"Bio - Warfare During Host Pathogen Interactions in Indigenous Crop Plants" by Md. Kamaruzzaman Shakil


Published on

This is a analysis of some collected information of the subject of my M.S. theory semester. Course title was Plant Pathogenesis and Genetics of Plant Pathogens

Published in: Education
  • Be the first to comment

  • Be the first to like this

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

"Bio - Warfare During Host Pathogen Interactions in Indigenous Crop Plants" by Md. Kamaruzzaman Shakil

  1. 1. AN ASSIGNMENT ON BIO - WARFARE DURING HOST - PATHOGEN INTERACTIONS IN INDIGENOUS CROP PLANTS Course No.: P.Path.- 501 Course Title: Plant Pathogenesis and Genetics of plant pathogens SUBMITED TO SUBMITED BYDr. A. Q. M. Bazlur Rashid Md. KamaruzzamanProfessor ID No. 11 Ag.P.Path. JJ 07 MDepartment of Plant Pathology Reg. No. 33141 Department of Plant PathologyBangladesh Agricultural Bangladesh Agricultural UniversityUniversity MymensinghMymensingh Ph.- +8801722449614 DEPARTMENT OF PLANT PATHOLOGY BANGLADESH AGRICULTURAL UNIVERSITY MYMENSINGH
  2. 2. AbstractPlants represent a rich source of nutrients for many organisms including bacteria, fungi,protists, insects, and vertebrates. Although lacking an immune system comparable toanimals, plants have developed a stunning array of structural, chemical, and protein-baseddefenses designed to detect invading organisms and stop them before they are able tocause extensive damage. Humans depend almost exclusively on plants for food, andplants provide many important non-food products including wood, dyes, textiles,medicines, cosmetics, soaps, rubber, plastics, inks, and industrial chemicals.Understanding how plants defend themselves from pathogens and herbivores is essentialin order to protect our food supply and develop highly disease-resistant plant species.Plant diseases caused by fungi and oomycetes result in significant economic losses everyyear. Although phylogenetically distant, the infection processes by these organisms sharemany common features. These include dispersal of an infectious particle, host adhesion,recognition, penetration, invasive growth, and lesion development. Bacteria pathogenicfor plants are responsible for devastating losses in agriculture. The use of antibiotics tocontrol such infections is restricted in many countries due to worries over the evolutionand transmission of antibiotic resistance. The advent of genome sequencing has enabled abetter understanding, at the molecular level, of the strategies and mechanisms ofpathogenesis, evolution of resistance to plant defence mechanisms, and the conversion ofnon-pathogenic into pathogenic bacteria. 1
  3. 3. Introduction:A pathogen is a microorganism that is able to cause disease in a plant, animal or insect.Pathogenicity is the ability to produce disease in a host organism. Microbes express theirpathogenicity by means of their virulence, a term which refers to the degree ofpathogenicity. Hence, the determinants of virulence of a pathogen are any of its genetic orbiochemical or structural features that enable it to produce disease in a host.The relationship between a host and a pathogen is dynamic, since each modifies theactivities and functions of the other. The outcome of such a relationship depends on thevirulence of the pathogen and the relative degree of resistance or susceptibility of thehost, due mainly to the effectiveness of the host defense mechanisms.Plant-interacting micro-organisms can establish either mutualistic or pathogenicassociations. Although the outcome is completely different, common molecularmechanisms that mediate communication between the interacting partners seem to beinvolved. Specifically, nitrogen-fixing bacterial symbiosis of legume plants, collectivelytermed rhizobia, and phytopathogenic bacteria have adopted similar strategies and genetictraits to colonize, invade and establish a chronic infection in the plant host. Quorum-sensing signals and identical two-component regulatory systems are used by thesebacteria to coordinate, in a cell density-dependent manner or in response to changingenvironmental conditions, the expression of important factors for host colonization andinfection. The success of invasion and survival within the host also requires that rhizobiaand pathogens suppress and/or overcome plant defense responses triggered aftermicrobial recognition, a process in which surface polysaccharides, antioxidant systems,ethylene biosynthesis inhibitors and virulence genes are involved.In view of the above facts, the present study was undertaken to achieve the followingobjectives – 1. To know about host- pathogen interaction. 2. To get knowledge about bio-warfare and penetration mechanisms. 3. To know about various weapons of fungi, bacteria, viruses and nematodes. 2
  4. 4. Plant pathogens:Plant pathology (also phytopathology) is the scientific study of plant diseases caused bypathogens (infectious diseases) and environmental conditions (physiological factors).Organisms that cause infectious disease include fungi, oomycetes, bacteria, viruses,viroids, virus-like organisms, phytoplasmas, protozoa, nematodes and parasitic plants.Not included are ectoparasites like insects, mites, vertebrate or other pests that affectplant health by consumption of plant tissues. Plant pathology also involves the study ofpathogen identification, disease etiology, disease cycles, economic impact, plant diseaseepidemiology, plant disease resistance, how plant diseases affect humans and animals,pathosystem genetics, and management of plant diseases. On the other hand, plantpathogen is an organism that causes a disease on a plant. Although relatives of some plantpathogens are human or animal pathogens, most plant pathogens only harm plants. Someplant pathogens make immuno-depressed people also sick. Organisms that cause plantdiseases reduce our ability to produce food and support the economy. All plants fromcitrus to grains to ornamental plants are susceptible to plant diseases. Plant diseases causebillions of dollars’ worth of direct and indirect losses every year (Citrus greeningexample). Emerging plant pathogens require preparation and planned, scientifically-basedresponse to lessen the impact on our farmers and the economy. Management of plantdiseases includes management of overall plant health. Healthy plants are less likely to getdiseases, just like healthy humans. You can help reduce the impact of both emerging andendemic plant pathogens by remembering not to transport unhealthy plant parts orproducts. An endemic pathogen is one that has become established in a new environmentand can no longer be eradicated. At that point, response switches from keeping it out oreradicating it to managing it through plant health, antimicrobial chemistries andmonitoring production. The major pathogen of plant are as follows-Fungi:The majority of phytopathogenic fungi belong to the Ascomycetes and theBasidiomycetes. The fungi reproduce both sexually and asexually via the production ofspores and other structures. Spores may be spread long distances by air or water, or theymay be soil borne. Many soil inhabiting fungi are capable of living saprotrophically,carrying out the part of their lifecycle in the soil. These are known as facultativesaprotrophs. Fungal diseases may be controlled through the use of fungicides and otheragriculture practices, however new races of fungi often evolve that are resistant to variousfungicides. A successful infection requires the establishment of a parasitic relationshipbetween the pathogen and the host, once the host has gained entry to the plant. There aretwo broad categories of pathogens –  Biotrophs:Those that establish an infection in living tissue. Biotrophs are less dangerous thannecrotrophs.  Necrotrophs: Those that kill cells before colonising them, by secreting toxins that diffuse ahead of theadvancing pathogen. 3
  5. 5. These two kinds of pathogens are also sometimes known as sneaks and thugs, becauseof the tactics they use to acquire nutrients from their hosts. Fig. Powdery mildew (Biotrophic) & Rice blast (necrotrophic) fungus  Hemibiotrophic:Hemibiotrophic begin frist biotrophic phase, then necrotrophic, intermediate hostrange e.g., Phytophthora (potato blight disease)Bacteria:Bacteria are microscopic, single-celled prokaryotic organisms, without a definednucleus, that reproduce asexually by binary fission (one cell splitting into two). Theyoccur singly or in colonies of cells. Bacteria are classified into two main groups based oncell wall structure, which can be determined by a simple staining procedure called theGram stain. Gram negative bacteria stain red or pink and Gram positive bacteria stainpurple. The difference in color is directly related to the chemical composition andstructure of their cell walls. The cells can be rod-shaped, spherical, spiral-shaped, orfilamentous. Only a few of the latter are known to cause diseases in plants. Most bacteriaare motile and have whip-like flagella that propel them through films of water.. Mostplant pathogenic bacteria are rod shaped (bacilli). Fig. Crown gall disease caused by Agrobacterium Fig. Infected stem 4
  6. 6. Viruses:Plant viruses are pathogens which are composed mainly of a nucleic acid (genome)normally surrounded by a protein shell (coat); they replicate only in compatible cells,usually with the induction of symptoms in the affected plant. Viroids are among thesmallest infections agents known. Their circular, single-stranded ribonucleic acid (RNA)molecule is less than one-tenth the size of the smallest viruses. There are many types ofplant virus, and some are even asymptomatic. Normally plant viruses only cause a loss ofcrop yield. Therefore it is not economically viable to try to control them, the exceptionbeing when they infect perennial species, such as fruit trees.Most plant viruses havesmall, single stranded RNA genomesPlant viruses must be transmitted from plant to plantby a vector. This is often by an insect (for example, aphids), but some fungi, nematodesand protozoa have been shown to be viral vectors. Fig. Tobacco mosaic virusNematodes:Nematodes are small, multicellular wormlike creatures. Many live freely in the soil, butthere are some species which parasitize plant roots. They are a problem in tropical andsubtropical regions of the world, where they may infect crops. Potato cyst nematodes(Globodera pallida and G. rostochiensis) are widely distributed in Europe and North andSouth America and cause $300 million worth of damage in Europe every year. Root knotnematodes have quite a large host range, whereas cyst nematodes tend to only be able toinfect a few species. Nematodes are able to cause radical changes in root cells in order tofacilitate their lifestyle. 5
  7. 7. Protozoa:There are a few examples of plant diseases caused by protozoa. They are transmitted aszoospores which are very durable, and may be able to survive in a resting state in the soilfor many years. They have also been shown to transmit plant viruses. When the motilezoospores come into contact with a root hair they produce a plasmodium and invade theroots. Fig. Leishmania donovani, (a species of protozoa) in a bone marrow cellParasitic plants:Parasitic plants such as mistletoe and dodder are included in the study of phytopathology.Dodder, for example, is used as a conduit for the transmission of viruses or virus-likeagents from a host plant to either a plant that is not typically a host or for an agent that isnot graft-transmissible. Fig. Cuscuta europaea on Sambucus ebulus 6
  8. 8. Economic significance:Plant diseases caused by fungi and oomycetes result in significant economic losses everyyear. Although phylogenetically distant, the infection processes by these organisms sharemany common features. These include dispersal of an infectious particle, host adhesion,recognition, penetration, invasive growth, and lesion development. Diseases are importantto humans because they cause damage to plants and plant products, commonly with anassociated economic effect, either positive or negative. Negative economic effects include–  Germination failure: Basic and primary loss of crop production due to seed borne pathogen. In diseased seed, pathogen kills the sprouting plumule in the seed. When farmer sow the seed under favorable condition, it germinates within 24 hours. On the same time pathogen germinate rather than more quickly. This pathogenic inoculum inhibit the germination ability of the seedlings.  Seedling diseases: In case of infected seed, when it germinate some seedlings are found healthy. But after some days this seedlings are infected by diseases. Infected seeds encourage different pathogen to make diseases. This is the major reason for destruction of seedlings but sometimes this infection symptom does not appeared immediately in case of seed borne diseases.  Adult plant infection: Adult plant are infected by the seed borne pathogen and almost all times yields are drastically reduced. In rice some pathogens like Pyricularia, Drechslera, Xanthomonas etc. which causes serious yield loss in other rice grown areas are common in Bangladesh and assumed to cause severe damage to the crop here also. Ahmed (1968) reported that stem rot alone damages 5 lakh bales of jute fibers. The value of five lakh bales of jute is TK. 800 million approximately at present world market.  crop failure: Diseases are responsible for the destruction of crop losses, in this why this is very important to know about all of the responsible causes responsible 7
  9. 9. for diseases. Ultimate goal of all kinds of diseases are lowering of diseases and we should try to control the pathogenicity of the pathogens.  Incremental loss from lower quality or failure to meet market standards: Diseases infestation results in contamination and loss of quantity in the crops; the quality losses may be due to relation in nutritional value. Or in marketability (lowering of grade). Loss is easily overlooked; this is the type of damage done to stored grain. A more common loss of quantity is the effect of diseases on the appearance of the crop, for example skeletonized or discolored vegetables or other crops have a lower market value than intact ones.Plant diseases are also responsible for the creation of new industries to develop controlmethods. Newly developed pesticide, fungicide, bio control agent helps to provideemployment opportunity.Description of various weapons of fungi, bacteria, viruses and nematodes used in thebio-warfare:Biological warfare (BW) also known as germ warfare are bacteria, viruses, fungi, orbiological toxins, used to kill or incapacitate humans, animals or plants as an act of war.Biological weapons (often termed "bio-weapons" or "bio-agents") are living organisms orreplicating entities (viruses) that reproduce or replicate within their host victims.Entomological (insect) warfare is also considered a type of BW. Here , the objectives ofpathogen to develop diseases at any cost and plant trying to kill / stop pathogenicorganisms.Biological weapons may be employed in various ways to gain a strategic or tacticaladvantage over an adversary, either by threat or by actual deployment. Like some of thechemical weapons, biological weapons may also be useful as area denial weapons. Theseagents may be lethal or non-lethal, and may be targeted against a single individual, agroup of people, or even an entire population. They may be developed, acquired,stockpiled or deployed by nation states or by non-national groups Fig. Logo of bio warfareDescription of various weapons:Modified hypha:Hyphae may be modified in many different ways to serve specific functions. Someparasitic fungi form haustoria that function in absorption within the host cells. The 8
  10. 10. arbuscules of mutualistic mycorrhizal fungi serve a similar function in nutrient exchange,so are important in assisting nutrient and water absorption by plants. Hyphae are foundenveloping the gonidia in lichens, making up a large part of their structure. In nematode-trapping fungi, hyphae may be modified into trapping structures such as constricting ringsand adhesive nets. Mycelial cords can be formed to transfer nutrients over largerdistances. Fig. Modified hypha penetrating host cellHaustoria:A specialized absorbing structure of a parasitic plant, such as the rootlike outgrowth ofthe dodder, that obtains food from a host plant. In parasitic fungi, haustoria arespecialized hyphae that penetrate the cells of other organisms and absorb nutrientsdirectly from them. Fungi in all major divisions form haustoria. Haustoria take severalforms. Generally, on penetration, the fungus increases the surface area in contact withhost plasma membrane releasing enzymes that break down the cell wall, enabling greaterpotential movement of organic carbon from host to fungus. Thus, an insect host aparasitic fungus such as Cordyceps may look as though it is being "eaten from the insideout" as the haustoria expand inside of it. Fig. Haustoria with conidiumAppressorium: 9
  11. 11. An appressorium is a flattened, hyphal "pressing" organ, from which a minute infectionpeg grows and enters the host, using turgor pressure capable of punching through evenMylar. Fungi that exhibit appressorial formation include the necrotroph Pyrenophorateres.Appressorium are the tube which enters the host, puts out branches between the cells ofthe host, and forms a mycelial network within the invaded tissue. The germ tubes of somefungi produce special pressing organs called appressoria, from which a microscopic,needlelike peg presses against and punctures the epidermis of the host; after penetration, amycelium develops in the usual manner. Many parasitic fungi absorb nutrient throughappressoria from host body. Fig. AppressoriaCapsules:The cell capsule is a very large structure of some prokaryotic cells, such as bacterial cells.It is a layer that lies outside the cell wall of bacteria. It is a well-organized layer, noteasily washed off, and it can be the cause of various diseases. .some bacteria form anorganized glycocalyx called a capsule around their cell walls which increases thevirulence of the species. The capsule helps resist host defenses by interfering withphagocytosis. If the human body produces antibodies against the capsule, this can allowdestruction of the bacteria byphagocytosis. Fig. Bacteria with capsule 10
  12. 12. Stylet:The stylet or stomatostyle, is the primitive mouth-parts of some nematodes and somenemerteans. It actually presents as a hardened protrusible opening to the stomach.The stylet is adapted for the piercing of cell walls, providing the operative organism withaccess to the nutrients contained within the prey cell. All plant-parasitic nematodes have astylet or mouth-spear that is similar in structure and function to a hypodermic needle. Thenematode uses the stylet to puncture plant cells, and then inject digestive juices and ingestplant fluids through it. All of the plant-parasitic nematodes that are important turfgrasspests feed on roots. Fig. stylet of nematodeToxins:Pathogens often benefit by producing toxins, which kill the tissue in advance ofenzymatic degradation. In many pathogens, particularly non-obligate pathogens, toxinscause the majority of damage to the hostEnzymesSome of the pathogen Produce enzymes that break down key structural components ofplant cells and their walls by soft-rotting bacteria that degrade the pectin ayer that holdsplant cells together.Mechanism of penetration & host tissue disintegration:Successful infection of a host plant by a pathogen involves the movement of the pathogentoward the host, attachment of the pathogen to the plant surface, penetration of the hostby the pathogen, and the proliferation of the pathogen inside the host immediatelyfollowing entrance.Microorganisms have various strategies to establish an infection in a host. Some micro-organisms recognize molecules on the surface of the host cell, and use these as receptors.The binding of bacteria or viruses to receptors brings the microorganism in close contactwith the host surface. 11
  13. 13. Fig. The mode of penetration by pathogenic organismsFungi: Penetration of a host by an invading fungus gives rise to the potential establishment ofphysiological contact between the two organisms. A fungus will usually use acombination of methods to gain access to host tissue.Physical mechanismsNatural Openings: Plants have several types of natural openings utilized by fungi. Themost common are stomates. Some fungi sense the location of openings by chemical orthigmatropic (touch) stimuli. Other natural openings include lenticels (open pores onwoody stems). Fig. open stomata 2. Wounds: Damage to a plant surface may result from animal and insect activities,environmental causes (e.g. hail), and mechanical injury (tree falling against stem,pruning). These sites provide ideal penetration sites for some types of fungi.3. Direct Penetration: After contact between a germ tube and the plant surface, the directpenetration of plant cells requires a combination of mechanical force and enzymatic 12
  14. 14. softening of the cuticle. Mechanical force is often achieved by a bulbous appressoriumand penetration peg. Fig. Direct penetration through penetration pegChemical MechanismsEnzymatic penetration of cell walls:During germination and penetration, fungi generally secrete a mixture of hydrolyticenzymes including cutinases, cellulases, pectinases, and proteases. Although theseenzymes are also required by saprophytes, their structures and biosynthetic regulationmay be adaptated to the specific needs of pathogens. For instance, different cutinaseisozymes are expressed during saprophytic and parasitic stages of Alternaria brassicicola.Many fungal genes encoding various hydrolytic enzymes have been cloned. Usually,however, the infection phenotype of gene disruption/replacement mutants does not differfrom wild-type. In particular, enzymatic degradation of cutin, the structural polymer ofthe plant cuticle, has been postulated to be crucial for fungal pathogenicity and cutinase tobe a key player in the penetration process.BacteriaBacteria are one of the many harmful germs throughout the body and in the environment.Germs and bacteria are almost everywhere in the world. Bacteria gets into the body whenthere is an open wound or an open patch of skin. When a knee is scraped and a person hasan open wound, it gives bacteria a chance to come directly into the body.Methods by which bacteria cause disease- Adhesion: Many bacteria must first bind to host cell surfaces. Many bacterial and hostmolecules that are involved in the adhesion of bacteria to host cells have been identified.Often, the host cell receptors for bacteria are essential proteins for other functions. Colonization: Some virulent bacteria produce special proteins that allow them tocolonize parts of the host body. Helicobacter pylori is able to survive in the acidicenvironment of the human stomach by producing the enzyme urease. Colonization of thestomach lining by this bacterium can lead to Gastric ulcer and cancer. The virulence ofvarious strains of Helicobacter pylori tends to correlate with the level of production ofurease. 13
  15. 15. Invasion: Some virulent bacteria produce proteins that either disrupt host cellmembranes or stimulate endocytosis into host cells. These virulence factors allow thebacteria to enter host cells and facilitate entry into the body across epithelial tissue layersat the body surface. Immune response inhibitors: Many bacteria produce virulence factors that inhibit thehosts immune system defenses. For example, a common bacterial strategy is to produceproteins that bind host antibodies. The polysaccharide capsule of Streptococcuspneumoniae inhibits phagocytosis of the bacterium by host immune cells. Toxins: Many virulence factors are proteins made by bacteria that poison host cellsand cause tissue damage. For example, there are many food poisoning toxins produced bybacteria that can contaminate human foods. Some of these can remain in "spoiled" foodeven after cooking and cause illness when the contaminated food is consumed. Somebacterial toxins are chemically altered and inactivated by the heat of cooking.Most bacterial pathogen damage host cell by in four main ways: 1. By using hosts nutrients (mainly iron) 2. By causing direct damage in the immediate area of the invasion 3. By producing toxins that may be transported by blood and lymph to damage sites far from the original invasion 4. By causing the host to react with a hypersensitivity reactionVirusesViruses require living cells for their replication. Some viruses, such as tobacco mosaicvirus (TMV) and cucumber mosaic virus, are found in many plant species.The replication of a plant virus appears to proceed according to the following generalscheme: introduction of the virus to a plant through a wound, release of the nucleic acidfrom the protein coat, association of viral RNA (or messenger RNA of DNA viruses) withcellular ribosomes for its translation to the proteins required for virus synthesis,replication of the nucleic acid and production of coat protein, and assembly of the nucleicacid and coat protein to form complete virus particles.Initially, most plant viruses multiply at the site of infection, giving rise to localizedsymptoms such as necrotic spots on the leaves. Subsequently, the virus may be distributedto all parts of the plant either by direct cell-to-cell spread or by the vascular system,resulting in a systemic infection involving the whole plant. However, the problem theseviruses face in reinfection and recruitment of new cells is the same as they face initially -how to cross the barrier of the plant cell wall. Plant cell walls necessarily containchannels called plasmodesmata which allow plant cells to communicate with each otherand to pass metabolites between them. Fig. Virus replication 14
  16. 16. The replication of viroids is not clearly understood at present. Cell-to-cell spread ofviruses usually occurs, and eventually the virus spreads throughout the plant. In someplants, the cells surrounding the initially infected cells die, and the virus usually does notspread further.NematodesPlant-parasitic nematodes have evolved diverse parasitic relationships with their hostplants to obtain nutrients that are necessary to support their development andreproduction. There are different types of plant-parasitic nematodes with characteristicpatterns of plant infestation:  Ectoparasites feed on the outside of plant roots causing severe moisture stress and a dramatic reduction in yield, e.g. sting, awl and stubby-root nematodes. Fig. Ectoparasitic nematode feed outside the host  Endoparasites enter the plant roots and root hairs resulting in malformation and yield reduction, e.g. reniform, cyst and root-knot nematodes Fig. Endoparasitic nematode feed inside the hostEndoparasitic nematode species must penetrate host tissues directly, usingmechanical and/or biochemical methods. Secreted proteases from parasiticnematodes appear to aid in the penetration and migration through animal tissues. Forplant-parasitic nematodes, a cell wall composed primarily of cellulose poses a 15
  17. 17. formidable barrier to penetration. Thrusts of the nematode stylet combined withesophageal gland secretions mediate penetration and migration through planttissues. Plant-parasitic nematodes possess an arsenal of hydrolytic enzymes fordigesting cell wall polymers. Genes encoding secreted cell-wall-modifying enzymeshave been localized to nematode esophageal gland cells including enzymes thatdegrade the pectic polysaccharides (pectate lyases and polygalacturonases)comprising the middle lamella between plant cells and enzymes that degrade thecellulose (endoglucanases) and hemicellulose (xylanase) structural components ofthe cell wall Interestingly, the cell-wall-modifying enzymes appear to beactive only in the subventral gland cells and, in the case of the cyst nematodeendoglucanases, they are only active during nemat ode migration within roots,whereas plant endoglucanases upregulated in feeding sites probably modifythe walls comprising these specialized cells which named gall.Disease development:Pathogenicity is the ability of an organism to enter a host and cause disease. The degreeof pathogenicity, that is, the comparative ability to cause disease, is known as virulence.The terms pathogenic and nonpathogenic refer to the relative virulence of the organism orits ability to cause disease under certain conditions. This ability depends not only uponthe properties of the organism but also upon the ability of the host to defend itself (itsimmunity) and prevent injury. The concept of pathogenicity and virulence has nomeaning without reference to a specific host.While necrotrophs have little effect on plant physiology, since they kill host cells beforecolonising them, biotrophic pathogens become incorporated into and subtly modifyvarious aspects of host physiology, such as respiration, photosynthesis, translocation,transpiration and growth and development. The respiration rate of plants invariablyincreases following infection by fungi, bacteria or viruses. The higher rate of glucosecatabolism causes a measurable increase in the temperature of infected leaves. An earlystep in the plants response to infection is an oxidative burst, which is manifested as arapid increase in oxygen consumption, and the release of reactive oxygen species, such ashydrogen peroxide (H2O2) and the superoxide anion (O2-). The oxidative burst is involvedin a range of disease resistance and wound repair mechanisms Link to Rapid ActiveDefense. In resistant plants, the increase in respiration and glucose catabolism is used toproduce defence-related metabolites via the pentose phosphate pathway. In susceptibleplants, the extra energy produced is used by the growing pathogen.Pathogens also affect photosynthesis, both directly and indirectly. Pathogens that causedefoliation rob the plant of photosynthetic tissue, while necrotrophs decrease thephotosynthetic rate by damaging chloroplasts and killing cells. Biotrophs affectphotosynthesis in varying degrees, depending on the severity of the infection. Abiotrophic infection site becomes a strong metabolic sink, changing the pattern of nutrienttranslocation within the plant, and causing net influx of nutrients into infected leaves tosatisfy the demands of the pathogen. The depletion, diversion and retention ofphotosynthetic products by the pathogen stunts plant growth, and further reduced theplants photosynthetic efficiency. In addition, pathogens affect water relations in theplants they infect. Biotrophs have little effect on transpiration rate until sporulationruptures the cuticle, at which point the plant wilts rapidly. Pathogens that infect the roots 16
  18. 18. directly affect the plants ability to absorb water by killing the root system, thus producingsecondary symptoms such as wilting and defoliation. Pathogens of the vascular systemsimilarly affect water movement by blocking xylem vessels. Growth and development ingeneral are affected by pathogen infection, as a result of the changes in source-sinkpatterns in the plant. Many pathogens disturb the hormone balance in plants by eitherreleasing plant hormones themselves, or by triggering an increase or a decrease insynthesis or degradation of hormones in the plant. This can cause a variety of symptoms,such as the formation of adventitious roots, gall development, and epinasty (the down-turning of petioles).Factors that affect disease developmentPathogen Host Environment  Presence of pathogen  Susceptibility  Temperature  Pathogenicity  Growth stage & form  Rainfall / Dew  Adaptability  Population density &  Leaf wetness period structure  Dispersal efficiency  Soil properties  General health  Survival efficiency  Wind  Reproductive fitness  Fire history  Air pollution  Herbicide damageOverall diseases development process includes major steps. They are as follows-  Enzymatic degradation:In their most basic form, pathogens secrete enzymes, which catalyze the breakdown ofhost tissues, similar to the digestion of food in mammals.  Toxins:Pathogens often benefit by producing toxins, which kill the tissue in advance ofenzymatic degradation. In many pathogens, particularly non-obligate pathogens, toxinscause the majority of damage to the host.  Growth regulators:Pathogens often find it advantageous to produce growth regulators (or cause the host toproduce them). The most common are those that cause translocation of nutrients to host 17
  19. 19. cells and/or cause host cells to enlarge or divide in the vicinity of the pathogen, thusproviding an increase in food for the pathogen. Obligate pathogens are very good at thistechnique because it allows the host to go on living, but still provides extra food for thepathogen.  Genetic manipulations:All viruses plus a few bacteria are able to force the plant to produce pathogen geneproducts from pathogen genetic material. This starves plant cells and disrupts theirfunction. 18
  20. 20. Conclusion:Most of the pathogens can only cause disease on a relatively small group of host plantsbecause of the slightly different set of specialized genes and molecular mechanismsrequired for each host-pathogen interaction. On the other hand, against pathogenicity,plant show resistance. The cell wall is a major line of defense against fungal and bacterialpathogens. It provides an excellent structural barrier that also incorporates a wide varietyof chemical defenses that can be rapidly activated when the cell detects the presence ofpotential pathogens. All plant cells have a primary cell wall, which provides structuralsupport and is essential for turgor pressure, and many also form a secondary cell wall thatdevelops inside of the primary cell wall after the cell stops growing.Many cell walls also contain lignin, a heterogeneous polymer composed of phenoliccompounds that gives the cell rigidity. Lignin is the primary component of wood, and cellwalls that become “lignified” are highly impermeable to pathogens and difficult for smallinsects to chew. Cutin, suberin, and waxes are fatty substances that may be deposited ineither primary or secondary cell walls (or both) and outer protective tissues of the plantbody, including bark. So that biological warfare conduct in indigenous crop plant withrespective wapons. Growth and development in general are affected by pathogeninfection, as a result of the changes in source-sink patterns in the plant. Many pathogensdisturb the hormone balance in plants by either releasing plant hormones themselves, orby triggering an increase or a decrease in synthesis or degradation of hormones in theplant. This can cause a variety of symptoms, such as the formation of adventitious rootsand gall development.Minimizing plant disease requires understanding the mechanisms of survival and spread.A competitive exclusion mechanism by beneficial organism can be effective in protectionagainst disease. (Biological Control of Plant Pathogens). 19
  21. 21. References:American Phytopathological Society. 2003. Microbial genomic sequencing. Perspectives of the American Phytopathological Society (revised 2003). 21 pp.Anderson RV, Byers JR (1975) Ultrastructure of the esophageal procorpus in the plant parasitic nematode, Tylenchorhynchus dubius, and functional aspects in relation to feeding. Can. J. Zool. 53:1581-1595.Arnold, D.L., Pitman, A., and Jackson, R.W. 2003. Pathogenicity and other genomic islands in plant pathogenic bacteria. Mol. Plant Pathol. 4:407-420.Atkinson HJ, Harris PD (1989) Changes in nematode antigens recognized by monoclonal antibodies during early infections of soya beans with the cyst nematode Heterodera glycines. Parasitology 98:479-487.Baum TJ, Hiatt A, Parrott WA, Pratt LH, Hussey RS (1996) Expression in tobacco of a functional monoclonal antibody specific to stylet secretions of the root-knot nematode. Mol. Plant-Microbe Interac. 9: 382-387.Bird AF (1971) Specialized adaptation of nematodes to parasitism. In: Zuckerman BM, Mai WF, Rohde RA (eds), Plant Parasitic Nematodes Vol. II, pp.35-49. Academic Press, New York, USA.Bird AF (1983) Changes in the dimensions of the esophageal glands in root-knot nematodes during the onset of parasitism. Int. J. Parasitol. 13:343-348.Bird DMcK (1996) Manipulation of host gene expression by root-knot nematodes. J. Parasitol. 82:881-888.Burgess TL, Kelly RB (1987) Constitutive and regulated secretion of proteins. Annu. Rev. Cell Biol. 3:243-293.Cao, H., Baldini, R.L. and Rahme, L.G. 2001. Common mechanisms for pathogens of plants and animals. Annu. Rev. Phytopathol. 39:259-284.Fire A, Xu S, Montgomery MK, Kostas SA, Driver SE, Mello CC (1998) Potent and specific genetic interference by double-stranded RNA in Caenorhabditis elegans. Nature 391:806-811.Gao B, Allen R, Maier T, Davis EL, Baum TJ, Hussey RS (2001a) Identification of putative parasitism genes expressed in the esophageal gland cells of the soybean cyst nematode, Heterodera glycines. Mol. Plant-Microbe Interac. 14:1247-1254.Glidewell DC, Mims CW. Ultrastructure of the haustorial apparatus in the rust fungus Kunkelia nitens. Botanical Gazette. 1979;140:148–152. doi: 10.1086/337071. 20
  22. 22. Hussey RS, Davis EL, Ray C (1994) Meloidogyne stylet secretions. In: Lamberti F, De Giorgi C, Bird D Mck (eds), Advances in Molecular Plant Nematology. pp.233- 249. Plenum Press, New York.Hussey RS, Mims CW (1991) Ultrastructure of feeding tubes formed in giant-cells induced in plants by the root-knot nematode Meloidogyne incognita. Protoplasma 162:99-107.Hussey RS, Paguio OR, Seabury F (1990) Localization and purification of a secretory protein from the esophageal glands of Meloidogyne incognita with monoclonal antibodies. Phytopathology 80:709-714.Jaubert S, Laffaire JB, Abad P, Rosso M-N (2002) A polygalacturonase of animal origin isolated from the root-knot nematode Meloidogyne incognita. FEBS Letters 522:109-112.Klement, Z., Farkas, G. L. and Lovrekovich, L. 1964. Hypersensitive reaction induced by phytopathogenic bacteria in the tobacco leaf. Phytopathology 54:474-477.Lambert KN, Allen KD, Sussex IM (1999) Cloning and characterization of an esophageal-gland-specific chorismate mutase from the phytoparasitic nematode Meloidogyne javanica. Mol. Plant-Microbe Interac. 12:328-336.Lindow, Steven E. 1987. Competitive exclusion of epiphytic bacteria by ice- Pseudomonas syringae mutants. Appl. Environ. Microbiol. 53:2520-2527.Mazarei M, Ying Z, Houtz RL (1998) Functional analysis of the rubisco large subunit N- methyltransferase promoter from tobacco and its regulation by light in soybean hairy roots. Plant Cell Rep. 17:907-912.Mitchell HJ, Hardham AR. Characterisation of the water expulsion vacuole in Phytophthora nicotianae zoospores. Protoplasma. 1999;206:118–130. doi: 10.1007/BF01279258.Money NP. Why oomycetes have not stopped being fungi. Mycology Research. 1998;102:767–768. doi: 10.1017/S095375629700556X.Nakai K, Horton P (1999) PSORT: a program for detecting sorting signals in proteins and predicting their subcellular localization. Trends Biochem. Sci. 24:34-35.Nielsen H, Engelbrecht J, Brunak S, von Heijne G (1997) Identification of prokaryotic and eukaryotic signal peptides and prediction of their cleavage sites. Protein Eng.10:1- 6.Ophel, K.M., Bird, A.F. and Kerr, A. 1993. Association of bacteriophage particles with toxin production by Clavibacter toxicus, the causal agent of annual ryegrass toxicity. Phytopathology 83: 676-681. 21
  23. 23. Park G, Xue C, Zheng L, Lam S, Xu J-R. MST12 regulates infectious growth but not appressorium formation in the rice blast fungus Magnaporthe grisea. Mol Plant- Micro Interact. 2002;15:183–192. doi: 10.1094/MPMI.2002.15.3.183.Ponciano, G., Ishihara, H., Tsuyumu, S. and Leach, J.E. 2003. Bacterial effectors in plant disease and defense: keys to durable resistance? Plant Dis. 87:1271-1282.Popeijus H, Blok V, Cardle L, Bakker E , Phillips MS , Helder J, Smant G , Jones J (2000a) Analysis of genes expressed in second stage juveniles of the potato cyst nematodes Globodera rostochiensis and G. pallida using the expressed sequence tag approach. Nematology 2:567-574.Popeijus HE, Overmars H, Jones J, Blok V, Goverse A, Helder J, Schots A , Bakker J, Smant G (2000b). Degradation of plant cell walls by nematodes. Nature 406:36- 37.Rosso M-N, Piotte C, Favery B, Arthaud L, Hussey RS, de Boer JM, Baum TJ, Abad P (1999) Isolation of a cDNA encoding a b-1,4-endoglucanase in the root-knot nematode Meloidogyne incognita during plant parasitism. Mol. Plant-Microbe Interac. 12:585-591.Schaad, N. W., Jones, J. B. and Chun, W. (ed.). 2001. Laboratory guide for identification of plant pathogenic bacteria. 3rd ed. American Phytopathological Society Press. St. Paul, MN.Trail F. Fungal cannons: explosive spore discharge in the Ascomycota. FEMS Microbiol Lett. 2007;276:12–18. doi: 10.1111/j.1574-6968.2007.00900.x.Urwin PE, Lilley CJ, Atkinson HJ (2002) Ingestion of double-stranded RNA by preparasitic juvenile cyst nematodes leads to RNA interference. Mol. Plant- Microbe Interact. 15:747-752.Vidhyasekaran, P. 2002. Bacterial disease resistance in plants. Molecular biology and biotechnological applications. 452 pp. The Haworth Press, Binghamton, NY.Walker SK, Chitcholtan K, Yu YP, Christenhusz GM, Garrill A. Invasive hyphal growth: An F-actin depleted zone is associated with invasive hyphae of the oomycetes Achlya bisexualis and Phytophthora cinnamomi. Fungal Genetics and Biology. 2006;43:357–365. doi: 10.1016/j.fgb.2006.01.004.Williamson VM, Hussey RS (1996) Nematode pathogenesis and resistance in plants. Plant Cell 8:1735-1745.Young, J.M., Saddler, G.S., Takikawa, Y., DeBoer, S.H., Vauterin, L., Gardan, L., Gvozdyak, R. I. and Stead, D.E. 1996. Names of plant pathogenic bacteria 1864- 1995. Rev. Plant Pathol. 75:721-763. 22
  24. 24. Zhao X, Kim Y, Park G, Xu J-R. A mitogen-activated protein kinase cascade regulating infection-related morphogenesis in Magnaporthe grisea. The Plant Cell. 2005;17:1317–1329. 23