Gotowa bibliografia na temat „Pycnidiospore”

Seasonal and diurnal patterns of spore dispersal by Leptosphaeria maculans, which causes blackleg disease of canola, were studied in two consecutive field seasons using a 7-day Burkard spore sampler and rotorod impaction spore samplers. Ascospores of L. maculans were trapped from mid-June to the end of July, whereas pycnidiospores were trapped from mid-July until the end of July or early August. Ascospores and pycnidiospores were trapped between 9:00 P.M. and 4:00 A.M., when air temperatures were 13 to 18°C and relative humidity was >80%. Peak ascospore and pycnidiospore dispersal was associated with rain events. Peak ascospore dispersal was found to occur several hours after rainfall ≥2 mm, and ascospore dispersal continued for approximately 3 days after such events. Peak pycnidiospore dispersal occurred during the same hours as rain events. More ascospores and pycnidiospores were carried in the direction of prevailing winds than in other directions. To the south of the inoculated area, the gradients of disease incidence and stem disease severity were -19.2 and -0.8 m-1, respectively. Disease incidence and stem severity declined by 50% 12.5 and 5.5 m from the inoculated area, respectively. To the north of the inoculated area, the gradients of disease incidence and stem severity were -21.5 and -0.7 m-1, respectively. Disease incidence and stem severity declined by 50% 14.0 and 5.2 m from the inoculated area, respectively. In 2001, ascospores and pycnidiospores were trapped within 25 m of the inoculated area, whereas pycnidiospores were trapped up to 45 m from the inoculated area.

A potential microbial fungicide, Paenibacillus lentimorbus isolate CBCA-2, against Botryosphaeria dothidea, the pistachio panicle and shoot blight fungus, was obtained from healthy pistachio leaves by both in vitro and in vivo screening techniques. CBCA-2 caused 100% inhibition of pycnidiospore germination after 24 h incubation at 25°C. Malformation of pycnidiospores and hyphae, and lysis and swollen pycnidiospores of B. dothidea occurred in the presence of cell suspensions of CBCA-2. Among the five media tested, nutrient yeast dextrose broth significantly increased the production of antifungal compounds. Application of culture filtrates of CBCA-2 suppressed disease on detached pistachio leaves, but washed bacterial cells did not inhibit lesion development. Development of lesions on excised dormant stems was inhibited only when the culture filtrate was applied before fungal inoculation. Survival of the CBCA-2 after treatment with azoxystrobin (Abound), benomyl (Benlate), tebuconazole (Elite), propiconazole (Break), or trifloxystrobin (Flint) at the highest recommended concentration was not affected, but survival was affected by iprodione (Rovral). Spraying a suspension of CBCA-2 on pruning wounds before inoculation with pycnidiospores of B. dothidea significantly reduced infection compared with the unsprayed, inoculated controls.

Daily and seasonal spore dispersal of Mycosphaerella pinodes (Berk & Bloxam) Vestergren and the relationship of spore dispersal to distance and disease severity were investigated in a pea field in western Canada during two consecutive years. Most ascospores were released in response to rain events, during the first 23–27 d after the inoculum source area was infested with naturally diseased pea residue, whereas most pycnidiospores were trapped during the first 20 d. For both ascospores and pycnidiospores, the highest peaks of spore release occurred during the first 14–20 d after infestation. Few spores were trapped after day 27 after infestation. Daily peaks of ascospore and pycnidiospore release occurred between 1700 and 0400 hours. Most ascospores were released 1–2 d after a rain event and the largest peak appeared the first day after rain. In contrast, most pycnidiospores were released on the same day as rain occurred or the following day. The release of both spore types was associated with rainfall events ≥2 mm during the first 27 d after infestation but not with rainfall events after 27 d. Ascospore density was negatively correlated with distance from the inoculum source (r ≤ –0.92) and positively related to the disease severity (r ≥ 0.92). Disease severity decreased with increasing distance from the inoculum source. The patterns of spore dispersal associated with rain events have practical applications in the disease forecasting and spraying of chemicals to control the disease.Key words: field pea, mycosphaerella blight, rainfall, spore release.

Isolates of Stenocarpella maydis from seed companies and plant disease clinics in the United States and the Republic of South Africa were assayed for isozyme polymorphisms and cultural variability. A low level of isozyme polymorphisms was detected in this collection of isolates. Isozyme polymorphisms were detected for α-esterase, hexose kinase, and malate dehydroge-nase of the enzymes assayed. Fungi often have limited variability among isozyme profiles, and this is especially true for fungi that have host specialization such as biotrophs or fungi with formae speciales designations. Optimum growth temperature, colony color, and pycnidiospore production were also measured. All isolates had an optimum temperature of 28 to 31°C for colony growth on acidified potato dextrose agar. Colony color and pycnidiospore production were variable over the course of several experiments, indicating that these phenotypes are poor genetic markers.

Observations on Ampelomyces quisqualis disclosed that the pycnidium may originate either from one cell of a single pycnidiospore, or from one hyphal cell. In the first case the pycnidiospore becomes two celled and swollen and a profuse germination of one of the two swollen spore cells can be observed. Later, the short hyphae branches, interweave, and anastomose to form a compact network around the mother spore, the pycnidium primordium. Similarly, we observed profuse branching in a single hyphal cell. The newly formed branches interweave and anastomose to form a compact network which gives rise to the pycnidium primordium. Hyphal rings were also observed throughout this study, but no pycnidia arose from these structures. During the vegetative growth of the fungus, hyphal anastomosis seems to be a frequent pattern. It seems that the pycnidial ontogeny of A. quisqualis does not conform to any known developmental type.

Citrus black spot, a major citrus disease caused by Guignardia citricarpa, was recently introduced in Florida. The nonpathogenic fungal endophyte G. mangiferae is commonly found in the same citrus tissues as G. citricarpa. Quantitative polymerase chain reaction (qPCR) assays based on internal transcribed spacer (ITS)-1 genes were developed to detect, quantify, and distinguish between these morphologically similar organisms in environmental samples. The primer/probe sets GCITS and GMITS were more than 95% efficient in single-set reactions in complex environmental DNA samples. Detection of 10 fg of G. citricarpa and G. mangiferae DNA was possible. Pycnidiospore disruption resulted in detection of single pycnidiospores with 78 (59 to 102; 95% confidence interval [CI]) and 112 (92 to 136; 95% CI) ITS copies for G. citricarpa and G. mangiferae, respectively. Detection was from partially decomposed leaves where fruiting bodies cannot be morphologically distinguished. Temperature and wetting period have significant effects on Guignardia spp. pseudothecia production in leaf litter. Based on relative biomass or the proportion of nuclei detected, G. citricarpa and G. mangiferae respond more strongly to wetting period than temperature. This qPCR assay will provide additional epidemiological data on black spot in tissues where G. citricarpa and G. mangiferae are not easily distinguished.

Six spring-type Brassica napus L. cultivars, either susceptible or with polygenic or monogenic resistance, were inoculated with Leptosphaeria maculans (Desmaz.) Ces. & De Not. (organism causing phoma stem canker in crucifers) to investigate differences in the responses of host stem tissues to the pathogen. At growth stage 1.06, plants were inoculated with pycnidiospores at the junction of the petiole and stem. The pre-penetration and penetration phases were examined along with the histological, ultrastructural, and histochemical responses. The processes of pycnidiospore attachment, germination, and penetration through the stomata of petioles and stems were found to be similar in all cultivars. Specific post-penetration defense reactions identified were lignification, suberisation, and additional cambium formation in the resistant cultivars. In ‘Surpass 400’, which has monogenic resistance, these responses occurred 4–5 d earlier than in polygenically resistant cultivars, and were more intense (preventing hyphal penetration of the additional cambium layer), and resulted in a hypersensitive reaction without pycnidia formation. Our study clearly emphasizes the variatiability in location, timing, and histochemistry of stem responses between compatible and incompatible interactions and will improve our overall understanding of the role and importance of the mechanisms of resistance in spring-type B. napus to L. maculans.

Citrus black spot (CBS) is caused by Phyllosticta citricarpa, which is classified as a quarantine organism in certain countries whose concerns are that CBS-infected fruit may be a pathway for introduction of the pathogen. This study evaluated the reproductive capability and viability of P. citricarpa under simulated conditions in which the whole fruit, peel segments, or citrus pulp with CBS lesions were discarded. Naturally infected ‘Midknight’ Valencia orange and ‘Eureka’ lemon fruit, either treated using standard postharvest sanitation, fungicide, and wax coating treatments or untreated, were placed into cold storage for 5 weeks (oranges at 4 °C and lemons at 7 °C). Thereafter, treated and untreated fruit were incubated for a further 2 weeks at conditions conducive for CBS symptom expression and formation of pycnidia. The ability of pycnidia to secrete viable pycnidiospores after whole fruit and peel segments or peel pieces from citrus pulp were exposed to sunlight at warm temperatures (±28 °C) and ±75% relative humidity levels was then investigated. The combination of postharvest treatments and cold storage effectively controlled CBS latent infections (>83.6% control) and pycnidium formation (<1.4% of lesions formed pycnidia), and the wax coating completely inhibited pycnidiospore release in fruit and peel segments. Pycnidiospores were secreted only from lesions on untreated fruit and peel segments and at low levels (4.3–8.6%) from peel pieces from pulped treated fruit. However, spore release rapidly declined when exposed to sunlight conditions (1.4% and 0% after 2 and 3 days, respectively). The generally poor reproductive ability and viability of CBS fruit lesions on harvested fruit, particularly when exposed to sunlight conditions, supports the conclusion that citrus fruit without leaves is not an epidemiologically significant pathway for the entry, establishment, and spread of P. citricarpa.

Eighty-six isolates of Botryosphaeria dothidea, the causal agent of Botryosphaeria panicle and shoot blight of pistachio, were collected from pistachio and other plant hosts in California. The isolates were characterized by microsatellite-primed polymerase chain reaction (MP-PCR), sequences of the nuclear ribosomal DNA internal transcribed spacer region (ITS1, 5.8S gene, and ITS2), morphological and cultural characters, osmotic and fungicide sensitivity, and pathogenicity on pistachio. Three groups of these isolates were identified based upon analysis of MP-PCR data and ITS sequences. Group I contained 43 pycnidiospore-derived isolates collected from pistachio and other hosts. Group II consisted of 20 ascosporic isolates obtained from a single sequoia plant. Group III consisted of 20 ascosporic isolates from three shoots on a single blackberry plant, two pycnidiospore-derived isolates from incense cedar, and one from pistachio. Group I predominated over the other two groups in California pistachio orchards. B. dothidea isolates of group III grew faster on acidified potato dextrose agar (APDA) than the isolates of groups I and II. Isolates of group III produced pycnidia on both APDA and autoclaved pistachio shoots, but the isolates of the other two groups produced pycnidia on only autoclaved pistachio shoots. Additionally, significant differences in osmotic and fungicide sensitivities were observed among these three groups. Results from lathhouse inoculations demonstrated that the representative isolates for each of the three groups were all capable of infecting pistachio and producing characteristic disease symptoms of Botryosphaeria blight. The virulence of group II isolates on pistachio was, however, significantly lower than that of group I isolates.

Les maladies foliaires fongiques sont une contrainte majeure des systèmes céréaliers. Elles constituent par ailleurs de précieux modèles d'étude pour comprendre comment commence une épidémie, questionnement récurrent en épidémiologie végétale. Dans cette thèse ont été étudiés trois des principaux déterminants des phases précoces des épidémies de septoriose du blé causée par Zymoseptoria tritici : quantité, efficacité et origine de l'inoculum primaire. L'étude a porté sur deux épidémies successives dans deux parcelles de blé proches l’une de l’autre au sein d'un dispositif pluriannuel (2011-2013 ; Grignon, France). La première parcelle, caractérisée par l'absence de résidus, était exposée à des sources distantes d'inoculum primaire, et la seconde, en monoculture de blé depuis plusieurs années, présentait une quantité importante de résidus contaminés agissant comme source locale d'inoculum primaire. Dans la première partie de la thèse, la capture d’ascospores à l’aide d’un piège volumétrique couplé à une quantification de l'ADN par qPCR a permis de quantifier l'inoculum primaire présent dans l'air au-dessus des parcelles pendant les phases épidémiques précoces. Les limites de détection et de quantification ont été déterminées, discutées et utilisées afin d'estimer de faibles quantités d’ascospores. Ni la présence locale de résidus contaminés ni la quantité d’inoculum au-dessus des parcelles n'ont été corrélées avec la précocité des deux épidémies. Dans la seconde partie, la pathogénicité des ascospores et des pycnidiospores de Z. tritici a été estimée sur plante adulte et comparée. La période de latence consécutive à une infection par ascospore a été plus longue de 60 degrés-jour qu’après une infection par une pycnidiospore. Dans la troisième partie de la thèse, qui visait à identifier l'origine de l'inoculum primaire, deux stratégies ont été adoptées. La première stratégie a consisté à rechercher des changements dans la structure génétique de différentes sous-populations collectées dans les deux parcelles sur une période de trois années en utilisant des marqueurs neutres (SSR). Aucune structure n'a été identifiée, mais de légères différenciations chez certaines sous-populations, cohérentes avec le contexte épidémiologique (nature du cycle de reproduction dont elles découlent, période épidémique, intensité de maladie), ont été mises en évidence. Ces résultats n'ont toutefois pas permis de déterminer l'origine de l'inoculum primaire puisqu'aucune différence entre les sous-populations résidantes (locales) et immigrantes (distantes), ni de discontinuité génétique entre sous-populations de fin (saison n) et de début d'épidémie (saison n+1), n'a été mise en évidence. La seconde stratégie a consisté à comparer le profil d'agressivité (capacité de sporulation et période de latence) d’une population de Z. tritici collectée en début d’épidémie dans la parcelle en monoculture de blé, à celui d'une population résidante (ascospores issues des résidus présents dans la parcelle) et d'une population immigrante (lésions provoquées par des ascospores d'origine distante). Le profil de la population testée, plus proche de celui de la population résidante, a suggéré que l'épidémie avait été déclenchée majoritairement par un inoculum primaire d’origine locale. Il ressort de cette étude de cas qu’une gestion quantitative (réduction) de l'inoculum primaire serait probablement très peu efficace, tandis que sa gestion qualitative, tenant compte de l'adaptation différentielle de populations pathogènes à leurs hôtes, mériterait d’être intégrée dans des stratégies de protection (alternance de variétés dans le temps). Pour finir, la définition du début et de la fin d'une épidémie a été discutée, selon que l’on se place à une échelle annuelle (absence de l’hôte comme critère de début/fin) ou pluriannuelle (discontinuité de pression pathogène comme critère de début/fin, indépendamment de l’absence de l'hôte)
Fungal foliar diseases are a major constraint to cereal production systems. They constitute relevant models to elucidate how an epidemic begins, which is a recurrent question in plant disease epidemiology. In this thesis three of the main components of the early stages of the epidemics of septoria tritici blotch, a wheat disease caused by Zymoseptoria tritici, were studied: the quantity, the efficiency and the origin of primary inoculum. The study focused on epidemics occurring over the 2011-2013 cultural seasons in two wheat plots located close to each other in Grignon (France). The first plot, characterized by the absence of debris, was exposed to distant sources of primary inoculum, while the second plot, grown in wheat for several years, had a large amount of contaminated debris acting as a local source of primary inoculum. In the first part of the thesis, ascospore trapping using a volumetric spore trap combined with DNA quantification by qPCR allowed to quantify the inoculums present in the air above the wheat plots during the early stages of the epidemics. The limits of detection and quantification were determined, discussed and used to estimate small amounts of ascospores. Neither the local presence of contaminated debris nor the quantity of inoculum above the plots was correlated with the earliness of the epidemics. In the second part, the pathogenicity of Z. tritici ascospores and pycnidiospores was estimated on adult plants. The latent period following infections by ascospores was 60 degree-days longer than following infection by pycnidiospores. In the third part of the thesis, which aimed to identify the source of primary inoculum, two strategies were developed. The first strategy investigated changes in the genetic structure of different subpopulations collected from both wheat plots over a period of three years using neutral markers (SSR). No structure was identified, but slight differentiations in some subpopulations, consistent with the epidemiological context (nature of the reproduction cycle from which they derived, epidemic period, disease intensity) were highlighted. These results, however, did not allow to determine the origin of the primary inoculum because no difference between resident (local) and immigrant (distant) subpopulations, or a genetic discontinuity between subpopulations from the end (season n) and the beginning of epidemics (season n + 1), were identified. The second strategy compared the aggressiveness profile (sporulation capacity and latent period) of a Z. tritici population collected at the beginning of an epidemic in the monoculture wheat plot and of a resident population (ascospores ejected from debris present in the plot) and to an immigrant population (leaf lesions caused by ascospores of distant origin). The profile of the tested population, closer to that of the resident population, suggested that the epidemic was mainly initiated by primary inoculum of local origin. This case study showed that a quantitative management (reduction) of the primary inoculum would be probably inefficient, while its qualitative management, taking into account the differential adaptation of pathogen populations to their hosts, deserves to be taken into account in crop protection strategies (alternating wheat cultivars in time). Finally, the definition of the beginning and the end of an epidemic was discussed, depending if we consider an annual scale (absence of the host as a beginning or end criterion) or a multiannual scale (pathogen pressure discontinuity as the beginning or end criterion, regardless of the absence of the host)

La lutte contre le Phoma du colza, causé par le champignon Leptosphaeria maculans, repose principalement sur la culture de variétés résistantes dont l’efficacité est peu durable. La reproduction sexuée confère un fort potentiel adaptatif au champignon confronté aux pressions de sélection exercées par les variétés résistantes : elle permet l’acquisition et l’association d’allèle de virulence, alors que les ascospores issues de la reproduction sexuée assurent la transmission de la maladie d’une saison culturale à la suivante. Nous faison l’hypothèse qu’en début de contournement de résistance, la transmission dela virulence d’une génération à la suivante est limitée d’une part par la faible probabilité de reproduction sexuée entre isolats virulents et d’autre part par une dispersion des ascospores spatialement limitée. Pour tester cette hypothèse nous avons étudié (i) la dispersion des pycnidiospores. Sous un générateur de gouttes en air calme, les pycnidiospores sont dispersées par les gouttelettes de pluie à moins de 40 cm de la macule source ; des résidus porteurs de pycnides peuvent causer des infections primaires de la maladie. Le succès de la phase systémique détecté par l’expression de nécroses au collet sur des plantules inoculées en conditions contrôlées augmente avec le nombre de points d’infection, mais diminue en présence de la résistance partielle ; la compétition entre individus peut limiter la présence concoittante des types sexuels au collet de la plante. Par conséquent dans des champs avec des populations de L. Maculans à faible densité, la dispersion des pycnidiospores par la pluie peut accroître la taille de la populatino pathogène et permettre la rencontre d’individus initialement distants, tandis que la progression systémique du champignon peut limiter la rencontre locale d’isolats virulents sexuellement compatibles
Management of homa stem canker of oilseed rape,caused by Leptosphaeria maculans, primarily relies on the cultivation of resistant varieties that lack durable efficiency. Sexual reproduction enhances the evolutionary potential of the fungus submitted to the selection pressure exerted by resistant varieties by allowing acquisition and association of virulence alleles and season-to-season transmission of the disease through ascospore dispersal. We hypothesize that for small, emergent virulent populations, sexual reproduction could be restricted by the reduced mating probability of individuals and that season-to-season transmission of virulent individuals through ascopsore dispersal can be spatially limited. To test these hypotheses, we investigated (i) rain-splash dispersal of pycnidiospores, (ii) systemic growth of the fungus in stem and (iii) the spatial genetic structure of populations to infer ascospore dispersal distances. Pycnidiospores were splash-dispersed over short distances (within 40 cm from the source) from phoma leaf sports, while oilseed rape stubble carrying pycnidia constituted a potential source of primary infections

La lutte contre le Phoma du colza, causé par le champignon Leptosphaeria maculans, repose principalement sur la culture de variétés résistantes dont l'efficacité est peu durable. La reproduction sexuée confère un fort potentiel adaptatif au champignon confronté aux pressions de sélection exercées par les variétés résistantes : elle permet l'acquisition et l'association d'allèles de virulence, alors que les ascospores issues de la reproduction sexuée assurent la transmission de la maladie d'une saison culturale à la suivante. Nous faisons l'hypothèse qu'en début de contournement de résistance, la transmission de la virulence d'une génération à la suivante est limitée d'une part par la faible probabilité de reproduction sexuée entre isolats virulents et d'autre part par une dispersion des ascospores spatialement limitée. Pour tester cette hypothèse nous avons étudié (i) la dispersion des pycnidiospores par la pluie, (ii) la progression systémique du champignon dans la tige de colza et (iii) la structure spatiale des populations de L. maculans pour inférer les distances de dispersion des ascospores. Sous un générateur de gouttes en air calme, les pycnidiospores sont dispersées par les gouttelettes de pluie à moins de 40 cm de la macule source ; des résidus porteurs de pycnides peuvent causer des infections primaires de la maladie. Le succès de la phase systémique détecté par l'expression de nécroses au collet sur des plantules inoculées en conditions contrôlées augmente avec le nombre de points d'infection, mais diminue en présence de la résistance partielle ; la compétition entre individus peut limiter la présence concomitante des types sexuels au collet de la plante. Par conséquent, dans des champs avec des populations de L. maculans à faible densité, la dispersion des pycnidiospores par la pluie peut accroître la taille de la population pathogène et permettre la rencontre d'individus initialement distants, tandis que la progression systémique du champignon peut limiter la rencontre locale d'isolats virulents sexuellement compatibles. Pour 29 populations françaises génotypées à l'aide de marqueurs minisatellites, l'essentiel de la diversité génotypique est détectée à l'échelle d'une population (champ) ; l'absence de différenciation génétique entre populations distantes n'a pas permis de mettre en évidence une limitation des flux de gènes à l'échelle spatiale analysée. Ces résultats suggèrent que la dispersion du Phoma par les ascospores est beaucoup plus élevée que supposée et/ou que les tailles efficaces des populations du champignon dans une parcelle sont très grandes. Ces connaissances épidémiologiques devront être prises en compte pour améliorer les stratégies de déploiement durable des variétés résistantes.