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S Pennazio

Publications and source records attributed to S Pennazio.

At least 19 recordsLinked to original sources

The origin of modern plant virology.

Plant virology, born with Mayer's work, saw a first (embryonic) phase of development during two decades (1900-1920) with outstanding contributions from Dimitri Ivanovski, Martinus Beijerinck, Erwin Baur and Harry Allard. Between 1920 and 1930 a second phase saw the elaboration of surprising hypotheses concerning the enigmatic nature of viruses and experimental evidence of great stress was obtained. Revolutionary renewal began from the mid-1930s on the basis of a body of knowledge which was organically assembled into the first textbook of plant virology published by Kenneth Smith in 1933. In 1922, the geneticist Hermann Muller put forward the hypothesis that considered viruses as possible genes. The theory was resumed in an apparently independent way by Benjamin Duggar and Joanne Karrer Armstrong in 1923, who considered TMV a biocolloidal self-reproducing protein, like genes appeared to be. This hypothesis, even if neglected by virologists, anticipated by some decades the functional nature of viruses and represented the first conceptual response to virus enigma. Considerable experimental results were obtained by James Johnson, who showed that plants could be infected by different viruses and who introduced a first rational system of plant virus classification. Harold McKinney showed that TMV could mutate. Harold Storey, Kenneth Smith and Harry Severin demonstrated that several viruses could be transmitted by insects and supplied the first interpretation of the relationship between virus and insect. Mayme Dvorak and Helen Purdy obtained the first experimental evidence of the antigenic power of plant viruses. Virus purification, first tentatively accomplished with physical methods, was brilliantly performed by chemical means. Finally, Francis Holmes elaborated the first suitable test to estimate virus infectivity. The evolution of plant virology from an empirical discipline to a biological science took place thanks to the work of one group of American and English scientists who must be regarded as the fathers of modern plant virology.

History, 20th Century↗

A history of plant virology. Cross protection.

Cross protection is a type of induced resistance developing in plants against viruses. Its basis is that prior infection with one virus affords protection against closely related ones. Its history started about seventy years ago, when the Dutchman Thung and the Englishman Salaman described the phenomenon independently. During the 1930s, several virologists confirmed the discovery, which was considered the first possibility to protect plants against virus infection. Growing interest also led plant virologists to formulate the first hypotheses on its mechanism, with the onset of a still unsolved debate. The hypotheses, that have been succeeded until the 1970s, included (i) antibody formation, (ii) exhaustion of essential metabolites, (iii) limited sites for virus multiplication, and (iv) specific adsorption by new cell compounds. These hypotheses were re-proposed and discussed on several occasions without arriving at a final conclusion. The statement of molecular genetics of viruses produced new interesting "theories", fundamentally based on the interference between virus strains. A model developed by the Americans Palukaitis and Zaitlin in 1984 indicates that excess of progeny positive-sense RNA of the protecting strain would sequester the minus-strand RNA of the challenging strain. Other models involve a function of the coat protein, or gene recombination. However, no model that could unify all the various facets of cross protection has hitherto been proposed. All that has not stopped the phenomenon having practical application. From the first attempts against a severe disease of cocoa in West Africa realized by Posnette in the 1940s, a number of crops (such as tomato, tobacco, citrus, cucurbits, grapevine, soybean, papaya, and so on) have been submitted to this practice. During the 1980s, cross protection came to a standstill because of the development of new resistant or tolerant cultivars. Its story is by no means ended, and much work is needed to understand its limits and possibilities.

Botany↗

A history of plant virology. Mendelian genetics and resistance of plants to viruses.

Virology was borne at the end of the nineteenth century, some years before the re-discovery of the so-called "Mendel's Laws". The rapid development of genetics was helpful to horticulturists and plant pathologists to produce hybrids of important cropping species resistant to several virus diseases. The concepts of Mendelian genetics were applied to plant virology by Francis Oliver Holmes, an American scientist who must be considered a pioneer in several fields of modern plant virology. During the Thirties, Holmes studied in particular the hypersensitive response of solanaceous plants to TMV and discovered the N dominant gene of tobacco hypersensitive to this virus. After the Second World War, the theoretic and practical support given by geneticists assisted plant virologists in better understanding the mechanism of inheritance of the character "resistance". The major problems posed by breeding for plant resistance were detected and critically discussed in several reviews published between the Fifties and the Sixties. These results, together with the discovery of the genetic functions of RNA virus raised interest on the possible relations between viral and plant genes. This fundamental subject saw the entry into the virological scene of molecular genetics, and in 1970 the Russian virologist Joseph Atabekov introduced host specificity to viruses as a central point of plant virology. From the mid 1980s, this point attracted the interest of several virologists, and many results led to several theoretic models of genetic interactions between plant and virus products. In the last fifteen years, the introduction of transgenic plants has given a remarkable contribution to the question of host specificity, which, however, still awaits a general explanation.

Botany↗

Plasmodesmata and plant viruses. A centenary story.

The passage of plant viruses from a cell to adjacent ones remained for a long time an unexplained event. Only during the thirties did Samuel and other plant virologists put forward the hypothesis that the passage occurred through plasmodesmata, i.e. those protoplasmic connections between plant cells described since the late 19th century. A direct relation between viruses and plasmodesmata was first demonstrated by electron microscopy during the late 1960s by Esau and co-workers, and then widely confirmed. The mechanism of the passage was investigated in depth starting from the 1970s, and research received a remarkable impulse after that a well-defined model of plasmodesmata had been obtained thank, in particular, to work of the Robards' and Gunning's groups. In this context, the discovery of the polycystronic functionality of the viral genomes was fundamental. A protein coded by tobacco mosaic virus, discovered in 1982 independently by the Soviet group of Atabekov and the American group of Zaitlin, was demonstrated to be indispensable for the transport of virus infection from cell to cell through plasmodesmata. Elegant investigations on this 'movement protein' demonstrated that it actually increases the permeability of plasmodesmata. The relation between viruses and plasmodesmata is one of the most interesting and investigated theme of research, which is receiving much attention from plant virologists, physiologists and molecular biologists. The current status of knowledge still presents unsolved questions, and the story is far from over.

History, 20th Century↗

A short history of plant virology. III. The thirties.

The Thirties testified on the outstanding development of plant virology: the new discoveries formalized the concept of virus on a physicochemical background. Plant viruses, which had received their own taxonomical position at the end of the Twenties, were no longer considered as simple "infective pathogens" as their size, shape and chemical nature were determined, particularly for one of them--tobacco mosaic virus (TMV). This paramount contribution was achieved as a consequence of a functional interaction between biology on one side, and chemistry and physics on the other side, from the development of which molecular biology was born. The chemical characterization of TMV developed from the first determination of nitrogen presence in purified virus, performed by Carl Vinson, through the identification of TMV as Wendell Stanley's infective, autoreplicative protein macromolecule, to the final discovery of its nucleoprotein nature by the British group of Frederick Bawden. Thorough analytical techniques--in particular electron microscopy--led to disclose the exact shape and size of TMV particle. These discoveries, that opened a new era of virology, were corroborated by new knowledge that, although less explosive, can be considered of great importance for the development of plant virology. The methodologies to estimate viral activity; the study of the relationships between viruses and insect vectors; the studies on virus spread within plants; the identification of non-sterile type of resistance and of correlation between single plant genes and viral pathogenesis benefited plant virology of a set of knowledge that, together with the discoveries on the physico-chemical properties of TMV, raised plant virology from a secondary branch of plant pathology to a new independent science by itself.

History, 20th Century↗

Endogenous changes in citokinin activity in systemically virus-infected plants.

Viral diseases may alter cytokinin activity in plants, an effect associated with morphological and physiological changes. Experimental evidence indicates that the level of cytokinins may be both reduced or increased depending on different viral diseases. Circumstantial evidence suggests a change in virus-diseased plants showing specific alterations such as tumors and disorders in carbon partitioning and chlorophyll metabolism. The knowledge reached on cytokinin changes is not yet adequate to the importance of their role during viral pathogenesis. Furthermore, unclear results are available on the effect of cytokinins on virus replication. There is little information on how systemic virus infection alters cytokinin metabolism and no information on how this alteration can affect plant metabolism. Nevertheless, a possible control of some viral diseases by biomanipulation of plants to modify the endogenous levels of such hormone may be suggested, provided that higher levels of cytokinins do not increase the rate of virus replication.

Adenine↗

A short history of plant virology. II. The twenties.

Plant virology, born at the end of the last century, consolidated during the Twenties. Important new viral diseases were described and their causal agents partially purified and characterized not least because of the development of methods and techniques. An interesting debate concerned the so called "intracellular bodies", which were finally demonstrated to be aggregates of virus particles. Discoveries mainly arrived from experimental investigations on tobacco mosaic virus, and concerned the identification of strains, the demonstration of antigenic property, and the protein nature of viruses. A new concept of virus drew great advantage from the first attempts of classification and nomenclature, and a debate on the living or non-living nature of viruses, universally accepted as a new class of pathogens, was opened. The idea of viruses as self-reproducing particles was first advanced, although on a controversial basis. On the contrary, there was only erratic investigations on the physiological alterations produced by viral diseases in plants and on the relationships between viruses and vectors. In spite of this gaps, the Twenties must be mentioned as the years of the turning-point towards a biochemical concept of viruses, which will be achieved in the next decade.

Antigens, Viral↗

History of therapy of plant viral diseases.

Sixty years of therapy of virus-infected plants have been examined by analyzing the development of therapeutic techniques which have been successful, i.e. thermotherapy, chemotherapy and meristem tip culture. The reasons that gave rise to the practice of combining techniques have also been investigated. The results have only slightly improved our knowledge of virus biology, but have made possible the micropropagation of marketable virus-free germoplasm.

History, 19th Century↗

Plant hormones and plant virus diseases. The auxins.

Systemic virus infection impairs the steady state of auxin hormone in plant with consequent morphogenetic alterations. Most reports indicate a reduction of auxin activity in diseased plants, generally associated with stunting, but a substantial increase in auxin activity has sometimes been observed in cases of severe symptomatology. Treatments of virus-diseased plants with exogenous auxins may inhibit virus replication and reduce symptom severity, although results have been obtained by empirical application and must therefore be considered with caution. There is no information on how virus infection alters auxin metabolism or how this alteration affects both plant growth and development. The considerable progress reached in auxin biochemistry now allows more accurate re-investigations of this important relationship.

Indoleacetic Acids↗

The hypersensitive reaction of higher plants to viruses: a molecular approach.

The molecular basis of necrosis and localization, the two fundamental processes involved in plant hypersensitivity, are critically examined. Cell death, followed by visible necrosis, is discussed in relation to: (i) the role of wounding; (ii) the possible occurrence of signal molecules; (iii) the series of biochemical events leading to necrosis; and (iv) the events restricting the necrotic lesion within a limited area. Localization of virus infection is considered as a consequence of two events, (i) the synthesis of antiviral factors around the lesion, and (ii) the inhibition of the synthesis of the protein responsible for cell-to-cell spread of virus infection. The present knowledge, however, supplies only poor information on both the first events of cell-virus interaction and the chemical nature and role of putative signal molecules.

Cell Death↗

Two-dimensional polyacrylamide gel electrophoresis of extracellular soybean pathogenesis-related proteins using PhastSystem.

Acidic and basic pathogenesis-related proteins (PR-Ps) were extracted from the intercellular fluid (IF) of soybean leaves, locally infected with tobacco necrosis virus and showing necrotic local lesions. Proteins were detected by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) using PhastSystem and precast commercially available gels. Extracts from healthy leaves were run as controls. PR-Ps were first run under native PAGE conditions or isoelectric focusing (IEF), the gels stained with Coomassie Blue, then run under sodium dodecyl sulfate (SDS)-denaturing conditions and finally stained with silver. Ten major acidic PR-Ps were separated; their Mr's were close to those found by conventional PAGE. Their isoelectric points ranged from 3.5 to 5.0. Ten basic PR-Ps were separated and their Mr's estimated. None of these acidic or basic soybean PR-Ps was a glycoprotein. PAGE with PhastSystem and precast gels gives reliable results, comparable with those from conventional 2D-PAGE, with simpler experimental procedures. By electrophoresing Coomassie-stained gels with SDS in the second dimension, we were able to control the first-dimensional separation and to avoid laborious protocols generally adopted with unstained gels.

Electrophoresis, Gel, Two-Dimensional↗

Quantitative determination by ELISA of tobacco necrosis virus from necrotic local lesions in tobacco.

The amounts of tobacco necrosis virus antigen from necrotic lesions in tobacco leaves were estimated by ELISA. Less than 10% variation among different plates was obtained for the same sample placed in 3 wells randomly selected among the 60 internal wells of the plates, including in each test a dilution series of purified virus. Huxley's simple allometry equations y = bxm (y, absorbance; x, virus concentration) were calculated for each plate and gave reproducible results within a large range of virus concentration. The amount of viral antigen recovered from the necrotic centres of lesions was always significantly lower than those from the living tissues of the halo surrounding the centre. The serological activity recovered from both necrotic and halo tissues was not increased upon various treatments with disaggregating agents. During the continuous growth of the lesions the amounts of viral antigen extracted from the necrotic centre linearly decreased with time, suggesting virus degradation, whereas the amounts of antigen extracted from the living halo tissues increased with time, indicating that mechanisms of restricting viral spread and multiplication were not operating.

Antigens, Viral↗

Resistance to tobacco necrosis virus induced by salicylate in detached tobacco leaves.

Sodium salicylate reduced both the size and viral antigen content of non-self-limiting necrotic lesions produced by tobacco necrosis virus (TNV) in detached tobacco leaves during the partly localized reaction to virus. The antiviral effect of salicylate occurred at concentrations close to the limits of toxicity, and depended on the timing of administration. Both viral antigen accumulation and lesion size were strongly inhibited by a continuous supply of salicylate before or just after virus infection. Salicylate treatment did not prevent TNV accumulation when given after the establishment of infection or when arrested 24 h after TNV inoculation. Both procedures, however, did limit lesion enlargement. These results constitute a limit for the use of salicylate as a chemotherapeutic agent but do not exclude its use in limiting the pathogenetic effects of the virus. The salicylate treatments induced the formation of four pathogenesis-related proteins (PRs). The PRs formation was stimulated during the first 8 h of treatment and persisted for some time after the salicylate supply was discontinued. No correlation was found between the presence of PRs and the reduction of TNV accumulation: low salicylate concentrations (0.25 mM) inducing the formation of the PRs did not induce resistance against the multiplication and/or cell-to-cell spread of TNV.

Plant Viruses↗

Effects of monoparacoumarylputrescinium chloride on the hypersensitive reaction of Gomphrena globosa leaves to tomato bushy stunt virus.

Monoparacoumarylputrescinium chloride (pCPH), supplied to detached leaves of Gomphrena globosa via the petiole, induced interference with tomato bushy stunt virus infection by reducing the number and size of the necrotic local lesions. The phenolic compound neither inactivated directly the virus in vitro, nor induced interference when supplied just after virus inoculation, all this indicating an effect on cell metabolism. The interference was positively correlated to both pCPH concentration and time of induction (viz., the intervals between pCPH supply and inoculation). Coumaric acid did not, whereas putrescine, but not spermidine or spermine, did induce interference. Disc electrophoresis in polyacrylamide gels revealed no changes in the soluble protein constitution between pCPH-treated and control leaves.

Coumaric Acids↗