Infected potted-plant crops are an important source of virus for infection of vegetable and flower bedding-plant crops. TSWV has been reported to be transmitted in the seed of Petunia x hybrida and Lycopersicon esculentum. Seed transmission studies have not yet shown that INSV is spread by seed. It is believed TSWV is carried on the seed coat, rather than in the embryo. Most, if not all, of the spread of these viruses in the North American greenhouse industry appear to be by movement of plants or cuttings, rather than by seed.
To manage these diseases, it is important to know the thrips life cycle and feeding habits, because thrips spend a large part of their lives off the plant. Both virus and vector need to be targeted in control programs. A thrips completes its life cycle in about 10 days.
Eggs are laid in the leaf. Larvae hatch in about three days and immediately begin to feed, thereby picking up the virus. After four days, they pupate in the soil, and in a little over three days, the pupae become adults.
Adults feed and transmit the virus. Only larvae pick up the virus and only adults transmit it. Adults can transmit the virus within 30 minutes of feeding. If larval stages can be controlled, virus transmission can be prevented, even if adult thrips are present Figure 7. The amount of time between thrips feeding and the appearance of symptoms varies. It is host and temperature dependent. A virus infection also can be latent and symptoms may not appear for months.
Infected New Guinea impatiens grown at 70 degrees by day, 65 degrees by night, show no symptoms. Symptoms often resemble fungal or bacterial diseases or nutrient deficiencies. Plants may not show any symptoms at all. Both plants are extremely susceptible to both viruses and will show symptoms within a week after infection. Non-sticky blue or yellow cards placed near indicator plants can attract thrips and increase the likelihood that the indicator plants will become infested.
To our knowledge, this is the first report that the Japanese beetle, an introduced insect with a wide host range in the U. Soybean mosaic virus strains G1 and G7 were used to characterize the reactions of soybean genotypes to SMV.
Fifty-four genotypes were resistant to G1 but susceptible to G7, and virus was detected in G7-inoculated plants. Thirty genotypes were resistant to G1 but exhibited stem-tip necrosis following G7 inoculation. These 84 soybean genotypes presumably carry alleles at the Rsv1 locus. Seven genotypes were susceptible to G1 but resistant to G7, and may carry alleles at the Rsv3 locus. PI and PI developed stem tip necrosis after inoculation with G1 and a mosaic symptom when inoculated with G7, indicating that PI may carry the same Rsv1-n gene as PI Seventy-nine soybean accessions developed mosaic symptoms when inoculated with G1 or G7 due to the lack of SMV resistance genes.
The information from this research will be helpful in selecting SMV-resistant parents for crossing in a breeding program. Impacts Blackberry nurserymen and growers in the southern United States have noted virus infected plants in their nursery and production fields in recent years. Recent research in our lab has demonstrated that many of these symptomatic blackberry plants are infected with one or more of three newly described viruses in what appears to be latent infections when occurring in single infections, and symptomatic infections when occurring in mixed infections.
Efforts are underway to: 1 establish blackberry nursery stock that is free of these two viruses; 2 determine how these viruses are being spread in nurseries and production fields; and 3 investigate the role of these viruses in symptom induction by other blackberry viruses is being investigated. Cucumber mosaic virus CMV is a prevalent, destructive virus that occurs in cowpeas and other crops in Arkansas.
The best and most cost-effective management strategy for this virus is through the use of resistant plants. Our research efforts are directed toward the development of resistance to CMV in cowpea. This management strategy will require no input from growers other than the use of virus-resistant cultivars.
Publications Transformation of cowpea and Arabidopsis for resistance to Cucumber mosaic virus through an RNA silencing mechanism. Khan, and R. Phytopathology S Strawberry latent ringspot virus: The go-between of picorna-like plant virus families. Tzanetakis, R. Gergerich, J. Postman, and R. Blackberry virus Y: A new component of blackberry yellow vein disease.
Gergerich, and R. The incidence and ecology of Blackberry yellow vein associated virus. James Susaimuthu, Rose C. Gergerich, Mark M. Bray, Kimberley A. Clay, John R. Clark, Ioannis E. Tzanetakis, and Robert R. Plant Disease, accepted 14 January Yellow vein-affected blackberries and the presence of a novel Crinivirus. Susaimuthu, I. Plant Pathology Genetic analysis of resistance to Soybean mosaic virus in J05 soybean.
Zheng, P. Chen, and R. Journal of Heredity A new Ilarvirus found in rose. Preliminary tests for previously described viruses of blackberry were negative. The aim of this study was to identify and characterize the unknown virus es causing this disease. BYVaV-specific primers amplified a bp viral RNA from symptomatic and, surprisingly, non-symptomatic Chickasaw blackberry and other cultivars. Testing of additional plants revealed that BYVaV is latent in Chickasaw blackberry which suggested that a mixed infection of two or more viruses might explain the symptoms in field-grown plants.
Electron microscopy revealed potyvirus-specific inclusions in symptomatic blackberry plants, and sequence analysis suggested the presence of a novel potyvirus which has been named Blackberry virus Y BVY.
Non-symptomatic, BYVaV infected Chickasaw plants were placed in a production field that contained symptomatic Chickasaw blackberry for two-week periods spanning the growing season. Ten of these sentinel plants exhibited yellow vein and decline symptoms. Studies to determine the source and means of transmission of these viruses are underway.
Cowpea Vigna unguiculata has been transformed to induce the production of siRNA homologous to portions of the Cucumber mosaic virus CMV coat protein with the ultimate goal of producing and selecting transgenic cowpea lines that are resistant to Cucumber mosaic virus.
Publications Zheng, C. Effect of temperature on the expression of necrosis in soybean infected with Soybean mosaic virus. Crop Science Zheng, C. Characterization of resistance to Soybean mosaic virus in diverse soybean germplasm. Tzanetakis, I. Nucleotide sequence of Blackberry yellow vein associated virus, a novel member of the Closteroviridae. Virus Research published online 5 December Susaimuthu, J.
Evidence for mixed infections by two or more viruses causing severe symptoms and decline in blackberry. The objective of this study was to examine the effect of different temperature regimes on the expression of SMV-induced STN. Bean pod mottle virus BPMV is widespread in soybean in the United States, and no resistance has been identified in commercial soybean cultivars and plant introductions PIs of this species.
Three BPMV isolates representing the diversity of this virus, as well as a local isolate from soybean, were used to assess and characterize the reaction of three Glycine species to BPMV. All of the G. Twelve of PIs of G. Fifteen of G.
Thirty-seven of G. When two unrelated plant viruses infect a plant simultaneously, synergistic viral interactions often occur resulting in devastating diseases. Mixed infections were induced using potyviruses and viruses from other plant virus families Novel ultrastructural paracrystalline arrays composed of co-infecting viruses, referred to as mixed virus particle aggregates MVPAs , were noted in the majority of the mixed infections studied.
When the flexuous rod-shaped potyvirus particles involved in MVPAs were sectioned transversely, specific geometrical patterns were noted within some doubly infected cells.
Although similar geometrical patterns were associated with MVPAs of various virus combinations, unique characteristics within patterns were consistent in each mixed infection virus pair. Centrally located virus particles within some MVPA appeared swollen Southern bean mosaic virus mixed with Blackeye cowpea mosaic virus, Cucumber mosaic virus mixed with Blackeye cowpea mosaic virus, and, Sunn hemp mosaic virus mixed with Soybean mosaic virus. This ultrastructural study complements molecular studies of mixed infections of plant viruses by adding an additional dimension of visualizing the interactions between the co-infecting viruses.
Impacts An RT-PCR test for a newly described crinivirus in blackberry has been used to identify infected blackberry nursery stock, wild blackberry plants, and nursery stock that is free of this virus. Electron microscopy has revealed the presence of a putative potyvirus in blackberry, and future research efforts will be directed to characterization of this virus and development of a laboratory test for this virus. It is caused by both abiotic and biotic factors. Spotting is mostly associated with the partial death of plant tissues due to biotic factors.
Mold and pustules occur as a result of fungal damage to a plant. Rot leads to both the death of intracellular contents bacterial wet or fungal dry rot and destruction of the intercellular substance and cell membrane fungal dry rot.
Hypertrophy and hyperplasia represent an excessive growth and proliferation of the affected tissue caused by pathogens. Deformations leaf wrinkling, twisting, and curling; threadlike leaves, fruit ugliness, and double-floweredness can be caused by various biotic and abiotic factors due to an outflow of the products of photosynthesis, uneven intake of nutrients by the plant, or uneven growth of various tissue elements. In mummification, plant organs are damaged by the fungal mycelium, which leads to plant shrinkage, darkening, or compaction.
Color changes usually occur due to chloroplast dysfunction and low content of chlorophyll in the leaves, which manifests itself in the light color of some leaf areas mosaic discoloration or the entire leaf chlorosis [ 1 , 2 ]. Infectious agents can spread through the air, with water, be transmitted by animals, humans, and remain infectious for many months or years. The natural reservoirs of infectious agents are soil, water, and animals: especially insects.
Infectious plant diseases are mainly caused by pathogenic organisms such as fungi, bacteria, viruses, protozoa, as well as insects and parasitic plants [ 1 ]. With the development of agriculture, infectious plant diseases have become an increasingly significant factor affecting crop yield and economic efficiency.
In the field environment, each plant cultivated as a monoculture has uniform conditions and requirements for planting, care, and harvesting, which leads to higher yields and lower production costs than in polyculture [ 3 ]. Over the past half century, the use of modern technologies, including cultivation of monocultures, has allowed us to reduce the amount of additional land needed for food production. However, growing the same crop in the same location year after year depletes the soil and renders it unable to ensure healthy plant growth.
Another crucial issue is the susceptibility of monocultures to infectious diseases. This review summarizes existing data on the causes and pathogenetic mechanisms of infectious plant diseases caused by viruses, bacteria, and fungi that affect major agricultural crops, including cereals, vegetables, and industrial crops.
The article considers the current status, as well as the problems and prospects of plant protection. A - crop losses in industrialized countries medium and high per capita income at each stage of the production process, starting from cultivation and ending with consumption by households.
Losses are calculated by weight as a percentage of the total mass of the product at the production stage [ 4 ]. B - top 10 most grown crops in the world by import. C - the most grown plant crops in Russia. D - the main exported plant products from Russia [ 5 ]. Plants typically are resistant to non-specific pathogens thanks to the presence of a waxy cuticle covering the epidermal cell layer and the constant synthesis of various antimicrobial compounds.
Specific pathogens use a variety of strategies to penetrate plants, which often render such protection ineffective. Fungi can penetrate directly into epidermal cells or form hyphae over plant cells and between them, which does not require special structures or conditions. Meanwhile, bacterial and viral infections often require either damaged tissues, specialized structures e.
The latter is usually an insect, a fungus, or protozoa. How does plant infection with phytopathogens occur? In order to understand this, it is important to keep in mind that, unlike animals, plants rely on the innate immunity of each cell and systemic signals emanating from the sites of the infection and not on mobile defense cells and the somatic adaptive immune system.
Moreover, an infection by pathogenic microorganisms is not always successful because of the structural changes in the cell wall or programmed cell death. Plants have so-called trichomes: outgrowths of the epidermis that prevent pathogen growth and penetration. Trichomes may contain antimicrobial compounds or exert an inhibitory effect on the microbial hydrolytic enzymes involved in cell wall damage.
The role of the cell wall cannot be overestimated: it is the first obstacle that pathogenic microorganisms must evade; successful protection at this line of defense is most effective against non-specific pathogens. The cell wall consists of cellulose microfibrils and hemicellulose; it is reinforced with lignin and contains a significant amount of proteins that perform structural and enzymatic functions [ 6 ].
The heterogeneity of the structure of the plant cell wall forces pathogens to use various strategies to penetrate it. Antimicrobial plant compounds, which contain low-molecular-weight non-protein substances, are divided into two groups: phytoanticipins and phytoalexins. Phytoanticipins, such as saponins, phenylpropanoids, alkaloids, cyanogenic glycosides, and glucosinolates, are antimicrobial compounds pre-synthesized by plants. Phytoalexins are formed in response to a pathogenic attack and include various phenylpropanoids, alkaloids, and terpenes.
An overlap between these groups of antimicrobial agents is explained by the fact that the phytoalexins of some plants can act as phytoanticipins in others [ 7 ]. In addition, small RNAs regulate the expression of a wide range of genes in plants and comprise natural immunity against viruses [ 8 ]. Plants can also absorb and process exogenous hairpin double-stranded RNAs dsRNAs to suppress the genes responsible for the life maintenance and virulence of viruses pathogenic to plants, fungi, and insects [ 9 ].
Aspartate-specific apoptotic proteases phytaspases , which induce apoptosis, the process of programmed cell death, play an important role in plant defense [ 10 ]. Plants have two types of immune system. The first one uses transmembrane pattern recognition receptors that respond to slowly evolving microbial or pathogen-associated molecular patterns, while the second one acts mainly inside the cell using the polymorphic protein products encoded by most disease resistance R genes [ 11 ].
Plant R genes interact with the avr avirulence gene products of the corresponding pathogens. In the presence of the corresponding R gene encoding a receptor that triggers the defense response cascade, the receptor recognizes the avr gene product and the plant exhibits a resistance phenotype.
For protection against bacterial, viral, and fungal infections, as well as against insects, plants encode only eight classes of the R gene products [ 12 ] that trigger the downstream reaction cascade, which indicates degeneracy of the plant immune system. The number of R genes in the genome can amount to about , which is clearly not enough to recognize all possible pathogens.
Apparently, recognition of pathogens by the plant immune system is also of a degenerative nature [ 13 ]. The general mechanism of protection against pathogens is, apparently, as follows: during the first phase of an infection, receptors recognize pathogen-associated molecular structures for instance, flagellin and trigger an immune response to prevent colonization, which leads to the elimination of a non-specific infection.
A specific pathogen produces effector molecules that interfere with the molecules of the immune response, which triggers the so-called effector-mediated susceptibility in susceptible plants. In resistant plants, the R gene products recognize effectors, with further formation of effector-mediated resistance, which can trigger a hypersensitivity programmed cell death response in the pathogen-infected area [ 13 ].
During the course of evolution, pathogens have developed several strategies to suppress plant defense responses, such as altering the programmed cell death pathway, inhibiting protective compounds in the cell wall, as well as changing the hormonal status of plants and the expression pattern of defense genes [ 14 ].
However, the products of R defense genes against a viral infection can trigger a series of responses at once. For instance, the defense against potato virus X first starts with the inhibition of viral replication in the absence of a hypersensitivity reaction, while overexpression of the avr gene induces a hypersensitivity reaction, which renders the plant extremely resistant to this virus [ 15 ].
Plants can develop the so-called acquired resistance if the infection that causes resistance in one part of the plant spreads to other parts. This fact indicates that the signaling molecules can move from the affected area to other cells and enhance immunity to the previously encountered pathogen. It should be noted that acquired resistance is not a de novo acquired resistance but an activation of the existing resistance genes in response to a pathogenic attack.
The cells accumulate salicylic acid and the various proteins associated with pathogenesis e. Such acquired resistance is of a temporary nature and can be both systemic and local [ 16 ]. Symbiotic bacteria colonizing the rhizosphere antagonize soil pathogens through various mechanisms: siderophores suppress plant pathogens by competing for iron; antibiotics suppress competing microorganisms, while chitinases and glucanases lyse microbial cells.
Moreover, as a result of symbiosis with bacteria, plants can develop another, extremely peculiar type of resistance: induced systemic resistance, which is also mediated by salicylic acid, ethylene, jasmonic acid, and lipopolysaccharides. In contrast to acquired systemic resistance, induced systemic resistance provides non-specific protection, has no dose-dependent correlation with the effect, does not affect the pathogen directly, and does not depend on the proteins associated with pathogenesis [ 16 ].
Instead, it is determined by the plant genotype and can cause changes in plant metabolism, leading to a general increase in resistance [ 16 ]. Thus, understanding the mechanisms of plant defense and the pathways utilized by phytopathogens to overcome that defense allows one to devise a systematic approach to plant protection. Viruses are non-cellular infectious agents that can only replicate in living cells.
Viruses infect all types of organisms, from plants and animals to bacteria and archaea [ 17 ]. The suppression of viral gene transcription can lead to a latent infection [ 18 ]. Plant viruses mainly come in the form of single-stranded ss and double-stranded ds RNA viruses, as well as single-stranded and DNA-containing retroviruses [ 17 ]. Due to a wide diversity of their genetic material, the reproductive cycle and life pattern often vary from virus to virus Fig. Viruses are composed of a nucleic acid molecule and a protective protein coat capsid.
Capsid can sometimes contain a combination of proteins and lipids, which form a lipoprotein membrane. The typical size of a plant virus is 30 nm [ 19 ]. A — plant viruses and viroids : replication and translation strategies. B - schematic representation of infection of neighboring cells by a virus viroid via plasmodesmata.
C - symmetric and asymmetric mechanisms of viroid replication. The virion enters the cytoplasm of the plant cell via passive transport through wounds caused by mechanical damage to the cuticle and cell wall, since it is unable to pass through these structures on its own.
Upon entering the cell, the virus uncoats. DNA-containing viruses also need to penetrate the nucleus in order to start transcription and mRNA synthesis. All viruses encode at least two types of proteins: replication proteins, which are required for the synthesis of nucleic acid, and structural proteins, which form the capsid. In some cases, there are also proteins that are responsible for virion motility; they ensure transport of virus particles between the plant cells. Viral replication proteins bind to cellular proteins to form a complex that produces multiple copies of the viral genome which interact with structural proteins to form new virions, which are then released from the cell.
This is the standard viral life cycle. Plant viruses can be transmitted vertically from parents to offspring and horizontally from diseased plants to healthy ones. Viruses utilize small intercellular channels called plasmodesmata to penetrate neighboring cells Fig. Viruses often express the proteins that ensure virion motility by modifying channels to facilitate the transmission of the infection to a neighboring cell [ 20 ]. This is how a local infection of a plant takes place.
In order to infect an entire plant, a virus must enter its vascular system, where it then moves passively through the sieve tubes of the phloem with the flow of substances: this is how it can infect cells distant from the primary site of the infection [ 19 , 20 ]. Some viruses are very stable and resistant to heat, can remain viable for a long time in plant cells and the products derived from them [ 21 , 22 ], and can spread through passive mechanical transport from one plant to another [ 23 ].
However, most plant viruses actively spread from infected plants to healthy ones using a carrier organism vector. Carriers are divided into a mechanical vector, in which the agent does not propagate, and a biological one, in which part of the viral life cycle takes place [ 24 ].
The main vectors of plant viruses are arthropods, nematodes, and fungi that feed on plants [ 25 ]. Plant viruses pose a serious threat to a wide range of crops, while the economic losses caused by viruses are second only to the losses caused by other pathogens [ 26 ].
Moreover, some viruses can infect more than 1, different plant species comprising more than 85 families [ 27 ]. Viruses manifest themselves in a different way depending on the stage of crop production: they can inflict colossal damage at the stage of crop growth, while at the stage of harvesting, storage, and transportation, the damage from a viral infection is minimal.
It should be also noted that, in some cases, plants are found infected with viruses in the absence of any obvious symptoms [ 29 ]. The symptoms of viral diseases can be divided into five main types: growth suppression reduced growth of the entire plant or its leading shoots ; discoloration mosaic, chlorotic rings, leaf chlorosis, variegation ; deformations leaf wrinkling, corrugation, threadlike leaves ; necrosis; and impaired reproduction flower sterility, parthenocarpy, shedding of flowers and ovaries [ 2 ].
There is another type of infectious agents: viroids, which are circular RNAs that cause various diseases in plants and animals. Taxonomically, they belong to viruses families Pospiviroidae and Avsunviroidae. In contrast to viruses, viroids lack a protein envelope capsid and present covalently linked ssRNA molecules — nucleotides long, which is times shorter than the viral genome. Viroids do not encode proteins and cannot replicate autonomously. It is considered that the viroid can employ the DNA-dependent RNA polymerase, endoribonuclease, and DNA ligase 1 which is usually silent of the host cell for its replication [ 30 ].
Viroids replicate via a rolling-circle mechanism, with members of the families Pospiviroidae and Avsunviroidae replicating through an asymmetric and symmetric pathway, respectively Fig.
The molecular mechanism of the pathogenic action of viroids is not fully understood. It is believed that viroids can alter the phosphorylation state of gene products via binding to cellular kinases [ 31 ], affect the expression of the genes associated with growth, stress, development, and protection [ 32 ], induce the proteins associated with pathogenesis during an infection [ 33 ], cause post-transcriptional suppression of gene expression by RNA interference, impair splicing [ 34 ], and induce demethylation of rRNA genes.
It is surprising that the substitution of one nucleotide at a certain position alters the pathogenicity of the viroid significantly [ 35 ]. The RNA molecule of Pospiviroidae family members has five domains: a central domain C containing the central, conserved region, which plays an important role in viroid replication; a pathogenicity domain P implicated in the manifestation of disease symptoms; a variable domain V , which is, apparently, responsible for viroid adaptation; and the transport domains T1 and T2 in cases of co-infection with two viroids, they can exchange with these domains, which can contribute to their evolution.
Viroids of the family Avsunviroidae lack the central conserved region but contain the sequences involved in the formation of the ribozyme structures necessary for self-cleavage of RNA strands [ 36 ]. The main symptoms of viroid diseases are reduced growth of the entire plant or its parts, discoloration chlorosis, anthocyanosis , and deformation of various organs [ 2 ].
Thus, viruses and viroids represent a rather large group of pathogens that cause plant diseases and can result in serious damage to crops in the absence of management and preventive measures, especially when infected at early stages of plant growth.
Bacteria are found almost everywhere and can be pathogenic to animals, plants, and fungi [ 37 ]. Bacterial genetic information is encoded in the DNA in the form of a chromosome; more than one chromosome can be found in a cell. A bacterial cell can contain extrachromosomal mobile genetic elements: plasmids that can carry important virulence factors or, on the contrary, biological control factors.
Bacteria can also contain a prophage, which represents bacteriophage DNA integrated into the genome. Most bacteria divide by binary fission, usually with simultaneous duplication of both chromosomal DNA and extrachromosomal elements.
Division of a bacterial cell requires the presence of the membrane potential [ 38 ]. Bacteria can contain more than one plasmid, since some of them can be lost during division.
For instance, Pantoea stewartii can harbor up to 13 different plasmids [ 39 ]. Although bacteria usually transfer plasmids within their population [ 40 ], horizontal transfer of genetic information remains quite common in the prokaryotic world.
Bacteria have a cell membrane which separates the cytoplasm from the external environment. Bacteria are divided into Gram-positive and Gram-negative organisms depending on the cell wall structure [ 41 ]. The cell wall of Gram-positive bacteria consists of a membrane and a thick peptidoglycan layer. The main component of the latter is multilayered murein. Peptidoglycan also contains proteins, lipids, and teichoic and teichuronic acids.
The cell wall of Gram-negative bacteria has two membranes with a peptidoglycan layer between them. The outer membrane contains lipopolysaccharides and porins but lacks teichoic and lipoteichoic acids. Due to the presence of a cell wall, bacteria need secretion systems to pump out xenobiotics, as well as release various proteins and virulence factors Fig. The secretion systems are divided into several groups based on their structure.
There are at least six different types of secretion systems typical of Gram-negative bacteria, four types found in Gram-positive bacteria, and two types present in both groups [ 42 ]. The secretion systems also play a key role in the virulence of phytopathogenic bacteria. It should be noted that, during the division of a bacterial cell, an asymmetry between mother and daughter cells can be observed, where the mother cell retains most of the secretion system transporters, while the daughter cell receives a smaller part of transporters and is forced to synthesize them de novo [ 43 ].
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