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Chapter X EFFECT OF INFECTION ON PHYSIOLOGY OF THE HOST. In preceding chapters a brief account of the process of infection, its establishment, and the potential activities of the pathogen was given. After establishment of infection, when the infections causal agent of a disease starts parasitic or pathogenic action, host tissues show different types of responses to these activities. In the initial stages of penetration there may be a striking increase in protoplasmic strands and the nucleus of the cell may move to the site of penetration. Cytoplasmic particles, in rapid Brownian movement, appear fallowed by granulation of the cytoplasm and appearance of many more particles in Brownian movement.Later the cellcontents become yellow and finaly dark brown when Brownian movement ceases and the cell is dead. Normal physiological activities of the host cells are disturbed and anatomical and morphological changes (morbid anatomy ) Appear as visible changes. In pathogenesis the first stage after infection is the manifestation of these responses of the host cells which appear in the following forms: 1.- Structural changes: In diseased plants usually adnormal structures are seen. Examples are overgrowth (Hyoertrophy), sterile flowers, phyllody, hairy roots, witch´s broom, bunchy top, crown gall, root knots, etc.. These abnormalities are discussed in the present and the following chapters. However, the apperance of abnormal structures on the sick plants is not due to physical but to chemical reactions occurring within the plant body and are therefore, expression of physiological malfunctioning of the host cells. 2.- Physiological changes: Harmful effects of infection on host physiology are yhe main causes of symptom expression and loss. In this chapter, brief account of following harmful effects is given. - Desintegration of tissues by the action of enzymes of the pathogen. - Effect of pathogenesis on growth of the host plant due to growth regulators produced by the pathogen or by the host under the influence of the pathogen. - Effect on reproductionof the host. - Effect on uptake and translocation of nutrients and water. - Abnormal respiration of the host tissues due to disturbed enzyme system associated with respiration. - Reduction in photosynthesis due to destruction of leaves or loss of chlorophyll. - The role of toxins in disturbing the phisiology of the host has been discussed in the following chapter. Tissue desintegration Among diverse symptoms of plant diseases the most common are those caused by didintegration of tissues. There are very few diseases that do not show tissue disintegration and death of cells at some stage after infection by the pathogen. These symptoms are so prominent that they had attracted the attentoin of man in ancient times. Usually the word “rot” is used for such symptoms. The word is derived from “ret” connected with “retting”, the process of soaking fibre-bearing tissues in water and macerating the tissues by biological action to separate the fibre. Thus, in tissue disintregration the cells and tissues of the host plant are separated from each other resulting in condition known as rot. This condition is present even in many necrotic spots. The material binding the cells to form tissues is destroyed by the pathogen to enable it reach the host protoplasm. Such pathogens are mostly facultativa parasites or saprophytes. However, obligate parasites or pathogens and even non-parasitic causes of disease can induce tissue disintegration through indirect effects. As a result of tissue disintegration or rot the symptoms known as blight, canker, anthracnose, etc. Appear on the plant. Fungi, bacteria and nematodes bring about tissue disintegration through the action of enzymes secreted by them. These enzymes are of different types for action on different tissues and chemical constituents of the cell wall. (i) (ii) (iii) Cuticular enzymes: The epidermis of plant is covered by cuticle and propagules of the pathogen first contact the host on this surface. The major chemical substance in cuticle is a cutin framework with waxes embedded in it and extruded from its surface to give a waterproof surface (the cuticular wax). The central region of the cuticle consists of cutin, a polyester of hidroxylated monocarboxylic acids each containing 16 to 18 carbon atoms and 2 to 3 hydroxyl groups. On hydrolysis the polyesters yield fatty and hydroxy-fatty acids. The wax portin consists of complex mixtures of long chain paraffins, alcohols, ketones, esters and acids. Paraffins and esters predominate on the outer surface. Small quantities of other substances such as proteins, carbohydrates, pigments and occluded pectin and cellulose may also by present. The thickness of cuticle varies with plant species. The amount of wax also similarly varies with plant type. The role of fungal enzymes in degradation of complex chemical structure of cuticle is not well understood . It is presumed that the cuticular enzymes mainly help in penetration of infection thread by pressure. Various enzymes suggested to be envolved in dissolution of cuticle are: (1) cutinase which catalyses the breakdown of cutin, hydrolysing it into cutin acids ( fatty and hydroxy- fatty acids), (2) those enzymes which help in the breakdown of fatty acids, and (3) enzymes which degrade other cuticular substances such as proteins, cellulose, pectin, pigments, etc. Germinating spores of Colletotrichum gloesporioides are reported to degrade the cuticle of orange leaves (Chaudhuri, 1935). Similar reports exist for Sphaerotheca pannosa ( powdery mildew of rose), Venturia inaequalis(bittler rot of apple), and Helminthosporium victoriae (Blight of oats). Pectic enzymes: After cuticle has been penetrated the pathogen comes in contact with cell wall protecting the protoplasm. The main components of cell wall are pectin or pectic substances, cellulose, hemicellulose, lignin and a small quantity of protein. Fungi, bacteria and nematodes which feed on the protoplasm have to degrade these substances to dissolve the middle lamella and cell walls so that protoplasm may be reached. Pectin or pectic substanses are major chemical components of middle lamella which binds the cells together.The pathogens like fungi, bacteria and nematodes are knowm to contain pecticor pectinolytic enzymes and use these enzymes against this group of materials. Extensive literature exists on the significance of pectic enzymes in plant diseases. Pectic substances are polymers consisting primarily of - 1,4 linked galacturonic acid units. The carboxyl group on carbón 6 may be unesterified an is polygalacturonic acids which . if colloidal, are known as pectic acids which, if colloidal, are known as pectic acids..The esterified carboxyl group of pectic acids on esterification with methyl alcohol. Pectina are pectinic acids of hihg methoxy content or more of the methylated carboxyl groups. The degradation of pectyic substances is brought about by two groups of pectinolytic enzymes: The pectinesterases and polygalacturonases. Pectinesterases are widely distributed in plants and microorganisms. Those in fungi have a lower optimun pH for their activity. The pectinesterases or pectinmethilesterases (PME) catalyse hydrolysis of the methil ester groups of pectinic acids to methyl alcohol and pectinic acids of reduced methoxy content. Eventually pectic acid is formed. This is attacked by polygalacturonase group of enzymes which includes glycosidases and lyases (eliminative mechanism) . These enzymes break the links between adjacent galacturonic acid units. Polygalacturonase (PG) attacks pectic acid and polymathilgalacturonase (PMG) attacks pectin. The presence and amount of pectinolytic enzymes differ in different fungi and is governed by many factors such as pH. The fact that the same fungi will produce the same enzymes in the host also and the enzymes will play some role in pathogenesis. Under certain conditions the pectinolytic enzymes are inactivated or rendered ineffective. Phenolic compounds or their oxidation products common in darkened tissues at sites of injury inavtivate pectic and other enzymes. Indole acetic acid also inhibits certain pectic enzymes.. The degradation of pectic substances provides nutrients for many fungal pathogens and due to weakening of the cell wall facilitates inter- and intracellular invasión by hyphae. There is no evidence so far to show that pectic enzymes affect the protoplasm of host cell. These enzymes are apparently of primary importance in soft rot diseases such as those caused by Erwinia dissolvens, E. Carotovora, E aroideae, Pseudomonas spp. Botrytis cinerea, Sclerotinia sclerotiorum, Scleritium rolfsii, Rhizoctonia solani, species of Pythium , Phytophthora and Rhizopus. However, more specialised pathogens such as Puccinia graminis tritici also produce pectic enzymes duryn spore germination. This facilitates the movement of hyphae in between the cells. The activity of pectic enzymes may be aggravated by synergostic action of other enzymes and metabolites. In the invasion of Sclerotium rolfsii oxalic acid produced by the pathogen plays a similar role. ( iii).Cellulolytic enzymes: Cellulose is the major component and bassic unit of structural framework of plant cell wall . Comparatively little is known about the significance of celullolytic enzymes and enzymated degradation of cellulose in plant diseases. Howeber, since in most diseases where tissue desintegration is a common feature, degradation of cellulose does occur to ennable the pathogen dissolve the cell wall. Celllulolyted enzymes (celluloses) are fourd in fungi , bacteria, many nematodes and phanerogamic plant parasites . Some workers believe that a single enzyme converts cellulose into glucose by random cleavage of the molicule.. Others have suggested that native cellulose is converted to the disaccharide cellobiose by one enzyme and thence to glucose by a second one. Still others suggest that a series of steps are involved in the conversion of cellulose into glucose. The native cellulose molecules are released or loosened from the chains by the action of C1 enzymes. These loosened molecules then take up water and are hydrolysed by Cx enzymes to soluble low molecular cellosaccharides and finally to cellobiose and glucose. These are then attacked by -Glucosidases to form glucose. The degradation of pectic substances and cellulose not only helps the pathogens in invasion of tissues and their desintegration, it causes other effects also.. The degraded products are used by fungi as food. Large molecules released by degradation often cause plugging of vessels thus partly contributing to development of synptoms of wilt in many plants. (iv).- Hemicelluloses: In addition to cellulose and pectin, the plant cell walls contain the complex water –insoluble polysaccharides known as hemicelluloses which are attached with cellulose and lignin. The Hemicellulose are important constituents of mature and thickened cell walls. They contain complex mixtures of such pentosans as xylans , mannans, galactans and arabans. The process of degradation of hemicelluloses is not much known. Many parasitic and saprophytic microorganisms produce the enzymes hemicelluloses for hydrolysis of these polysaccharides and produce simpler sugars. Certain components of hemicelluloses are degraded by cellulolytic enzymes also. The degradation of hemicelluloses exposes the cellulose and lignin of the cell wall for action of enzymes of the fungi. Reports implicating hemicelluloses in plant diseases are few . Xylanase and arabinase has been found in hypocotyl of sunflower attacked by Sclerotinis sclerotiorum, Sclerotinia fructigena produces arabinofuranosidase in cultures . Scleritium rolfsii produces, exogalactonase endomannnse, galactosidase, and endoxylanase in culture. (v).- Lycnolitic enzymes: The most complex chemical compound in plant cell walls is lignin the mechanism of degradation of which is least known . Pectic materials and cellulose are the major constituents of of herbaceous agricultural crops which contain lignin mostly in walls of their xylem vessels and in fibrous tissues. Howeber, woody perennial plants contain relatively much larger amounts of lignin . In woody cells lignin constitutes almost all of the middle lamella and forms its own framework in the walls so that the latter are strengthened and remain intact even after cellulose and hemicellulose are removed. Deposition of lignin is usually followed by death of the cells and the fungi which attack lignified tissues are usually perthotrophos. Lignin is a three dimensional, branched polymer formed by the oxidative polymerisation of three substituted cinnamaryl alcohols: -coumaryl alcohol, coniferyl alcohol and sinapyl alcohol. The amount of these alcohols in lignin differs with plant species. Most of the knowledge about degradation of lignin has been accumulated from studies of the action of wood rotting fungi ( Basidiomycetes, chieffy white rot type) although the foot rot of cereals in which fairly high amounts of lignin are present indicates that lignolytic enzymes might be involved. It is believed that these fungi produce polyphenol oxidases and through their action assimilate and metabolise lignin . Many wood rotting fungi degrade lignin but cannot utilise it. Among other fungi reported to cause partial degradation of lignin are Alternaria, Cephalosporium, Chaetomium, Xylaria, Pestalozzia, Fusarium and Penicillium. Among phytopathogenic bacteria the species of Pseudomonas and Xanthomonas can cause degradation of lignin. (vi).- Ither enzymes involved in degradation of cell wall and cell contents: After decomposing the cell walls the fungal hyphae come in contact with the host protoplasm. They get the required food from this sourse. The protosplasm contains mainly proteins, starch and lipids. In addition, phosphorus, potash, sulphur and iron are also present . Nucleic acids and protein are constituents of the nucleus. There is little information as to whether protein breakdown plays any part in the degradation of cell walls. Mechanism of protein breakdown by plant pathogens is the same as found in plants and animals . The enzymes peptidase attack and break down the polypeptides into lower peptides and amino acids which are utilised by the pathogens, Starch is hydrolysed by enzymes amylase to produce glucose used by the pathogens as nutrients. Lipids are degraded by enzyme lipase. The nucleic acids (ribonucleic acid or RNA and deoxyribonucleic acid or DNA) are present in the cell and may be degraded by the action of plant pathogens.DNA is mainly present in the nucleus and in very small quantities in the chloroplasts and mitochondria. RNA is present throughout the cell. These acids contain linear chains of alternating molecules of phosphate and a sugar (ribose in RNA and deoxyribose in DNA). Hydrolisis of these acids by enzymes ribonuclease and deoxyribonuclease results in formation of mononucleotides. Nonspecific phosphatases hydrolyse nucleotides . Further action by deaminases separates de amino groups from the nucleosides and makes them available to the parasite. From the above description it is obvious that tissue desintegration is a function of enzymes secreted by the pathogenic organisms. The destruction of cell walls leads probably to plasmolysis of protoplasts and death of the cell and utilisation of cell contens by the parasite. These degrading processes result in rots, blights and cankers, etc. The tissues thus broken are only those present at the site where the parasite is active. Sometimes desintegration of tissues occurs at a distance from this site . It is due to traslocated toxins produced by the pathogen. Necrosis caused by many obligate parasites and pathogens including viruses is not due to enzymic acxtion of their own but due to indirect effect. This may include hypersensitive reaction of the host, toxins, starvation of the cells and nonavailability of materials required for synthesis of cell walls. In deficiency diseases the necrosis representing tissue desintegration is due to shortage of elements required for cell wall synthesis and inhibition of other cellular activities. Effect on Growth of the Host The growth of plants is controlled by naturally present growth regulators in the plant body, In some diseases this control is disturbed and various structural abnormalities appear on the host. The regulatory substances are of two types: growth promoting which include specific hormones and growth inhibitory substances. Auxins, gibberellins and cytokinins are the known growth promoting substances . In a broad sense, gibberellins and cytoquinins are also auxins but in strict sense only indole acetic acid ( IAA) is known as auxin. Dormin, ethylene, etc are growth inhibitors or induce such reactions in the plant that lead to premature ripening of fruits and untimely formation of abscission layers leading to fall of leaves, fruits and flowers. The growth inhibitors can inhibit the action of growth promotors or the farmer can be rendered ineffective by the latter. This depends on the condition of the plant and its response to infection by a pathogen. The pathogens ( fungi, bacteria, nematodes) also producegrowth regulators . When such substances are produced during the period of infection the host cells are induced to show growthresponses. These responses at wrong time produce adverse effect on normal growth of the plant. Pathogens also produce substances as metabolites that are not hormones but effect the regulatory mechanisms in the plant thereby causing unrestricted production of growth regulators by the plant. Production of growth promoting substances in excess of normal requirements of the plant causes overgrowth of cells and tissues. In addition to their own effect the growth inhibitors produced by the pathogen can render the growth promoting substeances of the plant ineffective or inhibit their production thus causing growth retardation or stunting of organs or the entire plant. The imbalance in growth promoting and growth inhibiting substances causes appearance of symptoms known as hypertrophy and atrophy. Hypertrophy may appear as tumours, galls, knots, abnormal increase in organss size ¨, witch¨s broom, etc. Auxins:The naturally occurring auxin in the plants is indole acetic acid (IAA). Many plants pathogens produce small quantities of IAA or induce the plant to produce more of this substance . Although tryptophan is most important precursor of this auxin, it appears that differentorganisms have envolved different pathways of IAA synthesis involving precursors other than tryptophan. It is also possiblethat some auxin, other than IAA or gibberelins, may be involved in pathogenesis. IAA regulates cell growth and differentiation. It also effects cell wall permeability . Due to effect of IAA on oxidative enzyme system of the plant there may be abnormal increase in respiration of the tissues. It has also been suggested that this auxin even effects the genetics of the plant. The increase in the amount of indole (indolyl) acetic acid has been noticed in many diseased conditions of plants. These diseases can be due to any type of infections causes such as bacteria, fungi, nematodes and virus. The fungi causing late blight of potato (Phytopthora infestans), smut of matize (Ustilago maydis), Panama disease of banana ( Fusarium oxysporium f. Sp cubense), downy mildews of maize and bajira ( Sclerospora sacchari, S. philippinensis, S graminicola) and the nematode causing root knot (Meloidogyne spp) not only induce the plant to synthesise more IAA but also themselves produce this auxin. The conversion of tryptophan into IAA takes place in following steps: Tryptophan Tryptophan Indole pyruvic Or Tryptamine Indole acetaldechyde IAA Indole acetaldechyde IAA It is not clearly understood whether the excess of IAA detected in diseased plants is due to the plant or the pathogen or due to interaction of both. It could be due to excessive production of IAA by the diseased plant or due to production of this compound by the pathogen in the plant tissues or it could be due to its reduced destruction in the diseased tissues. Plants contain enzymes (IAA oxidase) that can degrade indole acetic acid . These enzymes keep the amount of IAA in the plant under check to permit its normal growth. It is possible that the pathogen inactivates these IAA oxidising enzymes by its metabolites and thus the level of IAA in the plant continues to rise. This condition has been proved in maize smut ( Ustilago maydis ) and wheat rust (Puccinia graminis) Hyperauxinity (excess of IAA) has been detected in many other diseases such as rust of Euphorbia Cyparissias caused by Uromyces pisi , powdery mildew (Erisiphe graminis) on wheat and white blister of Brassica napus (Albugo candida). The production and activities of auxins have been studied in some detail in bacterial plant diseases. Two such examples are given here. In bacterial wilt and brown rot of potato caused by Pseudomonas solanacearum the bacterium grows in vascular bundles of the tuber and stem and causes vascular browning, rot and wilt. Biochemical analysis has shown that diseased plants contain 100 times more IAA than the Healthy plants. At the same time phenolic compounds (scopoletin) also increase 10 times. Phenols are known to suppres the activities of IAA oxidase. Thus, one of the explanations for increased amount of IAA in diseased potato plants can be that the rise in phenols in diseased tissues suppresses the IAA oxidising enzyme that regulates the production and accumulatiun of the auxin . However, the level of this auxin rises in the beginning of pathogenesis also suggesting that the plant also syntheses it to some extent. After the death of the plant rise in level of the cause continues. This suggests that the bacterium also synthesizes the auxin in dead tissues. Thus,all the three possbilities of the cause of hyperauxinity exist in this disease. The hifh level of IAA in the plant increases plasticity and permeability of cell walls. This makes the pectin , cellulose and proteins easily available to the pathogen. Although phenols help in lignin synthesis which makes tissues resistant this does not happen in the diseased plant because IAA interferes with lignification of tissues. Thus, the bacterium gets more time for tissue desintegration. Increased respiration and transpiration are other effects produced by IAA through altered cell wall permeability. The second example is that of Agrobacterium Tumafaciens . This bacterium attacks more than 100 plant species and produces galls on root crown, stems and petioles. Crown gall caused by this bacterium has served as the classic model for investigations of the role of auxins, indoleacetic acid and related indole compounds in plant pathogenesis . The extensive research on this disease , was spurred by its similarity to carcinigenesis in animals . The bacterium is not present in galled tissues. The gall or tumour is initiated in two phases. The first is conditioning phase in which a fresh wound is required without the presence of the bacterium. Then the bacterium enters the host and second phase stars. The conditioned cells are transformed into tumour cells by an agent, termed the tumour – inducing principle (TIP) produced by the bacterial pathogen. This phase occurs only at temperatures below 29 0C . Afterwards, there is no function of the host or the bacterium in the development of the tumour. The tumour cells multiply and develop the galls. The process cannot be checked by killing the bacterium. The tumour cells multiply and develop the galls. The process cannot be checked by killing the bacterium. The tumour cwlls contain more than normal quantity of IAA. In addition, they contain cytokinins.Althouth the bacterium is capable of porducing indole acetic acid the tumour cells free from bacteria also contain higher level of IAA suggesting that the cells themselves are capable of synthesising this auxin. Since the enzymes capable of oxidising IAA are in identical amounts in normal and tumour cells it is evident that the excess auxin in tumour cellsin due to its synthesis rather than due to lackof its degradation. However, the auxin alone has no capacity to convert the normal cells into tumour cells. Conclusive evidence of the identity of the transforming agebt (TIP) is lacking. At various times TIP has been suggested to be bacterium itself a virus associated with the bacterium , a metabolic product of the bacterium, a coverted host component, or most recently, bacterial DNA which is taken up, incorporated and translocated in the tissue. There are indications that several metabolic systems are gradually, but permanently, activated during the transition from a normal cell to fully altered tumour cell. Viral infections also disturb the balance of auxin in plant. An excess of auxin results in overgrowth or its deficiency causes atrophy or growth retardation in viral diseases . Howeer, the mechanism by which the virus alters the balance is not known. In some viral diseases there is no correlation between synthoms and the amount of auxin detected in the diseased organ. Gibberellins. The role of Gibberellins in pathogenesis, although well recognised,has been studied in relatively few diseases . The Gibberellins were discovered by Japanese workers investigating the bakanae or foolish scedling disease of rice caused by Gibberella fujikuroi, as ascomycetous fungus with its imperfect stage in Fusarium moniliforme. The disease is characterised by abnormal elongation of stem due to excessive elongation of internodes. Rellins, a group of chemically related growth regulators, were insolated from these seedlings. So far 38 of these compounds have been reported. They are different from each other in their structure and /or biological activity. The best known gibberellin is gibberellic acid (GA3). Gibberellins are considered as normal constituents of green plants and are also found in microorganisms. They perform numerous functions. Oue of the important functions is their role as chemical signals which activate cell extension, dormancy breaking and flowering etc. These chemical signals activate various enzymes in the plant body. Thus, during seed germination the embryo secretes the hormone which activates the cells of aleurone layer to secrete hydrolytic enzymes for liquefying the reserve starch. It also promotes enzymes that aid in digestion of endosperm cells and softening of seed coat. Other enzymes are also helped by Gibberellins. The proteinase enzymes synthesised under the signal from Gibberellins cause degradation of protein releasing various amino acids. Among these acids tryptophan, the precursor of IAA may be one. Thus, there is a close relationship between Gibberellins and IAA. Tissues treated with Gibberellins (Gibberellic acid) may develop higher concentration of IAA. The latter often helps the functions of Gibberellins and both substances seen to work synergistically for maximun stem elongation. It is possible that Gibberellic acid neutralizes some growth inhibiting system in the plant, such as IAA oxidase. Gibberellins have strong ggrowth promoting qualities. These include elongation of root and shoot, excessive flowering, fruiting, etc. Synthoms of growth inhibition can be reversed by appication of Gibberellic acid. These compounds are suspected to be operating in many other host- pathogen systems such as downy mildew of sugarcane (Sclerospora sacchari), rust caused by Uromyces Pisi on Euphorbia cyparassias, smut of Bromus caused by Ustilago hypodytes, etc. The site of activity of Gibberellins in the cell is close to the nucleic acid system. It activates inactive genes and in this process synthesises new messenger RNA which directs the synthesis of various enzymes for different functions. Cytokinins (kinins): The best known Cytokinin, is kinetin (6- furfuryl-amino- purine). These growth regulating substances are derivatives of adenine, a constituent of DNA and RNA. As such they are essential for growth and differentiation of cells and tissues. The type of tissues and plant organs is deternined by amount of Cytokinin in the primordial tissue. Low Cytokinin activity causes root formation while high levels of these substances. Induce bud formation. In presence of auxin these compounds induce rapid cell division. They prevent degardation of protein and nucleic acid thereby delay senescense. Amino acids and other chemicals flow towards points where Cytokinin activity is higjh. The mode of action of cytokinins is similar to that of gibberellins and they also often function synergistically with auxins. The significance of kinins in pathogenesis is uncertain. However , role of kinins in many host- pathogen interactions has been suspected. These include bean rust, root knot, Victoria blight and some bacterial disease. Increase in the level of kinin- like substances in leaves of bean (Phaseolus vulgaris) attacked by Uromyces phaceoli and leaves of Vicia faba attacked by Uromyces fabae is reported to induce formation of “green islans” around the infection centres. Nutriens accumulate in the green tissue. The tissues with low cytokinins thus become senescent. Growth and differentiation inhibitors. Many chemically different substances work as growth inhibitors in the plant and are synthesised by them. Excess of these substances causes such effects as inhibition of cell division, induction of dormancy, formation of abscission layer, epinasty, etc. The growth inhibitors may interact with growth promoting substances in the plant and render them ineffective. Thus, normal growth of the plant organs is arrested. Two such chemicals have been studied in some detail. They are dormin and ethylene Dormin or abscission II induces dormancy by converting developing leaf primordia of a bud into dud scales. The inhibitory effects of dormin are counteracted by presence or application of gibberellins. On the other hand, dormin can function as antagonist of gibberellins in the plant. Dormin can also mask the effect of IAA which cannot be reversed by application of additional IAA although gibberelins can offset this effect of dormin on IAA activity. The role of dormin in pathogenesis is not known. Ethylene (C2H4) is a highly active growth regulator best qualified for a primary role in pathogenesis . It is produced by plants independently or under the influence of pathogenesis.It is the earliest known growth regulator and is biologically active in even as low concentration as 0.1 part per million. Some promitent effects of ethylene are epinasty, tissue proliferation, marked increase in rate of respiration, premature senescence and shedding of leaves , and stimulation of root formation . It is highly mobile in plants, and does not accumulate in tissues. However, whent the pathway for its movement is blocked suchas when vascular occlusions and stomatal closure occur in bacterial and fungal wilts, ethylene may accumulate and synptoms of epinasty become apparent. A number of bacterial and fungal pathogens produce ethylene and in case of fusarium wilt of tomato (Fusarium oxysporium f. Sp. lycopersici), ethylene production by the pathogen is sufficient to account for the epinastic synptoms of the disease . However, in most cases, the production of ethylene is by the damaged tissues. In a number of viral diseases , leaves with necrotic local lesions produce more ethylene tham those from systematically infected plants without necrotic lesions. Necrosis induced by toxic chemicals also results in increased ethylene evolution. This suggests that in such cases ethylene is a product rather than cause of tissue damage.Banana plants attacked by Pseudomonas solanacearum (bacterial wilt) show premature ripening and yellowing of fruits which is linked with high level of ethylene in the yellowed fruits. Other species of Pseudomonas , some species of Xanthomonmas and Erwinia also produce such effects. From the above account of the effect of pathogenesis on growth of the plant in can be concluded that changes in growth pattern are caused by imbalance in production, accumulation and translocation of growth regulators in the plant. The normal plant synthesises growth promoting substances in quentities just enough for its normal growth. The plant also produces growth inhibitors to rergulate the activity of growth promoters and other chemical substances. In pathogenesis this regulatory mechanisms is disturbed or destroyed and as a consequence there is unregulated synthesis of growth hormones and other substances and therefore the changes in growth habit are seen. Effect on Reproduction of the Host From practical viewpoint the loss from disease is due to reproduction in reproductivity of the plant. Reproduction in plant is determined by its agen nutrition, enviroments ( light, moisture, temperature) and normal physiological activity . Disturbance in one physiological activity initiates a chain reaction that affects other activities thus influencing growth and reproduction. Inanimate causes or unfavourable environment mainly reduce the reproduction of plants. There are also many infectious diseases which reduce or completely suppress reproduction of the host. EXAMPLES OF PLANT DISEASES IN WHICH SYMPTOMS SUGGEST OVERACTIVITY OF GROWTH REGULATORS. Disease and Symptoms Crown gall Smut Wart Host I.- Galls caused by cellular proliferation. Many Maize Potato Parasite. Agrobacterium tumefaciens Ustilago maydis. Synchytrium endobioticum. II.-Increase in the lengthof stem. Downy mildew Bakanae disease Rust Rust Sugarcane Rice Euphorbia Wheat Sclerospora sacchari Giberella fujikuroi Uromyces pisi Puccinia graminis. III.- Suppression of abscission layer. Leaf blight Cherry Gnomonia erythrostroma. IV.-Stimulation of abscission layer. Leaf blight Coffee V.-Excessive abnormal branching Omphalia flavida Witches broom Witches broom Downy mildew Various trees Sweet pea Maize Many fungi. Corynebacterium fasciens Sclerospora sacchari As has been discussed in the preceding section the abscission layers aren formed by the action of growth regulators. Under normal conditions this layer develops when the fruit has ripened and contains viable seeds and when the leaf has reached senescence. However pathogenesis induces formationof these layers, through the activity of growth regulators formed by the pathogen or by the host, untimely. When abscission layer develops in immature fruits there is loss in reproduction. The infectious diseases, localised or systemic, affect physiological activities of the plant. When pathogenesis reaches a particular stage reproductive process of the plant is also aaffected. These effects can be direct as well as indirect. The direct effects usually lead to partial or complete destruction of fruits,seeds , etc. While indirect effects are the result of weakening of the plant or loss of the crop resulting from seeds produced by diseased plants. The processby which pathogens reduce reproduction in plants is mediated by the physical and chemical means given in the preceding sections. Some examples of direct and indirect effects on reproduction are given below. In many plant diseases the host produces normal fruits and viable seeds. However, the inoculum gets mixed with the seed and reaches the next crop where it harms the young plants or detroys the reproductive organs. In wilt disease of tomato (Fusarium oxysporium f. Sp. lycopersici) the fungos is often associated with the viable seeds and harms the young plants developing from these seeds. In seed rot and stalk rot of maize (Fusarium moniliforme, Cephalosporium acremonium, C. Maydis) the fungi are present in and on the seed. When the seed is planted these pathogens, depending on environments, many cause rottingof seedsand seelings. F. Moniliforme causes direct loss ol seeds also when it attacks the cobs and rot . In loose smut of wheat (Ustilago nuda tritici) the seed itself is not damaged by infection but the plant developing from it in the next season produces ears completely devoid of grains and full of smut spores. The green ear disease of bajra (Sclerospora graminicola ) is carried by seed and soil and the infection becomes systemic in the plant developing from contaminated seedor on contaminated soil. The plants turn yellow, remain stunted and may never reach the flowering stage . If ears develop they bear leafy structures in place of grains. Since the infection is systemic in such diseases there is complete loss of productivity in them. Downy mildews of maize caused by Sclerospora sacchari and Sclerophthora macrospora also often cause complete loss of seed formation. The direct infection and loss of floral organs and seed occurs in such localised diseases as smut of bajra. The grains are partielly or completely damaged although majority of grains remain unaffected. The loss of germinability of seeds is another factor in causing losses in yields. Many viral diseases of potato reduce the sprouting capacity of the tubers. In addition almost all diseases of potato caused by viruses cause reduction in number and size of tubers.The same is true for late blight of potato. The above examples are only of those diseases where the loss in reproductive parts or the pproduce is conspicuous and forms part of symptoms. But, loss of reproduction occurs in all diseases because of interference in physiological systems resulting in general weakness of the plant . The powdery mildews do not show serious effect on reproductive organs or seeds but the seeds are weak or pod development may by significantly reduced due to disturbed physiology of the host including serious loss of photosyntesis. The increased transpiration in plants affected by rusts also results in shrivelled grains of low viavility. Thus, the effects on reproductivity of the diseased plants, as stated earlier, are the result of direct consumption of floral or reproductive parts by the pathogen or due to altered physiology such as low uptake of water and nutrients (root diseases), low rate of translocation of water and nutrients, tissue desintegration before flowering, lack of normal photosynthesis ( powdery mildews) or photosyntetic area (leaf spot diseases). Effect on Uptake and Translocation of Water and Nutrients. Living cells of plants need sufficient water and nutrients (organic and minaral) for their normal activity. If there is interferebce with the availability of these requirements the cells fail to perform their physiological functions. Minerals and water are absorbed by roots and translocated by xylem vassels upwards towards leaves. A part of absorbed and translocated water and the entire, amount of mineral nutrition is used up for various activities of the cells. However, a major portion of water reaches the intercellular spaces and is diffused into the atmosphere through stomata and lenticels in the process of transpiration . The organic nutrition of the plant is mostly Synthesised by photosynthesis in the leaves and translocated through phloem vessels downwards up to the roots. The excess of organic nutrients, in various forms (amino acids, sugars, organic acids, etc) is exuded out into the soil in the root exudates. It is, thus, obvious that if due to effects of pathogenesis uptakeand and translocation of minerals and water is checked the plant tissue will starve and when due to starvation the physiological activities of these tissues are affected thrre will be deficiency of substances produced by these tissues for the entire plant. In this way the entire plant will be sick. For an example, if water is not absorbed by roots or there is obstruction in its translocation the leaves will cease to be active and photosynthetic activities will cease or decrease. The organic nutrition will not be available to roots. Thus, not only the leaves but roots also will be adversely affected. The effect of pathogens on photosynthesis is discussed elsewhere. Here only the uptake and translocation of minerals and water is being considered . Effect on absorption of water by roots.The water uptake capacity of roots can be affected inthree ways, viz, roots are injured, permeability of root, cell walls is altered and development of roots is checked.The fungi causing damping off and root rot and most of the phytopathogenic nematodes and some viruses cause sfficient injury to the roots before visible symptoms appear on the aerial parts. Such injuries or wounds reduce the number of active roots and water uptake is decreased in the same proportion.Some vascular parasites reduce the number of root hairs thus decreasing active surface area and therefore reduced uptake of water. Roots absorb water and mineral solutions through the process of osmosis. If the pathogen or its growth regulators, toxins and enzymes alter cell wall permeability of roots the osmosis is also affected. The role of enzymes and growth regulators on cell wall permeadility has already been discussed. Effect of toxins is given in a later chapter. The reduced osmotic activitycauses decrease in water uptake.If the root cells are killed, plant or pathogen generated toxins can enter the roots and affect physiological activities of the plant. Effect on translocation of water by xylem vassels: The fungi and bacteria causing damping off, stalk rots and canker can enter the xylem vessels. If the plant is young these vessels can be desintegrated . In affected vessels organs of the pathogen or biochemical substances produced by the pathogen or the diseaseed plant may also be present and cause obstructions. Desintegration as well as obstructions both reduce de water carrying capacity of the root system. The crown gall bacterium, Agrobacterium tumefaciens, club root fugus, Plasmodiophora brassicae, and the root knot nematodes ( Meloydogyne spp) develop galls on roots and stem due to overgrowth of cells. The xylem vessels abjacent to these proliferating tissues are crushed or dislocated and thus lose their normal water conducting capacity. A common example of malfuntioning of xylem is the group of wilt disease in which the pathogens invade the xylems vessels.. Although these pathogens (species of fusarium, Verticillium, Pseudomonas, Erwinia) can obstruct water transport by their physical presence sometimes the obstruction by fungal hyphae or bacterial cells is not much but symptoms of wilt appear. Obviously, some additonal factors apart from presence of pathogen organs operate in causation of obstruction intransport of water. In this way, it is apparent that translocation of water is reduced or obstructed by any of the following mechanisms in addition to desintegration of the xylem vessels: 1.- Presence of fungus mycelium , spores and slimy bacterial mass in the xylems: Plugging of xylem vessels has at least partly been atributed to presence of these forms of the pathogens causing vascular wilt diseases. 2.- Enzymes: The production of pectic enzymes in vascular infections by wilt causing pathogens has been noted . These enzyme degrade the middle lamella and release pectic acid and other substances which form gels and gums. These pathogens also produce cellulolytic enzymes. When middle lamella of xylem vessels are desintegrated by these enzymes the pectic substances form plugs which obstruct the passage. Browning of vessels is a common feature in vascular wilts. This is due to a pigment called melanin. The pigment is formed by the action of enzymes. The pectinolytic enzymes of the pathogen desintegrate the host cells and star oxidation of phenolic compounds. The oxidised products form moolecules of the pigment. Since the action of enzymes and growth regulators alters cell wall permeability these pigments easily enter the xylem vessels. 3.- Pathogenic polysaccharides. Bacteria and gungi are capable of producing polysaccharides that can induce wilt sumptoms in vitro. In many wilt diseases the symptoms have been atributed to these complex substances. These polysaccharides are different from those produced by the plant. The pathogenic polysaccharides are macromolecular substances that cannot pass through openings in cells walls. Their entrapping in the cell wall openings causes abstruction in the flow of water from one vessel to another and laterally to other cells. Increase is viscosity and thereby decrease in rate of flow of tracheal fluid is also attributed to polysaccharides and partly accounts for wilt symptoms. In bacrterial brown rot and wilt of potato (Pseudomonas solanacearum) the amount of polysaccharide produced by the pathogen is proportional to the severity of the symptoms. 4.- Hiperplasia: The tomato mosaic virus causes necrosis in the stem . Cells adjacent to necrotic area show hyperplasia and the vessels that come in the path of this overgrowth are rendered nonfuntional due to pressure. Adnormal development of xylem vessels . even in areas of the plant not yet invaded by the pathogen, often occurs in vascular wilts. The walls of the new vessels are thinner than normal and they are usually flattened instead of circular and appear collapsed. These changes in the xylem reduce water transport in the plant. 5.-Tyloses: The production of gels and gums as a result of enzymic action of the pathogen and formation of plugs was mentioned above.In many fungal, bacterial and viral vascular disease the presence of the pathogen , its toxins, and permanent deficiency of water causes development of tyloses in the xylem vessels . Tyloses are outgrowth of parenchyma adjacent to the xylem and appear as peg- like structure. They obstruct passage of water inthe same manner as the gels and gums. Effect on transpiration: In the above account only the uptake of water from soil has been mantioned. Pathogens also affect transpiration in addition to uptake and translocation of water , Increased transpiration has been noticed in most of the leaf diseases (rusts, powdery mildews, etc). The main cause of this increase in transpiration or loss of water from plant body is desintegration of the cuticle.Increased cell wall permeability and malfunctioning of stomata are also contributory factors. In rust diseases a major portion of leaf surface is exposed due to rupture of the epidermis by the pustules. This causes unrestricted loss of water. If there is no translocation of water from roots in proportion to water lost in transpiration symptoms of wilt may appear. The increased suction tension caused by increase in transpiration may result in collapse of vessels or formation of tyloses. In some diseases, such as blights, death of leaf cells reduces the number of healthy and active cells. This decreases the suction tension .Therefore the transport of water to leaves by the xylem vessels is also reduced. Reduced permeability of cell walls also produces similar effects. On the other hand in some wilt diseases the related toxinas (fuisaric acid, lycomarasmin, etc) enhance cell wall permeability. In this situation also the loss of water is increased. Physiological and pathological wilting: Wilt symptoms usually indicate water deficiency in the plant. This deficiency may occur in plant without infection due to non-availability of water. No pathogen is involved in these cases . The wilting thus caused is known as physiological wilting in contrast to pathological wilting in which non-availability of water in directly or indirectly associated with some pathogen. Soil moisture has no relationship with pathological wilting.. Effect on translocation of nutrients and their deficiency in plants: The materials from soil enter the roots as solutions in water and are translocated through the xylem. Therefore, the abnormalities thet obstruc water uptake and translocation affect the uptake and movement of mineral nutrients also. The organic nutrients synthesised in leaf cells enter the phloem vessels through plasmodesmata . Due to difference in osmotic pressure they move down the sieve tubes and during this downward movementthey continue passing again into the adjacent nonphosynthetic cells through plasmodesmata . These cells them use the nutrients for their vatious activities or store Smut