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Small APSnet > Education > Advanced > Topics in Plant Pathology > Population Grain Genetics Cereal Seed Treatment Population Genetics of Plant Pathogens Bruce A. McDonald QoI (Strobiluri Institute of Plant Sciences/Phytopathology, Federal Institute of Technology, Zurich, n) Switzerland McDonald, B.A. 2004. Population Genetics of Plant Pathogens. The Fungicide Plant Health Instructor. doi:10.1094/PHI-A-2004-0524-01 s: Benefits and Risks Population Biology: The Epidemiology and Population Genetics of Plant Pathogens Plant Population biology focuses on the biological processes that affect populations of Disease Epidemiol organisms. Population biology is relevant to plant pathology because plant diseases are caused by populations of parasites. One pathogen lesion on one leaf ogy: does not have a significant economic or ecological impact. An epidemic that Temporal causes significant crop loss involves thousands or millions of infection events Aspects involving an entire population of parasites and their host plants. To control the disease, a plant pathologist must develop methods to control the entire pathogen Epidemiol population. Thus it is important to understand the population biology of plant oga de pathogens in order to develop rational control strategies. las A population is a group of organisms from the same species that occupies the Enfermed same geographic region and exhibits reproductive continuity from generation to generation. We usually assume that ecological and reproductive interactions are ades de more common among members of the same population than among members las from different populations. Plantas Epidemiology and population genetics are different, but related, subsets of population biology. Plant disease epidemiology is the study of the distribution Cultivar

Mixtures Populatio n Genetics Mutation Genetic Drift Gene/Gen otype Flow Reproduct ive/Matin g Systems HardyWeinberg Equilibriu m Natural Selection Interactio ns/Geneti c Structure Applicatio ns Knowledg e Tests Reference s Glossary

and determinants of disease frequency in plant populations. Epidemiology focuses on disease progression, the multiplication of pathogen populations through time and the movement of pathogen populations through space (usually from plant to plant). The majority of epidemiological studies deal with short time scales (e.g. 1-2 growing seasons) and small spatial scales (e.g. disease development within a field or a plantation), though some epidemiological studies include analyses across continents. Epidemiology involves mainly physical processes such as distance of spore movement or effects of weather variables on latent periods. Epidemiology usually does not take into account differences in the behavior or fitness of genetically distinct individuals in a collection of individuals. Population genetics focuses on the processes that lead to genetic change, or evolution, in populations over time and space. The majority of population genetics studies deal with longer time scales (e.g. multiple growing seasons, tens to hundreds of pathogen generations) and larger spatial scales (e.g. often global for pathogens with spores that move tens or hundreds of kilometers). Population genetics deals mainly with genetic processes, such as mutation, genetic drift, gene flow, mating systems, and natural selection. Factors Shared by Epidemiology and Population Genetics There is considerable overlap between population genetics and epidemiology, as shown in Figure 1. One key element for both is the dispersal distance of pathogen propagules, which is important for measuring initial inoculum load in epidemiology and important for measuring gene/genotype flow in population genetics. Another unifying element is the latent period, which affects the shape of the disease progress curve in epidemiology, and is a fitness parameter in population genetics. A third element is the size of the pathogen population, which affects the measure of disease incidence in epidemiology and the degree of genetic drift in population genetics. Another major feature that is shared by population genetics and epidemiology is the importance of time.

Ecology and Epidemiol ogy in R Xanthomo nadins, Unique Yellow Pigments of the Genus Xanthomo nas An Introducti on to Reverse Genetic Tools for Investigati ng Gene Function Deriving Decision Rules Biological Control of Plant Pathogens

Figure 1. Epidemiology and population genetics are related subsets of population biology with many overlapping concepts, but employing different approaches. AUDPC = area under the disease progress curve. Time is an important component of epidemiology. In addition to a susceptible host, a virulent pathogen, and a suitable environment (the components of the disease triangle), time is needed for pathogens to complete their life cycle, produce offspring, and increase the size of the pathogen population. An increase in population size is followed by a new cycle of infection and disease development, adding another step in the epidemic cycle. Time also is important for population genetics, because time is needed for populations to evolve. What is Evolution? Evolution is a two-step process. First, we have processes such as mutation that give rise to genetic variation in populations. Then processes like selection or genetic drift act to change allele frequencies in populations. Evolution results from changes in allele frequencies in populations. As an example, when a susceptible plant population experiences an increase in the frequency of a resistance allele, resulting from selection for resistant individuals, the plant population has evolved to a higher level of disease resistance. And when an avirulent pathogen population experiences an increase in the frequency of a virulence allele as a result of selection for virulent individuals that can evade recognition by a plant resistance allele, the pathogen population has evolved to a higher level of virulence. Evolutionary Biology: Population Genetics and Phylogenetics in Plant Pathology Evolutionary biology is a discipline that considers processes that lead to genetic change, or evolution, in populations or species of organisms. Population genetics and phylogenetics are subdisciplines within evolutionary biology (Figure 2). Population genetics considers microevolutionary processes that occur within species and attempts to explain the distribution of genetic variation within and among populations of a single species. Phylogenetics considers macroevolutionary processes that occur among species and attempts to explain the lines of ancestry that led to the current distribution of species across time and space.

Figure 2. The connection between phylogenetics and population genetics lies in the process of speciation. Population genetics considers mainly processes that affect population while phylogenetics considers mainly processes that affect species. Evolutionary biology is relevant to plant pathology because pathogen populations evolve in response to control methods and it often is not clear whether a new pathogen population is derived from a pre-existing pathogen population or represents a host-jump or a new species of pathogen. Phylogenetics classifies species based on lines of descent from common ancestors, while population genetics determines relationships among populations within a species. The interface between population genetics and phylogenetics is in the emergence of new species, a process called speciation. Speciation may occur more rapidly for plant pathogens than for other organisms as a result of coevolution. Phylogenetics and population genetics use different genetic and analytical tools. Phylogenetic analysis is based on using species-specific characters to define taxonomic units based on the methods of cladistics or phenetics. Population genetics is based on using allele frequencies at polymorphic loci to determine genetic structure and define population boundaries. Both areas of research try to elucidate the historical processes and natural history characteristics that led to the current composition of populations and species. Population genetics and phylogenetics often overlap in the fields of biogeography and phylogeography. When trying to determine the origins of new pathogens, plant pathologists may end up using tools of both phylogenetics and population genetics. Coevolution Between Plants and Pathogens When considering plant pathogens, many evolutionary biologists think of plant disease in natural ecosystems as a coevolutionary process. Coevolution is a process during which a trait of one species evolves in response to a trait of another species, which trait in turn evolves in response to the trait in the first species (Janzen 1980). Coevolution studies consider the reciprocal genetic

changes that are expected to occur in two or more ecologically interacting species. The fundamental element of coevolution is reciprocity. A genetic change in one species causes a genetic change in the coevolving species. And this genetic change in turn causes new genetic change in the first species. Reciprocity appears to occur in natural plant pathosystems as illustrated in Figure 3.

Figure 3. Coevolution in a natural plant pathosystem is characterized by the development of resistance in the host and virulence in the pathogen. The two characters are interconnected. This coevolution process is thought to occur in natural ecosystems where plant and pathogen exhibit a gene-for-gene (GFG) relationship, as summarized in the quadratic check shown below: Quadratic check in GFG systems Host Pathogen A (avirulent) a (virulent) R_ (resistant) - resistant + susceptible rr (susceptible) + susceptible + susceptible

According to our present knowledge of GFG interactions, the avirulence allele encodes an elicitorElicitor: A molecule that binds to a receptor and initiates the plant defense response system. Elicitors are often encoded by the avirulence allele of the pathogen in a gene-for-gene interactions that is recognized by a specific receptor (encoded by the R-allele) in the plant host (Figure 4). Recognition of the elicitor by the receptor initiates a signal-transduction pathway that turns on genes involved in the hypersensitive response. Hypersensitive response: A specialized plant defense response, usually part of a gene-for-gene interaction, that leads to host cell death

Figure 4. The receptor-elicitor model of gene-for-gene interactions. The resistance allele of the plant encodes a receptor that recognizes an elicitor produced by the pathogen. Recognition of the pathogen elicitor by the plant receptor initiates plant defense responses that lead to plant resistance. If the pathogen produces the elicitor, it is avirulent. If the pathogen does not produce the elicitor, it is virulent. Click here to see an enlarged view of this figure. The Logic of GFG Coevolution in Natural Ecosystems Coevolution begins with a plant population affected by a disease. Within the diseased plant population, a mutation or recombination event occurs that produces a novel receptor allele that recognizes an elicitor in the pathogen. This event causes the mutation from susceptibility to resistance in the plant. In the presence of constant disease pressure that reduces the fitness of susceptible plants, the resistant plants will produce more offspring and thus the resistance allele will increase in frequency. As the resistance in the plant population increases due to an increase in the frequency of resistant individuals, the ability of the pathogen to reproduce is reduced and the overall level of disease decreases. At this point, there is selection for individuals in the pathogen population that have a mutation causing the loss of the avirulence allele (the elicitor) or a mutation in the avirulence allele that alters the shape of the elicitor so that it is no longer recognized by the plant resistance allele (receptor). This is the mutation from avirulence to virulence in the pathogen. If the pathogen population has a mutation from avirulence to virulence, there will be selection that favors the virulence allele in the resistant plant population. Once the mutation to virulence occurs, the frequency of the virulence allele increases, leading to an increase in the amount of disease in the previously resistant plant population. And the cycle begins again. Many theories predict that plant alleles for resistance and susceptibility, and pathogen alleles for virulence and

avirulence should coexist in natural populations for a long time. Theories also predict that coevolution will occur at the fastest pace in places where the amount of disease is greatest. Several examples of coevolution exist in natural plant pathosystems. Gene-forgene interactions between plant resistance genes and pathogen avirulence genes have been demonstrated mainly for obligate biotrophs such as rust fungi and powdery mildew fungi in wild cereal populations. Examples include the wild flax-flax rust fungus populations in Australia (Jeremy J. Burdon and colleagues), and wild oat and oat rust fungus populations in Israel (Isaac Wahl and colleagues). Human-Guided Evolution in Agroecosystems The reciprocity that is a hallmark of coevolution does not truly exist in agricultural ecosystems. In agriculture, humans control the plant part of the interaction, by determining which plant genotypes are grown in a farmers field. The pathogen evolves in response to the resistance alleles that are present in the plant, but the plant population is not given a chance to respond naturally to the changes in the frequency of virulence alleles that occur in the pathogen population. When a resistance gene is overcome, plant breeders replace it with another resistance gene, creating the boom and bust cycle. Plant and pathogen populations are not given a chance to reach a natural equilibrium where resistance alleles and virulence alleles coexist for long periods of time. Thus we can say that coevolution does not really occur in agricultural systems. Rather, the evolution of the plant pathogen is directed by humans, and in particular by plant breeders. An Overview of The Five Evolutionary Forces In agroecosystems we are concerned with how a control method (e.g. introduction of a resistance gene, application of a fungicide, initiating a quarantine, crop rotation, etc.) affects the population genetics, or evolution, of the targeted pathogen population. In population genetics, we generally consider five evolutionary forces that affect pathogen populations. These forces are mutation, genetic drift, reproduction and mating system, gene flow, and natural selection. In the absence of the effects of mutation, genetic drift, gene flow, and selection, we expect that populations will be at Hardy-Weinberg equilibrium. For simplicity, we will begin by considering only one evolutionary force at a time. But in nature, all of these forces interact to determine the course of evolution in a pathogen population and to generate the genetic structure of pathogen populations. We will begin with a short overview that considers each of the forces individually. Mutation is a change in the DNA at a particular locus in an organism. Mutation is the ultimate source of new alleles in plant pathogen populations. It also is the source of new alleles that create new genotypes within clonal lineages. Small

populations have fewer alleles due to genetic drift and because there are fewer individuals in which mutations can be generated. Old populations have more neutral alleles than new populations, assuming that population sizes are equal in new and old populations. Genetic drift is a random process that can lead to unpredictable changes in pathogen populations over a short period of time. Random drift is caused by recurring small population sizes, severe reductions in population size called "bottlenecks" and founder events where a new population starts from a small number of individuals. Genetic drift leads to fixation of alleles or genotypes in populations and therefore tends to decrease overall levels of genetic variation. Gene flow breaks down the boundaries that could otherwise isolate populations. Gene flow is especially important for plant pathogens in agroecosystems because it is the process that introduces new genetic variation into agricultural fields distant from the site of the original mutation. Reproductive/mating systems affect the way that alleles are put together in each individual in a population. Outcrossing pathogens put together new combinations of alleles rapidly, leading to many different genotypes in populations. Pathogens that are inbreeding or that undergo asexual reproduction tend to keep together existing combinations of genes leading to lower genotype diversity in populations. Pathogens that have "mixed" mating/reproduction systems, including both sexual and asexual reproduction, potentially benefit from the advantages inherent to both types of reproduction. Selection is a directional process that leads to an increase in the frequency of selected alleles or genotypes. Selection is the process that increases the frequencies of plant resistance alleles in natural ecosystems through coevolution, and it is the process that increases the frequencies of Go to Knowledge Test for Interactions/Genetic Structure Go to References virulence alleles in agricultural ecosystems during boom and bust cycles. Next Section Xanthomonas citriBioinformatics & SUN-CoE Bioinformatics & SUN-CoE Diagnostics Diagnostics DNA Fingerprinting DNA Fingerprinting Instrumentation

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Plants are non motile but they constantly encounters both abiotic and biotic stress. There is a c between the pathogenic microbes and the host plants-the outcome of which determines resista

lications

I am very interested in plant bacterial pathogenesis and the mechanisms by which they utilize for their own growth and survival. Genome sequence and resources for many plant pathoge now available like- Xanthomonas, Pseudomonas, Ralstonia including many of their model pl such as rice, Arabidopsis. I want to identify both host and pathogen factors that promot pathogenesis. a) Extracellular cell-cell communication system in plant

pathogen

Several plant pathogenic bacteria make extracellular signaling molecules in a density depen co-ordinate regulation of virulence factor synthesis. The phenomena called as quorum sensin important trait in the pathogenesis of many plant pathogenic bacteria like Xanthomonas, Ps

Xanthomonas makes an extracellular fatty acid like signaling molecule called as Diffus Molecule (DSF), which appears to differ in structure as well as mode of action in regul functions across closely related Xanthomonas. We will use both forward and reverse genet identify role of DSF like signaling molecules in Xanhomonas like- Rice pathogens= Xanth pv. oryzae, Xanthomonas oryzae pv. oryzaecola., crucifer pathogen= Xanthomonas campestris (Xcc) and the tomato pathogen=Xanthomonas campestris pv. vesicatoria (XCV).

Fig. 1. A simplified model of plant-microbe interaction. Plant pathogenic bacteria secret host modulating components by various secretion systems which include toxins, extracel and effectors. Plants recognize these effectors including microbial surface components li mount a defense response. Bacteria secrete quorum sensing molecules and regulate prod virulence functions. Integration of signals from the plant and the extracellular environm with two component signal transduction systems

1. Role of DSF in virulence of these pathogen-How DSF regulate virulence? Mech mediated signal transduction in regulating virulence factor synthesis. 2. What are the environmental conditions inside the plants which effect DSF production 3. Mode of DSF production inside the plant 4. Mechanism of DSF mediated biofilm formation both inside the plant (in planta) and in

Recently there is elucidation of genome sequence of several microbes. It appears that severa associated bacteria (which do not cause disease in plants but are associated with them (as epiphytes) encodes potential DSF like quorum sensing system, which rises interesting ques there is cross talk with DSF like signaling molecules between these pathogenic and non path ?. To what extent these cross talks influence the out come of the plant-microbe interacti

Resistance)? b) Role of di-Cylcic GMP as intracellular signaling molecule in

plan

Recent advances in plant-pathogen interaction as elucidated the role of cyclic di-GMP as signaling molecule which couples extracellular quorum sensing signal and is involved in va like-Biofilm formation, motility, quorum sensing and regulation of virulence gene expre Three protein domains-HD-GYP, GGDEF and EAL have been implicated in the synthesis a of di-Cyclic GMP (Fig. 3). Genome analysis indicates that various Xanthomonas have potential di-Cyclic GMP modulating activity. It will be interesting to determine the role of th pathogenesis and role of di-cyclic GMP in modulating behavior of the pathogens inside the h

Interestingly several two component signal transduction systems have the di-cyclic GM domains, role of these in virulence and adaptation inside the plant will give us underst pathogens couples different extracellular signals with physiological adaptation to different env 3).

Fig. 2. di-Cyclic GMP

Fig. 3. Two component signal transduction system with di-Cyclic GMP modulating dom quorum sensing and interaction of pathogen with plant.

c) Role of secretion of virulence factors and modulation of plant environment

Plants have an innate response to pathogen by which they can recognize a pathogen or a ben microbe. Some bacterial derived components like LPS (lipopolysaccharide), flagella etc. (Fig recognized by plants and they can mount a localized defense response. These components ar PAMP or MAMP (Pathogen associated molecular pattern; microbe associated molecular pa defense response in plants is mediated by the synthesis of defense proteins, reactive oxygen cross linking of cell wall, so that to restrict the spread of the pathogen (Fig. 1).

Pathogens are clever, as they have evolved several types of secretion systems which can deliver proteins inside the plant cell or in the near vicinity. These proteins can suppress th response, and hence the pathogen can multiply inside the plant and can cause disease.

We will be interested in determining role of PAMP and MAMPs in virulence and host mechanism of action of secreted bacterial effectors and how they are able to suppress the response. Using genetic screens for protein delivery system inside the plant cell and mediated transient transformation, we will be interested in identifying novel effectors as well the localization of these secreted effectors inside the plant cell. Based on these genetic stud finally address the actual biochemical roles of these effectors inside the plant cell.

To address the components of plant which are involved in defense response, we will use muta defense signaling pathways as well as transient loss of function studies using VIGS (Virus Silencing). d) Alternative secretion systems of plant pathogens and their role in plant colonization

Xanthomonas group of plant pathogens are interesting as they have a very wide host range as

exhibit variability in the mode of entry inside the plants. Genome sequence of several Xantho pathogens have now been completed and has elucidated some very exciting features. There a different kind of secretion system like-Type III (Fig. 1; syringe like apparatus which can dire bacterial effectors molecules inside the plant cell) and Type I and TypeII, which can deliver proteins in the vicinity of plant cell and can modulate pathogenesis. We will be interested in the role of these effectors secretion systems in virulence and role in fitness of these pathogen alternative secretion systems like Type IV and TypeV are present in Xanthomonas and pseud of plant pathogens. It will be also interesting to understand the role of these system in virulen effectors delivered by these alternative secretion systems e) Biology of Xanthomonas citri

Xanthomonas citri is an important member of the Xanthomonas group of plant pathogen. It c economically important disease called as Citrus Canker. In India, it causes severe economic citrus production. Very little information is known about the biology of this pathogen, its int host plant. Large genetic variation and lack of well defined resistance citrus plants makes it a pathosystem to work with. We will explore the biology of this pathogen by molecular geneti which will elucidate new virulence functions in this pathogen. Contact Information Email: Phone: Fax: subhadeep<at>cdfd.org.in +91-40-24749425 +91-40-24749448

Last updated on : Monday, 14th May, 2012

Copyright @ 2008 CDFD.

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PPT Slides of All Figures Understanding the mechanistic basis of why a certain pathogen causes disease in one host plant and not in another has long intrigued and motivated plant pathologists. Plants, in nature, are generally resistant to most pathogens. The ability of a pathogen to cause disease in a host plant is usually the exception, not the rule. This is because plants have an innate ability to recognize potential invading pathogens and to mount successful defenses. In a converse manner, successful pathogens cause disease because they are able to evade recognition or suppress host defense mechanisms or both. Since the early days of the 20th century, classical breeding for disease resistance in plants has been a major method for controlling plant diseases. However, it was not until the 1940s when H. H. Flor published his seminal work on the genetics of the interaction between flax and its obligate rust pathogen, Malamspora lini, that we gained a substantial understanding of the genetic interactions that control disease resistance in plants (10). Flor's work was novel, insightful, and under-appreciated at the time as he concurrently studied the inheritance of resistance in the host and virulence in the pathogen. This work resulted in formulation of the gene-for-gene hypothesis. In its most simple form, the gene-for-gene hypothesis states that plants contain single dominant resistance (R) genes that specifically recognize pathogens that contain complementary avirulence genes. Avirulence genes can be defined as genes in the pathogen that encode a protein product that is conditionally recognized directly or indirectly only by those plants that contain the complementary R gene. Specific recognition results in the induction of defense gene expression and the inhibition of pathogen growth. However, if the plant host does not contain the R gene, the pathogen is still capable of causing disease on that plant even though it still contains the avirulence gene. It was the work of H. H. Flor that set the stage for the subsequent molecular cloning of pathogen avirulence genes and plant R genes.

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MOLECULAR CLONING AND CHARACTERIZATION OF PATHOGEN AVIRULENCE GENES As a graduate student at U.C. Berkeley in the late 1970s, I became interested in studying why certain races of Pseudomonas syringae pv. phaseolicola (Psp) cause disease in certain cultivars of bean, but induced a hypersensitive resistance response in other cultivars. At the time it was known that a single dominant R gene was present in a certain cultivar of bean that specifically controlled resistance to certain races of Psp, but that others races of the pathogen could cause disease in that cultivar. A review article written by Al Ellingboe on the genetics of hostparasite interactions greatly influenced my thinking at the time (2). After many discussions concerning this article with my major advisor Nick Panopoulos we predicted that it should be possible to chemically mutagenize an avirulent race of Psp to cause disease in the previously resistant bean variety. We were right. The molecular cloning of the first pathogen avirulence gene occurred several years later in the early 1980s while I was a research scientist at one of the first plant biotechnology companies, International Plant Research Institute (IPRI) (15). A seminar by Fred Ausubel on the construction of a Rhizobium cosmid library and the cloning of Rhizobium genes (nod genes) by genetic complementation inspired the development of a strategy to clone a bacterial avirulence gene. We hypothesized that we could clone a bacterial avirulence gene based on the fact that in previous genetic studies with fungal pathogens, Flor had shown that avirulence genes were genetically dominant. In collaboration with Noel Keen we set out to clone an avirulence gene by constructing the genomic library of a race 6 strain of Pseudomonas syringae pv.glycinea (Psg) in a wide host range cosmid cloning vector, pLARF1. We reasoned that we could test the idea whether avirulence genes could be detected in bacteria by conjugating a cosmid genomic library of Psg race 6 into a Psg race 5 strain. Because the two races have the reciprocal phenotype on two different cultivars of soybean, we could test whether virulence or avirulence was dominant by inoculating the exconjugants on both cultivars and scoring the phenotype (TableI).

View this table: In this window In a new window Table I. Bacterial disease reactions on soybean cultivars

Our results, published in 1984, revealed that a Psg race 5 strain containing the avirulence gene avrA from race 6 was now recognized by the Harosoy cultivar and induced a hypersensitive response. We never detected any exconjugants that convertedPsg race 5 strains from an HR to a susceptible reaction on the cultivar Norchief confirming the dominant nature of theavrA gene. Although we cloned and sequenced a pathogen avirulence gene, we did not gain much insight into how this gene could trigger disease resistance in plants that contained a complementary R gene. The sequencing of avrA and the predicted protein sequence did not show homology to any proteins in any database and attempts to isolate a factor from bacterial supernatants were unsuccessful. A clue of how avirulence genes induced a resistance response in host plants had to await the cloning and characterization of the Hrp genes (see below) in phytopathogenic bacteria several years later.

Previous SectionNext Section Hrp GENES IN PHYTOPATHOGENIC BACTERIA ENCODE A SPECIALIZED TYPE III SECRETION APPARATUS TO DELIVER Avr (EFFECTOR) PROTEINS TO PLANT CELLS Early genetic studies in the 1980s carried out in the group of Nick Panopoulos resulted in the identification of bacterial genes controlling the ability of phytopathogenic bacteria to elicit a plant infection (9). These genes were termed Hrp genes, as bacteria containing these mutations concomitantly lost the ability to induce a HR on resistant plants and to cause disease in susceptible plants. Hrp genes were subsequently identified and characterized in several phytopathogenic genera, including Pseudomonas (Collmer group), Xanthomonas (Bonas group), Erwinia (Beer group), and Ralstonia (Boucher group). The Hrp genes are generally

organized as 23- to 25-Kb clusters of DNA that contain several operons and have been subdivided into group I (Erwinia and Pseudomonas) and group II (Xanthomonas and Ralstonia) based on DNA homology (1, 8). Subsequent work revealed that some avirulence genes were actually within or near Hrp loci. It is interesting that it was also revealed that Hrp genes and avr genes in Pseudomonas syringae are coregulated. However, how Hrp genes and avr genes were functionally related remained a mystery. A major breakthrough in our understanding of pathogen avirulence genes occurred when the sequencing of the Hrp regions of phytopathogenic bacteria (groups of Ulla Bonas and Christian Boucher) revealed strong homology to type III secretion machinery of mammalian pathogens such asYersinia, Salmonella, and Shigella (1). Such Type III secretory systems target virulence effector proteins to mammalian host cells, thereby interfering with the ability of the host to resist pathogen attack (3). Several laboratories working in this area have compelling evidence that phytopathogenic bacteria may deliver effector proteins directly to the plant host (13). It is difficult to conceptually imagine what the selective advantage would be for a pathogen to maintain avirulence genes that are recognized by plant hosts. Recent studies have suggested that Avr proteins are most likely to be virulence factors that have evolved to alter or suppress host defense mechanisms (7). Only those plants are protected that have co-evolved resistance mechanisms to specifically detect foreign Avr proteins delivered into the host cell. Although much had been learned by studying the pathogen avirulence genes, it was becoming clearer that plant molecular pathologists should begin to turn their attention to the plant side of the interaction, and to focus their efforts on cloning and characterizing genetically understood R genes whose cognate avirulence gene had already been identified.

Previous SectionNext Section ISOLATION AND MOLECULAR CLONING OF PLANT DISEASE RESISTANCE GENES

The identification of resistant germplasm in wild species of agronomic crops and the subsequent introgression into commercial cultivars has been the major focus of many plant breeders for the better part of the 20th century. Furthermore, most plant breeders chose to employ single dominant and semi-dominant genes in their breeding programs because of the ease and efficacy in which they could be introduced into agronomically acceptable cultivars. Thus as little as 10 years ago, the Holy Grail in the field of molecular plant pathology was the cloning and characterization of plant R genes. The fact that most characterized resistance genes were inherited as single genetic loci allowed plant biologists to employ genetic strategies to clone R genes. The development of transposon tagging and map-based cloning strategies to clone genes in the 1980s seemed like the best method of choice to clone R genes from plants. A major breakthrough was the cloning and characterization of the maize Hm1 disease resistance gene (6). The Hm1 gene controls resistance to certain isolates of Cochliobolus carbonum and was cloned by transposon tagging employing the maize transposonMu. The characterization of the Hm1 gene revealed that it encoded an NADPH-dependent reductase that inactivates the toxin produced by the invading fungus. In the next year a second R gene was isolated by Greg Martin and colleagues while he was working as a post-doctoral stuedent in the Tanksley laboratory at Cornell University. The Cornell group employed a map-based cloning strategy to identify the Pto resistance gene from tomato (11). This gene encodes a Ser/Thr kinase activity and is unrelated to theHm1 gene. Thus at this time, there was no indication of a common relationship between R genes from different plants that controlled unrelated types of pathogens. The pace of cloning R genes increased beginning in 1994 with the cloning and characterization of R genes for resistance to several classes of pathogens, including viral, bacterial, and fungal pathogens. The Arabidopsis RPS2 gene was cloned in my group and the group of Fred Ausubel, the tobacco N gene in the group of Barbara Baker, the tomatoCf9 gene in the group of Jonathan Jones, and theL6 gene of flax in the group of Jeff Ellis (14). Subsequent analyses of the predicted polypeptides revealed that all four proteins contain Leu rich repeat motifs, suggesting that plants may share common mechanisms for disease resistance to diverse pathogens (see Fig.1). In the following year, the groups of Jeff Dangl and Roger Innes reported the cloning of the ArabidopsisRPM1 gene (4). The sequencing of this gene further validated the

idea that disease resistance genes share common protein motifs. This was an extremely exciting time in plant biology: a major breakthrough was achieved that could have not been predicted based on previous knowledge (5). Furthermore, a comparison of the N, RPS2, RPM1, and L6 proteins revealed further similarities as significant homologous stretches of amino acids could be found throughout the proteins. Prominent among these is the presence of a nucleotide binding site (NBS) and a Leu zipper (LZ) or homology to the toll and interleukin 1 receptor (TIR) domains in the N terminus of these proteins (see Fig. 1). These analyses also suggested that additional R genes could be identified by employing PCR with degenerate oligonucleotides and that putative R genes could be inferred from DNA sequencing projects. These predictions have been validated, as at 481 sequences have been identified that are putative R genes containing NBS/LRR domains from three sources: cloned R genes, homologous sequences in public databases, and degenerate PCR cloning (12).

View larger version: In this page In a new window Download as PowerPoint Slide Fig. 1. Characterization of several of the first disease resistance proteins cloned revealed the presence of common motifs.

Previous SectionNext Section MAJOR UNANSWERED QUESTIONS AND FUTURE DIRECTIONS

Today's Holy Grail is to define the molecular basis of disease resistance specificity. We also need to elucidate the biochemical functions of pathogen avirulence proteins and plant R proteins. Moreover, we must focus on better understanding what controls the defense signal transduction pathways in the host leading to the expression of resistance. During the course of this work we expect to uncover the answer to the question: Do resistance proteins bind directly or indirectly to pathogen avirulence proteins or are there protein complexes that form that contain several yet to be identified proteins in addition to R and Avr proteins? The answer to this question is expected to come in the next few years as we begin to define the precise mechanisms involved in plant disease resistance. The major advances in this field up until this time have been shaped by genetic approaches, but it is also quite clear that a concomitant biochemical and cell biological effort will also be necessary to unravel the molecular complexities to understand the mechanisms involved in plant disease resistance. A major future goal is to be able to understand the molecular basis of disease resistance in enough detail to make precise predictions about engineering plants to express resistance proteins that can recognize pathogen molecules essential for pathogenicity. In this manner it is anticipated that biotechnological approaches can engineer durable disease resistance in agricultural crops.

JL (1995) Science 269:843846. Abstract/FREE Full Text 5. Hammond-Kosack KE,

Jones JDG

(1997) Annu Rev Plant Physiol Plant Mol Biol 48:575607.

Navigate This Article Top MOLECULAR CLONING AND CHARACTERIZATION OF PATHOGEN AVIRULENCE GENES Hrp GENES IN PHYTOPATHOGENIC BACTERIA ENCODE A SPECIALIZED TYPE III SECRETION APPARATUS TO DELIVER Avr (EFFECTOR) PROTEINS TO PLANT CELLS
ISOLATION AND MOLECULAR CLONING OF PLANT DISEASE RESISTANCE GENES MAJOR UNANSWERED QUESTIONS AND FUTURE DIRECTIONS Footnotes LITERATURE CITED

Cited By NOV 2008 Genetic Analysis of Phytophthora Root Rot Race-specific Resistance in Chile Pepper Journal of the American Society for Horticultural Science DEC 2007 NLR proteins: integral members of innate immunity and mediators of inflammatory diseases Journal of Leukocyte Biology JUN 2005 Eclair--a web service for unravelling species origin of sequences sampled from mixed host interfaces Nucleic Acids Research View citing article information

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APSnet > Education > Advanced > Topics in Plant Pathology > Population Genetics > Knowledge Tests

Population Genetics of Plant Pathogens

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Knowledge Test on Population Biology

Genetic Drift Gene/Genotype Flow Reproductive/Mating Systems Hardy-Weinberg Equilibrium Natural Selection Interactions/Genetic Structure Applications Knowledge Tests References Glossary

and Coevolution
1. What is a population and what is population genetics? 2. Why is population biology important for plant pathologists? 3. What is coevolution? 4. Why dont agroecosystems exhibit coevolution? 5. What are the five evolutionary factors most commonly considered by population geneticists?

Ecology and Epidemiology in R Xanthomonadins, Unique Yellow Pigments of the Genus Xanthomonas An Introduction to Reverse Genetic Tools for Investigating Gene Function Deriving Decision Rules Biological Control of Plant Pathogens

Knowledge Test on Mutation

1. Why is mutation important in the population genetics of organisms? 2. Does mutation acting alone cause changes in allele frequencies? 3. Why do large populations have more alleles than small populations? 4. Why do plant breeders seek the center of origin to find resistant germplasm? 5. What is a resistance gene pyramid? 6. How many resistance genes would a plant breeder need if a pathogen has a very large population size 12 (>10 individuals per field)? 7. How many resistance genes would a plant breeder need if a pathogen has a relatively small 5 population size (<10 individuals per field)?

Knowledge Test on Genetic Drift

1. What is genetic drift? Name three processes that cause genetic drift. 2. What is a genetic bottleneck and what is a founder effect? 3. How does genetic drift affect the distribution of genetic diversity among populations? 4. Why is genetic drift important in agroecosystems? 5. How can you calculate the predicted effect of genetic drift?

Knowledge Test on Gene/Genotype Flow

1. What is gene flow and how does it differ from genetic drift? 2. How does gene flow differ from genotype flow? 3. Why is gene flow important in agricultural ecosystems? 4. How does Nem relate genetic drift to gene flow? 5. What is a metapopulation and how is it relevant to agroecosystems?

Knowledge Test on Reproductive/Mating System

1. What is the difference between genetic assortative and genetic disassortative mating? 2. What is the difference between gene and genotype diversity?

How do you measure them? 3. Is gene diversity affected by mating system? How? 4. Is genotype diversity affected by mating system? How? 5. Why is mating/reproduction system relevant to plant pathology?

Knowledge Test on Natural Selection

1. What is the difference between the balance model and the neutral mutation model for explaining genetic variation in populations? 2. What is the difference between directional selection and stabilizing selection? 3. Define pathogen fitness. Name as many fitness parameters as you can imagine for a pathogen in an agricultural ecosystem. 4. What is Fishers Fundamental Theorem of Natural Selection? 5. What happens to the frequency of pathogen virulence alleles if there is no fitness cost associated with having unneeded virulence? 6. Have plant pathologists found evidence of selection against unneeded virulence genes?

Knowledge Test on Interactions/Genetic Structure

1. What is a boom-andbust cycle? How do they develop and why do they persist? 2. Why did the Puccinia graminis f. sp. tritici population stabilize in North America? 3. What is genetic structure? 4. Does gene flow make populations more genetically similar or more different? 5. How does sexual reproduction affect the genetic structure of populations? 6. Describe the evolutionary forces that affected Phytophthora infestans populations in Europe before 1960. Now describe the evolutionary forces that affect P. infestans populations in Europe in 2000. Which population poses a greater threat to potato production and why is the threat greater?

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Induced systemic resistance (ISR) in plants: mechanism of action

by Devendra K Choudhary, Anil Prakash, B N Johri Biological Sciences Miscellaneous Papers View in Mendeley Desktop In your librarySave reference to library

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References7Related research Indian Journal of Microbiology (2008)

Volume: 47, Issue: 4, Pages: 289-297

ISSN: 00468991 DOI: 10.1007/s12088-007-0054-2 Available from www.springerlink.com or Find this paper at:

openurl.ac.ukWorldCatGoogle ScholarEdit library access linksAbstract Plants possess a range of active defense apparatuses that can be actively expressed in response to biotic stresses (pathogens and parasites) of various scales (ranging from microscopic viruses to phytophagous insect). The timing of this defense response is critical and refl ects on the difference between coping and succumbing to such biotic challenge of necrotizing pathogens/parasites. If defense mechanisms are triggered by a stimulus prior to infection by a plant pathogen, disease can be reduced. Induced resistance is a state of enhanced

defensive capacity developed by a plant when appropriately stimulated. Systemic acquired resistance (SAR) and induced systemic resistance (ISR) are two forms of induced resistance wherein plant defenses are preconditioned by prior infection or treatment that results in resistance against subsequent challenge by a pathogen or parasite. Selected strains of plant growth-promoting rhizobacteria (PGPR) suppress diseases by antagonism between the bacteria and soil-borne pathogens as well as by inducing a systemic resistance in plant against both root and foliar pathogens. Rhizobacteria mediated ISR resembles that of pathogen induced SAR in that both types of induced resistance render uninfected plant parts more resistant towards a broad spectrum of plant pathogens. Several rhizobacteria trigger the salicylic acid (SA)-dependent SAR pathway by producing SA at the root surface whereas other rhizobacteria trigger different signaling pathway independent of SA. The existence of SA-independent ISR pathway has been studied in Arabidopsis thaliana, which is dependent on jasmonic acid (JA) and ethylene signaling. Specifi c Pseudomonas strains induce systemic resistance in viz., carnation, cucumber, radish, tobacco, and Arabidopsis, as evidenced by an enhanced defensive capacity upon challenge inoculation. Combination of ISR and SAR can increase protection against pathogens that are resisted through both pathways besides extended protection to a broader spectrum of pathogens than ISR/SAR alone. Beside Pseudomonas strains, ISR is conducted by Bacillus spp. wherein published results show that several specifi c strains of species B. amyloliquifaciens, B. subtilis, B. pasteurii, B. cereus, B. pumilus, B. mycoides, and B.sphaericus elicit signifi cant reduction in the incidence or severity of various diseases on a diversity of hosts.

Author-supplied keywords
induced systemic resistancejasmonate ethylene signallingling expressionpathogenesis related proteinssarsignal

Related research
1. Interactions of Bacillus spp. and plants--with special reference to induced systemic resistance (ISR). Devendra K Choudhary, Bhavdish N Johriin Microbiological research(2009)
Save reference to libraryRelated research18 readers

2.

The relationship between pathogen-induced systemic resistance ( ISR ) and multigenic ( horizontal ) resistance in plants Sadik Tuzunin Plant and Cell Physiology(2001)
Save reference to libraryRelated research18 readers

3.

Priming as a mechanism in induced systemic resistance of plants U Conrath, O Thulke, V Katz, S Schwindling, A Kohlerin European Journal of Plant Pathology(2001)
Save reference to libraryRelated research11 readers

4.

Induced systemic resistance (ISR) against pathogens in the context of induced plant defences M Heil, R M Bostockin Annals of Botany(2002)
Save reference to libraryRelated research6 readers

5.

The ecological concept of costs of induced systemic resistance ( ISR ) Martin Heil, Lehrstuhl Zoologie III, Am Hubland D Win European Journal of Plant Pathology(2001)
Save reference to libraryRelated research17 readers

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Induced systemic resistance (ISR) in plants: mechanism of action

Indian J. Microbiol. (December 2007) 47:289297 289 123 REVIEW Induced systemic resistance (ISR) in plants: mechanism of action Devendra K. Choudhary Anil Prakash B. N. Johri Received: 10 July 2007 / Final revision: 26 October 2007 / Accepted: 30 October 2007 Indian J. Microbiol. (December 2007) 47:289297 Abstract Plants possess a range of active defense apparatuses that can be actively expressed in response to biotic stresses (pathogens and parasites) of various scales (ranging from microscopic viruses to phytophagous insect). The timing of this defense response is critical and re ects on the difference between coping and succumbing to such biotic challenge of necrotizing pathogens/parasites. If defense mechanisms are triggered by a stimulus prior to infection by a plant pathogen, disease can be reduced. Induced resistance is a state of enhanced defensive capacity developed by a plant when appropriately stimulated. Systemic acquired resistance (SAR) and induced systemic resistance (ISR) are two forms of induced resistance wherein plant defenses are preconditioned by prior infection or treatment that results in resistance against subsequent challenge by a pathogen or parasite. Selected strains of plant growth-promoting rhizobacteria (PGPR) suppress diseases by antagonism between the bacteria and soil-borne pathogens as well as by inducing a systemic resistance in plant against both root and foliar pathogens. Rhizobacteria mediated ISR resembles that of pathogen induced SAR in that both types of induced resistance render uninfected plant parts more resistant towards a broad spectrum of plant pathogens. Several rhizobacteria trigger the salicylic acid (SA)-dependent SAR pathway by producing SA at the root surface whereas other rhizobacteria trigger different signaling pathway independent of SA. The existence of SA-independent ISR pathway has been studied in Arabidopsis thaliana, which is dependent on jasmonic acid (JA) and ethylene signaling. Speci c Pseudomonas strains induce systemic resistance in viz., carnation, cucumber, radish, tobacco, and Arabidopsis, as evidenced by an enhanced defensive capacity upon challenge inoculation. Combination of ISR and SAR can increase protection against pathogens that are resisted through both pathways besides extended protection to a broader spectrum of pathogens than ISR/SAR alone. Beside Pseudomonas strains, ISR is conducted by Bacillus spp. wherein published results show that several speci c strains of species B. amyloliquifaciens, B. subtilis, B. pasteurii, B. cereus, B. pumilus, B. mycoides, and B.sphaericus elicit signi cant reduction in the incidence or severity of various diseases on a diversity of hosts. Keywords Induced systemic resistance SAR Signalling and expression Jasmonate and ethylene signalling Pathogenesis-related proteins Introduction Imagine a place on Earth where an organism does not suffer from infectious disease and is unlikely to become infected even in presence of pathogens. Such rare places exist and one such habitat is natural suppressive soils1. In such soils

the by fungi, D.

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protected microorganisms plant-deleterious Prakash

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diseases which nematodes. N. Johri

caused include Patho(

) Department Barkatullah Bhopal India Tel: +91 Fax: +91 Email: devmicro@rediffmail.com

of / / 755 755 / / 462 2677748,

Biotechnology, University, 026, 49 2485656

Page 2

290 Indian J. Microbiol. (December 2007) 47:289297 123 genic microorganisms affecting plant health are major and chronic threats to food production and ecosystem stability worldwide. Crop rotation, breeding for resistant plant varieties and the application of pesticides are insuf cient to control root diseases of important crop plants. An initiative, simple explanation of how the biological control of soil-borne pathogens could work? There is a large body of literature describing potential use of plant associated bacteria, the so called plant growth-promoting bacteria (PGPB) as agents stimulating plant growth and managing soil and plant health. The most widely studied group of PGPB is plant growth-promoting rhizobacteria (PGPR) that colonize the root surface and the closely adhering soil interface, the rhizosphere. The widely recognized mechanism of biocontrol mediated by PGPB is competition for an ecological niche/substrate, production of inhibitory allelochemicals, and induction of systemic resistance (ISR) in host plants to a broad spectrum of pathogens2. Induced resistance is a physiological state of enhanced defensive capacity elicited by speci c environmental stimuli, whereby the plants innate defenses are potentiated against subsequent biotic challenges. This enhanced state of resistance is effective against a broad range of pathogens and parasites15. The two most clearly de ned forms of induced resistance are systemic acquired resistance (SAR), and induced systemic resistance (ISR), which can be differentiated on the basis of the nature of the elicitor and the regulatory pathways involved (Fig. 1). SAR can be triggered by exposing the plant to virulent, avirulent, and nonpathogenic microbes. Depending on the plant and elicitors, a set period of time is required for the establishment of SAR wherein accumulation of pathogenesis-related proteins (chitinase and glucanase), and salicylic acid takes place. ISR is potentiated by plant growth-promoting rhizobacteria (PGPR), of which best characterized are strains that belong to genus Pseudomonas that cause no visible damage to the plants root system3. Unlike SAR, ISR does not involve the accumulation of pathogenesis-related proteins or salicylic acid, but instead, relies on pathways regulated by jasmonate and ethylene5,52. Plant roots release substantial amounts of Cand Ncontaining compounds into the surrounding soil. Microorganisms are attracted to this nutritous environment and use the root exudates and lysates for growth and multiplication on the surface of root and in the adjacent rhizosphere soil. Because of the rapid consumption of the nutrients, bacterial growth in the rhizosphere remains nutrient-limited where roots are seldom colonized for more than about 15% of their surface area. The rhizosphere micr ora plays an important role in plant development and acclimation to environmental stresses3. Since the rhizosphere micro ora is extremely diverse, a dynamic interplay between the members of the microbial community occurs which is mediated by synergistic and antagonistic interactions within the limits of the nutrients available. In addition, signals are exchanged between fungi and bacteria and plant roots which re ect a highly dynamic belowground communication network. Plant growth-promoting rhizobacteria can suppress diseases through antagonism between bacteria and soil-borne pathogens, as well as by inducing a systemic resistance in the plant against both root and foliar pahogens. The induced resistance constitutes an increase in the level of basal re-

sistance to several pathogens simultaneously, which is of bene t under natural conditions where multiple pathogens exist. Several speci c Pseudomonas strains have been reported to induce systemic resistance in e.g., carnation, cucumber, radish, tobacco, and Arabidopsis. In addition, several other bacterial strains are reported to inducing resistance in different plant species, whereas others show speci city, indicating speci c recognition between bacteria and plants at the root surface. In carnation, radish and Arabidopsis, the O-antigenic side chain of the bacterial outer membrane lipopolysaccharide acts as an inducing determinant along with other bacterial traits. Pseudobactin siderophores have been implicated in the induction of resistance in tobacco and Arabidopsis together with other siderophore, psedomonine. These siderophores may explain induction of resistance associated with salicylic Fig. 1 The pathogen-induced SAR and the rhizobacteriamediated ISR signal transduction pathways in Arabidopsis (From Pieterse et al (2002) Signaling in Rhizobacteria-Induced Systemic Resistance in Arabidopsis thaliana. Reproduction with permission.

Related Full-Text Papers

1. Induced Disease Resistance Signaling in Plants Bas W M Verhagen, L C Van Loon Cornin Plant Biotechnology(2003)
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A Genomic Approach to Identify Regulatory Nodes in the Transcriptional Network of Systemic Acquired Resistance in Plants Dong Wang, Nita Amornsiripanitch, Xinnian Dongin PLoS Pathogens(2006)
Save PDF to library51 readers

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Induced systemic resistance (ISR) in plants: mechanism of action

by Devendra K Choudhary, Anil Prakash, B N Johri

Biological Sciences Miscellaneous Papers

Save reference to library Share

Overview References7 Related research

Indian Journal of Microbiology (2008)

Volume: 47, Issue: 4, Pages: 289-297 ISSN: 00468991 DOI: 10.1007/s12088-007-0054-2

Available from www.springerlink.com

or Find this paper at:

Abstract

Plants possess a range of active defense apparatuses that can be actively expressed in response to biotic stresses (pathogens and parasites) of various scales (ranging from microscopic viruses to phytophagous insect). The timing of this defense response is critical and refl ects on the difference between coping and succumbing to such biotic challenge of necrotizing pathogens/parasites. If defense mechanisms are triggered by a stimulus prior to infection by a plant pathogen, disease can be reduced. Induced resistance is a state of enhanced defensive capacity developed by a plant when appropriately stimulated. Systemic acquired resistance (SAR) and induced systemic resistance (ISR) are two forms of induced resistance wherein plant defenses are preconditioned by prior infection or treatment that results in resistance against subsequent challenge by a pathogen or parasite. Selected strains of plant growth-promoting rhizobacteria (PGPR) suppress diseases by antagonism between the bacteria and soil-borne pathogens as well as by inducing a systemic resistance in plant against both root and foliar pathogens. Rhizobacteria mediated ISR resembles that of

pathogen induced SAR in that both types of induced resistance render uninfected plant parts more resistant towards a broad spectrum of plant pathogens. Several rhizobacteria trigger the salicylic acid (SA)-dependent SAR pathway by producing SA at the root surface whereas other rhizobacteria trigger different signaling pathway independent of SA. The existence of SA-independent ISR pathway has been studied in Arabidopsis thaliana, which is dependent on jasmonic acid (JA) and ethylene signaling. Specifi c Pseudomonas strains induce systemic resistance in viz., carnation, cucumber, radish, tobacco, and Arabidopsis, as evidenced by an enhanced defensive capacity upon challenge inoculation. Combination of ISR and SAR can increase protection against pathogens that are resisted through both pathways besides extended protection to a broader spectrum of pathogens than ISR/SAR alone. Beside Pseudomonas strains, ISR is conducted by Bacillus spp. wherein published results show that several specifi c strains of species B. amyloliquifaciens, B. subtilis, B. pasteurii, B. cereus, B. pumilus, B. mycoides, and B.sphaericus elicit signifi cant reduction in the incidence or severity of various diseases on a diversity of hosts.

Author-supplied keywords

induced systemic resistancejasmonate ethylene signallingling expressionpathogenesis related proteinssarsignal

Related research

Interactions of Bacillus spp. and plants--with special reference to induced systemic resistance (ISR).

Devendra K Choudhary, Bhavdish N Johri in Microbiological research (2009)

Save reference to library Related research 18 readers

The relationship between pathogen-induced systemic resistance ( ISR ) and multigenic ( horizontal ) resistance in plants

Sadik Tuzun in Plant and Cell Physiology (2001)

Save reference to library Related research 18 readers

Priming as a mechanism in induced systemic resistance of plants

U Conrath, O Thulke, V Katz, S Schwindling, A Kohler in European Journal of Plant Pathology (2001)

Save reference to library Related research 11 readers

Induced systemic resistance (ISR) against pathogens in the context of induced plant defences

M Heil, R M Bostock in Annals of Botany (2002)

Save reference to library Related research 6 readers

The ecological concept of costs of induced systemic resistance ( ISR )

Martin Heil, Lehrstuhl Zoologie III, Am Hubland D W in European Journal of Plant Pathology (2001)

Save reference to library Related research 17 readers

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Induced Disease Resistance Signaling in Plants

Bas W M Verhagen, L C Van Loon Corn in Plant Biotechnology (2003)

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A Genomic Approach to Identify Regulatory Nodes in the Transcriptional Network of Systemic Acquired Resistance in Plants

Dong Wang, Nita Amornsiripanitch, Xinnian Dong in PLoS Pathogens (2006)

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Article # 1 Source: http://www.fs.fed.us/r8/foresthealth/laurelwilt/pla nt_susceptibility.shtml

Laurel Wilt
Plant Susceptibility
At this time only plant species in the family Lauraceae indigenous to the southeastern USA are known to be affected by laurel wilt. Redbay, a tree particularly abundant in maritime forests of Georgia, South Carolina and Florida, has been the primary species affected by the wilt. Sassafras, a less common tree in the coastal plains of the Southeast but with a more extensive range than redbay, has also been affected by the disease but to a lesser extent than redbay. The wilt fungus has also been isolated from dead and dying pondspice (Litsea aestivalis) and pondberry (Lindera melissaefolia), however the redbay ambrosia beetle has not been found in either of these species. Pondberry is a federally endangered species while pondspice is regarded as a threatened or endangered species in some southeastern states.

Figure 1. Redbay trees are very susceptible to laurel wilt. The wilt is currently occurring in forests of the coastal plains in South Carolina, Georgia and Florida, and is continuing to spread. Laboratory inoculation studies have confirmed that redbay and sassafras as well as spicebush (Lindera benzoin) are susceptible to the vascular wilt caused by the Raffaelea lauricola (Figure 2). Additional studies have found that avocado is also susceptible but some cultivars or age classes may be more resistant than redbay and sassafras. In inoculation studies, some avocado seedlings typically wilt and die rapidly, but others remain healthy or only exhibit symptoms such as shoot dieback or foliage discoloration and do not die. As the redbay ambrosia beetle and laurel wilt spread southward in Florida (Distribution Map), mostly in redbay, avocado plants in urban and rural landscapes also have been observed dying and confirmed to be infected with the disease. Some varieties of avocado appear to be more susceptible than others. The serious threat to the avocado industry in south Florida and elsewhere has aroused great concern and a significant research effort is underway to help manage this disease as it moves into the commercial avocado growing area (http://www.fl-dpi.com/enpp/pathology/laurel_wilt_disease.html).

Figure 2. Uninoculated "control" plants and plants inoculated with the laurel wilt fungus (Raffaelea lauricola) for: A. redbay (Persea borbonia); B. avocado (Persea americana); C. California bay (Umbellularia californica); and D. sassafras (Sassafras albidum).

California bay (Umbellularia californica), a species indigenous to the west coast of the United States, is also susceptible to disease caused by the laurel wilt fungus. In controlled inoculation studies California bay seedlings exhibited shoot and branch dieback. Studies have also been carried out on red maple, tulip poplar and red oak, and these species were not susceptible to the wilt. Numerous species in the Lauraceae occur in the Americas, particularly in the tropical forests of Central and South America where there is great diversification and the species of this family are major components of the forests. Testing is continuing to evaluate the susceptibility of other species in the Lauraceae, as well as other plant families. Additional studies are needed to evaluate the susceptibility of various plant species to the redbay ambrosia beetle since it appears that this beetle is the primary vector of the laurel wilt pathogen.

Additional Information
Smith, J.A., T.J. Dreaden, A.E. Mayfield, III, A. Boone, S.W. Fraedrich, and C. Bates. 2009. First Report of Laurel Wilt Disease Caused by Raffaelea lauricola on Sassafras in Florida and South Carolina. Plant Disease 93(10): 1079. Smith, J.A., L. Mount, A.E. Mayfield, III, C.A. Bates, W.A. Lamborn, and S.W. Fraedrich. 2009. First report of laurel wilt disease caused by Raffaelea lauricola on camphor in Florida and Georgia. Plant Disease 93(2): 198. Mayfield, A.E. III, J.E. Pea, J.H. Crane, J.A. Smith, C.L. Branch, E.D. Ottoson, and M. Hughes. 2008. Ability of the redbay ambrosia beetle (Coleoptera: Curculionidae: Scolytinae) to bore into young avocado (Lauraceae) plants and transmit the laurel wilt pathogen (Raffaelea lauricola)." Florida Entomologist 91(3): 485-487. [45 KB] Mayfield, A.E. III, J.A. Smith, M. Hughes, and T.J. Dreaden. 2008. First report of laurel wilt disease caused by a Raffaelea lauricola on avocado in Florida. Plant Disease 92(6): 976-976.

Smith, J.A., T.J. Dreaden, A.E. Mayfield, III, A. Boone, S.W. Fraedrich, and C. Bates. 2009. First Report of Laurel Wilt Disease Caused by Raffaelea lauricola on Sassafras in Florida and South Carolina." Plant Disease 93(10): 1079. Susceptibility of Native and Foreign Species in the Lauraceae and Other Families to Laurel Wilt, Steve Fraedrich, US Forest Service, Southern Research Station, Laurel Wilt Conference 27Feb-09 (Slideshow 1.3 MB). Susceptibility of Avocado to Laurel Wilt, Randy Ploetz, University of Florida , Laurel Wilt Conference 27-Feb-09 (Slideshow 3.2 MB). Laurel Wilt Disease Resistance Research, Jason Smith, University of Florida , Laurel Wilt Conference 27-Feb-09 (Slideshow 2.4 MB). Fraedrich, S.W. " Disease Notes: California Laurel is Susceptible to Laurel Wilt Caused by Raffaelea lauricola." Plant Disease 92.10 (2008): 1469. Mayfield, A.E. III, Crane, J.H., and Smith, J.A. 2008. Laurel Wilt: A Threat to Redbay, Avocado and Related Trees in Urban and Rural Landscapes. University of Florida , Institute of Food and Agricultural Sciences Extension, Document HS-1137. 6 p. Redbay (Persea borbonia) - Taxonomy & Identification - Kim D. Coder, University of Georgia, 1/19/2007 (Handout) Laurel Wilt: Hosts and Pathogenicity Tests, Stephen Fraedrich, USDA Forest Service. 1/19/2007. (942 KB)

Article # 2 source: http://www.factmonster.com/dk/science/encyclopedia/plantsensitivity.html

Like animals, plants sense changes in their surroundings and respond to them. Plants are able to detect and respond to light, gravity, changes in temperature, chemicals, and even touch. Unlike animals, plants do not have nerves or muscles, so they cannot move very fast. A plant usually responds to change by gradually altering its growth rate or its direction of growth. The slow movements that plants make towards or away from a stimulus, such as light, are known as tropisms. Tropisms are controlled with the help of special chemicals called PLANT GROWTH REGULATORS.

Light influences how shoots grow. They bend towards it, so that leaves will have the maximum amount for photosynthesis. Roots push down through soil because of the effect of gravity. They may also be drawn towards water, or away from bright light. Other factors, such as temperature and how wet the soil is, may affect when seeds germinate (sprout).

Over the course of a day, the flowerheads in a field of sunflowers gradually turn, tracking the Suns path across the sky. The movement is almost too slow to notice. In the morning, the flowerheads all face east and by evening they face west. This is called phototropism, which means the movement of part of a body towards light. It happens as chemicals shift from one side of the stems to the other.

TIME TO FLOWER
Many plants only bloom at certain times of year. They flower at the right time by responding to changes in light and temperature. A crocus plant is able to detect signs of spring, such as lengthening days (more light) and warmer soil (increased temperature). These changes cause chemical changes in the plant and the crocus starts to put out shoots and flowers.

SURVIVING WINTER
Deciduous plants such as Forsythia respond to the lack of light and warmth in winter by entering a resting period. In preparation, the plant produces chemicals that weaken the leaf stalks, so the leaves fall. Over winter, the plant does not need to make food. Its shoots and buds are inactive. When spring comes, the plant produces chemicals that make buds and shoots start to grow again.

REACHING OUT
Some plant parts respond to contact. Climbers, such as pea plants and this passion flower, put out long, reaching shoots called tendrils. When a tendril reaches something solid such as a garden cane or the stem of another plant it coils around it. By grasping at supports in this way, the plant is able to climb even higher.

MANGROVE ROOTS UNDERWATER

Roots usually respond to light by growing away from it, but the roots of mangrove trees behave differently. Mangroves grow in coastal swamps where there is little oxygen in the waterlogged soil. Their roots compensate for this by growing upwards out of the mud. Each low tide, the mangrove roots are exposed to the air and can collect plenty of oxygen.

PLANT GROWTH REGULATORS

Certain chemicals influence different aspects of a plants growth. These plant growth regulators may control how fast cells divide, or how they grow. Some are produced in the tips of shoots or roots. They can even change the direction the shoot or root takes as it grows. If cells on one side of the tip grow faster, the tip will start to curl in the opposite direction.

Article # 3 source: http://www.plantphysiol.org/content/135/1/530.full unable to open article # 4