required for systemic acquired resistance (SAR), namely salicylic acid (SA) accumulation and NIM1/NPR1. We present two important findings. First, SA accumulation and NIM1/NPR1 are required for lsd1-mediated runaway cell death following pathogen infection or application of chemicals that mimic SA action. This implies that lsd1-dependent cell death occurs ‘downstream’ of the accumulation of SA. As SA application triggers runaway cell death in lsd1 but not wild-type plants, we infer that LSD1 negatively regulates an SA-dependent signal leading to cell death. Thus SA is both a trigger and a required mediator of lsd1 runaway cell death. Second, neither SA accumulation nor NIM1/NPR1 function is required for the basal resistance operating in lsd1. Therefore LSD1 negatively regulates a basal defense pathway that can act upstream or independently of both NIM1/NPR1 function and SA accumulation following avirulent or virulent pathogen challenge. Our data, together with results from other studies, point to the existence of an SA-dependent ‘signal potentiation loop’ controlling HR. Continued escalation of signaling in the absence of LSD1 leads to runaway cell death. We propose that LSD1 is a key negative regulator of this signal potentiation.
    The Plant Journal 01/2002; 29(3). · 6.58 Impact Factor
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    ABSTRACT: Specific recognition of pathogens is mediated by plant disease resistance (R) genes and translated into a successful defense response. The extent of associated hypersensitive cell death varies from none to an area encompassing cells surrounding an infection site, depending on the R gene activated. We constructed double mutants in Arabidopsis between positive regulators of R function and a negative regulator of cell death, LSD1, to address whether genes required for normal R function also regulate the runaway cell death observed in lsd1 mutants. We report here that EDS1 and PAD4, two signaling genes that mediate some but not all R responses, also are required for runaway cell death in the lsd1 mutant. Importantly, this novel function of EDS1 and PAD4 is operative when runaway cell death in lsd1 is initiated through an R gene that does not require EDS1 or PAD4 for disease resistance. NDR1, another component of R signaling, also contributes to the control of plant cell death. The roles of EDS1 and PAD4 in regulating lsd1 runaway cell death are related to the interpretation of reactive oxygen intermediate-derived signals at infection sites. We further demonstrate that the fate of superoxide at infection sites is different from that observed at the leading margins of runaway cell death lesions in lsd1 mutants.
    The Plant Cell 11/2001; 13(10):2211-24. · 9.25 Impact Factor
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    ABSTRACT: Plant disease resistance (R) genes are introduced into high yielding crop varieties to improve resistance to agronomically important pathogens. The R gene-encoded proteins are recognitionally specific, interacting directly or indirectly with corresponding pathogen avirulence (avr) determinants, and are therefore under strong diversifying selection pressure to evolve new recognition capabilities. Genetic analyses in different plant species have also revealed more broadly recruited resistance signalling genes that provide further targets for manipulation in crop improvement strategies. Understanding the processes that regulate both plant-pathogen recognition and the induction of appropriate defences should provide fresh perspectives in combating plant disease. Many recent studies have utilized the model plant, Arabidopsis thaliana. Here, mutational screens have identified genes that are required for R gene function and for restriction of pathogen growth in compatible plant-pathogen interactions. Genetic analyses of these plant mutants suggest that whilst signalling pathways are conditioned by particular R protein structural types they are also influenced by pathogen lifestyle. Two Arabidopsis defence signalling genes, EDS1 and PAD4, are required for the accumulation of salicylic acid, a phenolic molecule required for systemic immunity. The cloning, molecular and biochemical characterization of these components suggests processes that may be important in their disease resistance signalling roles.
    Novartis Foundation symposium 02/2001; 236:153-61; discussion 161-4.
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    ABSTRACT: Lipid peroxidation was investigated in relation with the hypersensitive reaction in cryptogein-elicited tobacco leaves. A massive production of free polyunsaturated fatty acid (PUFA) hydroperoxides dependent on a 9-lipoxygenase (LOX) activity was characterized during the development of leaf necrosis. The process occurred after a lag phase of 12 h, was accompanied by the concomitant increase of 9-LOX activity, and preceded by a transient accumulation of LOX transcripts. Free radical-mediated lipid peroxidation represented 10% of the process. Inhibition and activation of the LOX pathway was shown to inhibit or to activate cell death, and evidence was provided that fatty acid hydroperoxides are able to mimic leaf necrotic symptoms. Within 24 h, about 50% of leaf PUFAs were consumed, chloroplast lipids being the major source of PUFAs. The results minimize the direct participation of active oxygen species from the oxidative burst in membrane lipid peroxidation. They suggest, furthermore, the involvement of lipase activity to provide the free PUFA substrates for LOX. The LOX-dependent peroxidative pathway, responsible for tissue necrosis, appears as being one of the features of hypersensitive programmed cell death.
    Journal of Biological Chemistry 01/2000; 274(51):36446-55. · 4.65 Impact Factor
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    ABSTRACT: We analyse the relationship between active oxygen species (AOS) production and pH changes induced in tobacco cells by cryptogein, a fungal proteinaceous elicitor of defence mechanisms in plants. When tobacco cells were treated with cryptogein, an intracellular acidification, an alkalinization of the extracellular medium and a transient burst of AOS (H2O2) were observed. Treatment of elicited cells with either diphenyleneiodonium (DPI), an inhibitor of the neutrophil NADPH oxidase, or Tiron, which scavenges O2·–, abolished AOS production. These data suggest the involvement of a NADPH oxidase-like enzyme leading to H2O2 production through O2·– dismutation. Although H2O2 production could be, per se, the origin of the pH changes observed, we showed that it was not the main cause, since DPI and Tiron did not inhibit extracellular alkalinization. On the other hand, cryptogein-induced changes in pH could be abolished using fusicoccin (FC), which is known to stimulate the plasmalemma H+-ATPase. Consequently, the observed changes in pH induced by cryptogein could be mainly due to the inhibition of the plasmalemma H+-ATPase activity. Furthermore, changes in extracellular pH were shown to modulate the intensity of AOS production by elicited cells. The possible regulation of the NAD(P)H oxidase activity of plant cells by changes in pH is further discussed.
    Plant Cell and Environment 01/1997; 20(12):1573-1579. · 5.14 Impact Factor
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    ABSTRACT: Excised leaves of Nicotiana tabacum var Xanthi and Nicotiana rustica were treated with cryptogein and capsicein, basic and acidic elicitins, respectively. Both compounds induced leaf necrosis, the intensity of which depended on concentration and duration of treatment. N. tabacum var Xanthi was the most sensitive species and cryptogein was the most active elicitin. Lipid peroxidation in elicitin-treated Nicotiana leaves was closely correlated with the appearance of necrosis. Elicitin treatments induced a rapid and transient burst of active oxygen species (AOS) in cell cultures of both Nicotiana species, with the production by Xanthi cells being 6-fold greater than that by N. rustica. Similar maximum AOS production levels were observed with both elicitins, but capsicein required 10-fold higher concentrations than those of cryptogein. Phytoalexin production was lower in response to both elicitins in N. tabacum var Xanthi cells than in N. rustica cells, and capsicein was the most efficient elicitor of this response. In cryptogein-treated cell suspensions, phytoalexin synthesis was unaffected by diphenyleneiodonium, which inhibited AOS generation, nor was it affected by tiron or catalase, which suppressed AOS accumulation in the extracellular medium. These results suggest that AOS production, lipid peroxidation, and necrosis are directly related, whereas phytoalexin production depends on neither the presence nor the intensity of these responses.
    Plant physiology 08/1996; 111(3):885-891. · 6.56 Impact Factor
  • Christine Rustérucci, Marie-Louise Milat, Jean-Pierre Blein
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    ABSTRACT: The O2− · scavenging properties of beticolin-1, a fungal toxin, have been studied using peroxidase-mediated luminol chemiluminescence. A comparison between beticolin-1, vitamin E and tiron is reported: beticolin-1 displays an anti-radical effect without inhibiting peroxidase activity in a larger range of concentrations (1 × 10−8−1 × 10−5 M) than vitamin E (3 × 10−7−1 × 10−5 M) or tiron (5 × 10−7−4 × 10−5 M). Maximal scavenging efficacy was higher for beticolin-1 and vitamin E than for tiron (88, 80 and 52%, respectively).
    Phytochemistry 01/1996; 42(4):979-983. · 3.05 Impact Factor
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    ABSTRACT: In order to initiate studies on signal transduction pathways leading from fungal elicitor perception to defence activation in plants, the effects of a cell wall crude elicitor from Phytophthora parasitica var. nicotianae and of cryptogein, a protein from the culture medium of Phytophthora cryptogea, were compared on Nicotiana tabacum L. cells. The two elicitors displayed similar biological activities towards induction of lipoxygenase (LOX; linoleate:oxygen oxidoreductase, EC 1.13.11.12) and proteinase inhibitors. When very rapid cellular responses were assessed, both elicitors enhanced extracellular pH and K+ efflux, whereas active oxygen species production was induced by cryptogein only. The data indicate that active oxygen species, though possibly involved in cryptogein toxicity, may not be necessary for defence induction.
    Plant Physiology and Biochemistry 01/1994; 32(3):373-378. · 2.78 Impact Factor

Publication Stats

1k Citations
107.35 Total Impact Points

Institutions

  • 2008–2014
    • Université de Picardie Jules Verne
      • BIOPI - Biologie des plantes et innovation
      Amiens, Picardie, France
  • 2001–2002
    • John Innes Centre
      • The Sainsbury Laboratory
      Norwich, England, United Kingdom
  • 1996
    • University of Burgundy
      Dijon, Bourgogne, France