368 research outputs found
Induced resistance in plants and the role of pathogenesis-related proteins
The nature of induced resistance
Resistance, according to Agrios (1988) is the ability
of an organism to exclude or overcome, completely
or in some degree, the effect of a pathogen or other
damaging factor. Disease resistance in plants is manifested
by limited symptoms, reflecting the inability
of the pathogen to grow or multiply and spread, and
often takes the form of a hypersensitive reaction (HR),
in which the pathogen remains confined to necrotic
lesions near the site of infection. Induced resistance is
the phenomenonthat a plant, once appropriately stimulated,
exhibits an enhanced resistance upon 'challenge'
inoculation with a pathogen. Although induced resistance
has been attracting attention recently (Ryals et
al., 1994; Hammerschmidt and Kuc, 1995), the first
systematic enquiry into induced resistance was made
by Ross (1961a,b). He observed that the inducible
resistance response to tobacco mosaic virus (TMV)
in N gene-containing, hypersensitively reacting tobacco
was not confined to the immediate vicinity of the
resulting local necrotic lesions, but extended to other
plant parts. A ring of tissue around the developing
lesions became fully refractory to subsequent infection
(localized acquired resistance; Ross, 1961a), whereas
challenge inoculation of distant tissues resulted in
much smaller, and occasionally fewer, lesions (systemic
acquired resistance (SAR); Ross, 1961b) than in
non-induced plants. Even leaves thatweremere initials
at the time of the primary inoculation became induced,
suggesting that as a result of the initial infection, a
signal was generated, transported and propagated, that
primed the plant to respond more effectively to subsequent
infection (Bozarth and Ross, 1964). Treatments that influenced lesion size after primary infection had
similar effects on lesions developing upon challenge
inoculation (Ross, 1966), leading to the conclusion
that the mechanisms responsible for resistance expression
were the same under both conditions. Only upon
challenge inoculation, defense mechanisms appeared
to be expressed earlier and to a greater extent (De Laat
and Van Loon, 1983; Dean and Kuc, 1987)
Модель системы стратегического управления оператором сотовой связи и алгоритм её проектирования
Розроблено модель системи стратегічного управління операторів стільникового зв’язку на підставі запропонованої стратегії як випереджальної дії щодо поточного і прогнозного впливу середовища підприємства. Обґрунтовано зміст основних блоків цілей, функцій, завдань, управління і ресурсів системи.
Ключові слова: управління оператором стільникового зв'язку, модель системи, підприємство.
----------Разработана модель системы стратегического управления оператором сотовой связи на основе предложенной трактовки стратегии как упреждающего воздействия на текущее и прогнозное влияние среды предприятия. Обоснована содержательная сторона основных блоков целей, функций, задач, управления и ресурсов системы.
Ключевые слова: управление оператором сотовой связи, модель системы, предприятие.
-----------The model of the strategic management system for a cellular mobile operator was developed on the basis of suggested treatment of the strategy as a warning impact on current and forecasted influence of the enterprise’s environment. The content of such main blocks as goals, functions, tasks, control and resources is motivated.
Key words: managing a cellular mobile operator, system model, enterprise.
---------
Pathogenese en symptoomexpressie in viruszieke tabak : een onderzoek naar veranderingen in oplosbare eiwitten
The nature and the severity of the reaction of a plant to infection by a virus are determined by the genetic properties of both virus and hostplant. The genetic information of both is expressed in the formation of proteins. Our aim was to gain insight into the specificity of the interaction between virus and hostplant by investigating the biochemical mechanism of pathogenesis and symptom expression. Hence, we attempted to show if differences in protein constitution between noninfected and infected plants could indeed be established and whether such differences can be regarded as characteristic of the infecting virus or of the hostplant. In this study we made use of tobacco varieties that differ in reaction type to tobacco mosaic virus (TMV) and of strains of this virus that are distinguished by the symptoms they induce in tobacco. As the multiplication of TMV most probably takes place in the cytoplasm, the soluble protein fraction was investigated. Previous investigations have emphasized alterations in enzyme activities as a result of infection. In contrast to this, our attention was focused on changes in the electrophoretic pattern of protein bands induced by infection, not manifesting themselves immediately under the form of enzymatic activity.By using electrophoresis in 5, 7.5 and 10% polyacrylamide gel, over fifty different protein components in the soluble protein fraction from leaves of Nicotiana tabacum could be distinguished. No differences in protein patterns were observed between noninfected plants of the varieties Samsun and Samsun NN, although Samsun plants react to infection with TMV W U1 by formation of systemic mosaic symptoms, while Samsun NN plants - which contain the factor N from N. glutinosa - develop local lesions at temperatures below 25°. However, in the two varieties different and characteristic changes in protein patterns appeared upon infection. Apart from a number of quantitative changes, one new band was present in mosaic-diseased Samsun plants four weeks after infection. This band was identified as the free coat protein of the virus by co-electrophoresis and serology. A reduction in the electrophoretic mobility of the major band was also recorded.In the inoculated leaves of Samsun NN plants four new protein components (I-IV) were present one week after infection. These new components are not related to TMV coat protein. In N. glutinosa one new band was induced and two bands increased markedly after infection with TMV W U1, while one other band disappeared. These bands differed in electrophoretic mobility from the new bands observed after infection of Samsun NN plants. Therefore, none of the new components I-IV can be regarded as product of the Hg chromosomes, that are derived from N. glutinosa and contain the factor N. This was further substantiated by patterns from Samsun plants showing semi-systemic yellow ringspot symptoms as a result of infection with TMV HR. In this combination, both free TMV HR coat protein and the new components I-IV were apparent.In Samsun plants infected by TMV W U1 or TMV HR only a limited number of quantitative changes was observed. Contrary to this, Samsun NN plants infected by TMV W U1 showed a considerable number of quantitative changes, most of which did not appear in the two combinations mentioned earlier. The extent of these changes correlated with the lesion density on the leaves.When systemic mosaic symptoms were induced in both Samsun and Samsun NN plants as a result of infection with TMV W U1 at 30°, identical changes in protein patterns were observed for both varieties. These changes were the same as those in the combination TMV W U1 - Samsun at 20° and those in the combination TMV W U1 - Samsun EN, in which identical symptoms are induced. on the other hand, the formation of local lesions on the variety Samsun EN upon infection with TMV HR led to the appearance of the new components I- IV. It follows that in the combination TMV - tobacco the changes in soluble proteins are connected with the type of symptoms - either mosaic or local lesions produced, and that in all cases they are hostplant dependent.The induction of local or systemic necrosis on Samsun and Samsun NN tobacco with tobacco necrosis virus (TNV), tobacco rattle virus (TRV) and potato virus Y n(PVY n) always led to the appearance of the four new components in both varieties,but the relative proportions of the bands varied with the variety used, and with the characteristic of the virus to remain local or become systemic. Relatively low concentrations of the four new components were observed after infection with cucumbermosaic virus, although no necrosis developed in these combinations. Bands I and II were present after infection with PVY o, that only causes mild mottling. Although potato virus X (PVX) induces a similar mottling, the new components were not detected in plants infected by this virus. In none of the combinations the presence of virus-specific proteins could be established.Many of the quantitative changes observed in the various combinations occurred under different conditions and evidently represented general reactions, as similar changes were detected after cutting or freezing of the leaves. Same changes, however, were characteristic of the type of symptoms produced after virus infection. Cutting or freezing of the leaves or production of artificial necrosis by spraying with HgCl 2 induced no new components. The greater part of the quantitative changes occurring as a result of necrosis induced by virus infection were not observed in HgCl 2 induced necrosis either. So necrosis due to virus infection and artificially induced necrosis can be clearly distinguished by the accompanying changes in the soluble protein fraction. Since cutting or freezing of the leaves induces changes that are only partly similar to those observed when necrosis is induced by virus infections, ageing and injury seem to be only minor facets of the metabolic alterations underlying this type of symptom.In the combination TMV W U1 - Samsun NN the four new components first appeared at the onset of necrosis, and the bands increased in intensity with time. By five clays after inoculation band I ceased to increase, whereas bands II, III and IV increased up to day 14. From day 7 onward, the four bands were also present in the young leaves that had developed after inoculation and neither showed symptoms nor contained virus. In these leaves also, the bands increased in intensity with time. These bands were also present in the young leaves that had developed after inoculation with TNV or TRV.In the combination TMV W U1 - Samsun NN the amount of the four new components correlated with lesion density. The increase in intensity of the bands was reduced by treatment of the leaves with actinomycin D (MD) two days after inoculation. AMD inhibited the incorporation of 35S- methionine and 14C-leucine in the soluble protein fraction by 56-60%. Infection with TMV in itself also strongly inhibited synthesis of soluble proteins. These two effects appeared to be at least additive. However, the inhibition of the amount of the new components by AMD always amounted to less than 50%. Although preferential synthesis of the new components could not be demonstrated by electrophoresis of labeled proteins, the ratios of the radioactivities incorporated into protein from infected and noninfected plants point to de novo synthesis which can be only partly inhibited by AMD.The new components are not isoenzymes; of thirty enzymes studied, and do not contain carbohydrate, lipid or RNA. Their strong colouration with coomassieblue may indicate a high content of basic amino acids.A possible relation between the occurrence of these new components in young, developing leaves not containing virus, and the ability of these leaves to react with the formation of small lesions after (a second) inoculation with a virus that induces local lesions, was further investigated. There appeared to be a distinct correlation between the presence of the new components and the state of systemic acquired resistance. However, when eluates from gel slices that contained the four new components were applied to the plants simultaneously or 24 hours before inoculation with TMV, no effect on number or size of the lesions could be demonstrated. On the other hand, the multiplication of TMV in leaves that developed after inoculation of Samsun plants with TNV did appear to be inhibited to a considerable extent as a result of the first infection.Ammonium sulfate fractionation of purified protein fractions from noninfected and TMV IV U1-infected Samsun NN plants revealed two other new components. Upon gelfiltration on Sephadex G 100, in addition to the new components I-IV, another eight, more slowly migrating components were detected. These twelve new components all have molecular weights between 10,000 and 20,000. A number of these were observed as quantitative changes upon electrophoresis of unfractionated extracts. During electrophoresis of extracts from noninfected plants separation due to differences in molecular size prevailed. Therefore, the new components differ from the majority of the other soluble proteins from tobacco leaves by their relatively small charges.In addition to these twelve new components, a new ribonuclease and a new peroxidase isoenzyme were detected. The peroxidase isoenzyme was distinguished by a low pH optimum and a far greater affinity towards guaiacol than towards o -diphenols. It was induced in all combinations in which necrosis due to virus infection occurs, and to a small extent after infection with PVX and PVY o. In the combination TMV W U1 - Samsun NN maximal activity was reached when symptom development could be considered complete. The new isoenzymes were not present in young, symptomless leaves not containing virus.On the basis of data given in the literature, it can be envisaged that the new components might also be present in tobacco plants which, upon TMV infection, react with systemic mosaic symptoms, but in that case only after the multiplicaticn of the virus has stopped. Therefore, it seems possible that both in hypersensitively reacting tobacco plants and in plants that react with systemic mosaic symptoms, the appearance of the new components is connected with a slowing down of viral synthesis through a direct or indirect inhibition of virus multiplication. Their presence, together with the occurrence of increased peroxidase activity - that is correlated with a decreased rate of lesion enlargement - might be responsible for the expression of acquired resistance to subsequent inoculation. However, this phenomenon could also be explained by inhibition of the formation of a specific protein which may not, or in turn may result in the induction of new proteins and enzymes.The induction of the hypersensitive reaction and of necrosis by viruses seems to be governed by a common mechanism. Presumably TMV W U1 in Samsun tobacco represses this mechanism. This would enable the virus to multiply and spread throughout the plant.</p
Inducing resistance: a summary of papers presented at the First International Symposium on Induced Resistance to Plant Diseases, Corfu, May 2000
The First International Symposium on Induced Resistance
to Plant Diseases, organized by Eris Tjamos,
brought together over 150 participants to discuss the
complexities, questions and future direction of research
on the mechanisms by which plants can become better
able to defend themselves against pathogen attack.
Although the term immunization has been used to
denote treatments that enhance the defensive capacity
of plants, the correspondence to vaccination in vertebrates
is far-fetched: the induced state is by no means
specific, but rather constitutes a more general increase
in plant resistance to various types of pathogens. Moreover,
it seldom prevents disease from occurring but
generally reduces its extent or severity. These characteristics
make induced resistance a powerful mechanism
to exploit for enhancing the overall resistance
in crop plants. Indeed, the first commercial chemical
triggering induced resistance in plants, acibenzolar-Smethyl
(BTH) was recently introduced on the market
by Novartis under the tradenames Actigard (USA) and
BION (Europe)
Identification of a Chitin-Binding Protein Secreted by Pseudomonas aeruginosa
One of the major proteins secreted by Pseudomonas aeruginosa is a 43-kDa protein, which is cleaved by
elastase into smaller fragments, including a 30-kDa and a 23-kDa fragment. The N-terminal 23-kDa fragment
was previously suggested as corresponding to a staphylolytic protease and was designated LasD (S. Park and
D. R. Galloway, Mol. Microbiol. 16:263-270, 1995). However, the sequence of the gene encoding this 43-kDa
protein revealed that the N-terminal half of the protein is homologous to the chitin-binding proteins CHB1 of
Streptomyces olivaceoviridis and CBP21 of Serratia marcescens and to the cellulose-binding protein p40 of Streptomyces
halstedii. Furthermore, a short C-terminal fragment shows homology to a part of chitinase A of Vibrio
harveyi. The full-length 43-kDa protein could bind chitin and was thereby protected against the proteolytic activity
of elastase, whereas the degradation products did not bind chitin. The purified 43-kDa chitin-binding
protein had no staphylolytic activity, and comparison of the enzymatic activities in the extracellular medium
of a wild-type strain and a chitin-binding protein-deficient mutant indicated that the 43-kDa protein supports
neither chitinolytic nor staphylolytic activity. We conclude that the 43-kDa protein, which was found to be
produced by many clinical isolates of P. aeruginosa, is a chitin-binding protein, and we propose to name it CbpD
(chitin-binding protein D)
Combining fluorescent Pseudomonas spp. strains to enhance suppression of fusarium wilt of radish
Fusarium wilt diseases, caused by the fungus Fusarium oxysporum, lead to significant yield losses of crops.
One strategy to control fusarium wilt is the use of antagonistic, root-colonizing Pseudomonas spp. It has been
demonstrated that different strains of these bacteria suppress disease by different mechanisms. Therefore, application
of a mixture of these biocontrol strains, and thus of several suppressive mechanisms, may represent a viable
control strategy. A prerequisite for biocontrol by combinations of biocontrol agents can be the compatibility of
the co-inoculated micro-organisms. Hence, compatibility between several Pseudomonas spp. strains, that have the
ability to suppress fusarium wilt of radish, was tested in vitro on KB agar plates. Growth of P. fluorescens strain
RS111 was strongly inhibited by Pseudomonas spp. strains RE8, RS13, RS56 and RS158, whereas a mutant of
strain RS111 (RS111-a) was insensitive to inhibition by these strains. Strains RS111 and RS111-a only slightly
inhibited some other strains. Suppression of fusarium wilt of radish in a potting soil bioassay by the incompatible
combination of RE8 and RS111 was comparable to the effects of the single strains. However, disease suppression
by the compatible combination of RE8 and RS111-a was significantly better as compared to the single strains. In
contrast, the incompatible combination of RS56 with RS111 resulted in enhanced disease suppression as compared
to the single strains. Increased disease suppression by combinations of RS13 or RS158 with RS111 or RS111-a was
not observed. This indicates that specific interactions between biocontrol strains influence disease suppression by
combinations of these strains
Characterization of Arabidopsis enhanced disease susceptibility mutants that are affected in systemically induced resistance
In Arabidopsis, the rhizobacterial strain Pseudomonas fluorescens WCS417r triggers jasmonate (JA)- and
ethylene (ET)-dependent induced systemic resistance (ISR) that is effective against different pathogens.
Arabidopsis genotypes unable to express rhizobacteria-mediated ISR against the bacterial pathogen
Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) exhibit enhanced disease susceptibility towards
this pathogen. To identify novel components controlling induced resistance, we tested 11 Arabidopsis
mutants with enhanced disease susceptibility (eds) to pathogenic P. syringae bacteria for WCS417rmediated
ISR and pathogen-induced systemic acquired resistance (SAR). Mutants eds4-1, eds8-1 and
eds10-1 failed to develop WCS417r-mediated ISR, while mutants eds5-1 and eds12-1 failed to express
pathogen-induced SAR. Whereas eds5-1 is known to be blocked in salicylic acid (SA) biosynthesis,
analysis of eds12-1 revealed that its impaired SAR response is caused by reduced sensitivity to this
molecule. Analysis of the ISR-impaired eds mutants revealed that they are non-responsive to induction
of resistance by methyl jasmonate (MeJA) (eds4-1, eds8-1 and eds10-1), or the ET precursor 1-
aminocyclopropane-1-carboxylate (ACC) (eds4-1 and eds10-1). Moreover, eds4-1 and eds8-1 showed
reduced expression of the plant defensin gene PDF1.2 after MeJA and ACC treatment, which was
associated with reduced sensitivity to either ET (eds4-1) or MeJA (eds8-1). Although blocked in
WCS417r-, MeJA- and ACC-induced ISR, eds10-1 behaved normally for several other responses to MeJA
or ACC. The results indicate that EDS12 is required for SAR and acts downstream of SA, whereas EDS4,
EDS8 and EDS10 are required for ISR acting either in JA signalling (EDS8), ET signalling (EDS4), or
downstream JA and ET signalling (EDS10) in the ISR pathway
Micro-organismen beschermen planten tegen rupsenvraat
Samenvatting van de voordracht te houden op 30 november 2005 tijdens de Najaarsvergadering van de KNPV (Koninklijke Nederlandse Plantenziektekundige Vereniging). Onderzoek naar inductie van resistentie in Arabidopsis tegen vraat van rupse
Електродинамічні характеристики розподілено-зв'язаних діелектричних хвилеводів з екраном змінної провідності
Широке розповсюдження та використання, як окремих приладів так і елементної бази електроніки НВЧ, отримали хвилеводні системи із розподіленим зв‘язком. Найбільш відомими серед них є спрямовані
відгалужувачі, хвилеводно-пучкові перетворювачі, елементи сумарнорізнецевих перетворювачів сигналів, пристрої на базі планарних лінз Люненберга. Тому питання оптимізації вже відомих та пошук нових
способів керування міжхвилеводним розподіленим зв‘язком в таких системах є актуальними
Inibição da germinação de basidiósporos de Crinipellis perniciosa por compostos voláteis produzidos por cinco actinomicetos residentes de filoplano de cacaueiro
- …