Role of Enzymes, Toxins, and Growth Regulators in Pathogenesis PDF

HOST PATHOGEN INTERACTION 63 spaces of host tissues. They sendoutspecial short branches which penetrate the host cells. Within the host cells (usually parenchyma) the branches get modified into special types of absorb...

HOST PATHOGEN INTERACTION 63 spaces of host tissues. They sendoutspecial short branches which penetrate the host cells. Within the host cells (usually parenchyma) the branches get modified into special types of absorbing organs, called haustoria. The S re haustoria absorb nutrients from the host and supplyit to the main bodyof pathogen. These pathogens soon start reproduction and multiplication. es ROLE OF ENZYMES, TOXINS AND GROWTH st REGULLATORS IN PATHOGENESIS to, (The establishment of pathogen in the host/nvolves a close biochemical the relationship between the two. It is accomplished in two ways (1) by the alis destruction of host cells and tissues and/or (ii) by nutritional relationship. e. Almost all the stages of pathogenesis(i.e.,pre- penetration, penetration and post- penetration) involve chemical interactien of pathogen with the host. e in The pathogen brings several morphological, anatomical and physiological pugo, disturbances in the host tissues mainly by secreting several injurious meta bolicproducts. These products may be of three main types (i) enzymes, (ü) ar wilt toxins and (iii) growth regulating substances.) ply in (a) ROLE OF ENZYMES ce only ing cel (Successful infection needs entry of pathogen and its subsequent es tablishment in the host The plant body of host is well protected by external ease oE cuticle and waxy substances. Thesc protcctive Tucifers epidermal layer coated with pathogen in order to cause pathogencsis layers must bé invaded)by obtain 2 enswhick Moreover, the pathogen must enter into the living host cells to nourishment. To achieve this objective, the pathogen must possess sufficicng es, smu mechanical strength and required chemical weapons to break through thc barriers of the host. The most important chemicalweapons which a pathogen ment frof (except viruses) possesses are the hydrolytic enzymes secreted extracellular stances t ly to disintegrate the protective layers of host. ses do n¢ The epidermalcell_ are usually coated externally by alayer of cuticle tly into th mainly made up of cutin. In many plants an additional layer of thin wax, in aucleus at the form of granular or rod like projections, is coated outside the cuticle. 0st nucle The layer of cuticle is followed by a thin layer of pectin Finally this layer etc. (Fig. and, requif merges with the primary wall made up of cellulose, hemicellulose, etc.)possess l pathogd6.4). A few thick walled cells of host (e.g., xylem vessels, fibres, The ligninis obiain th an additional secondary wall made up of bgnin, suberin, etc. Taphrina)sialso found as ne of the component ofpathogens middle lamella. which degrade the cell wall ate parasil The variousenzymes secreted by intercellu Components of host arc bricfly discussed below  on removesfungi. hordei rotting esterase 64 pathbarogens k degraded enzymes di(1961) ssolvpolingymerpathogen.ofcan Pect Cutin di sin te FIGURE grate Plant. ic of These Lig causi Li nignnin n :g leaves. are randated of : Suberin methbyoxyl demonst waxes es: enzymes (i) 1-4ßN-acet ylCutin 64 ey hystategitaacking : cellulo lytic fungual powderysecreted AcCording the Structure : Enzymatic groups in theis wax No also barks from carboxycutin-peroxidase two cnzyne The s) enzymes. iccurcifomi decomposi pat of and hogens ng mildew to plant main layer. and the glukicosami nds ne composition Edwards oftip pathogens. This has LAMELLA MIDOLE pecticdegradat treesion el(how of bcen AMELAEWA fies barley. of component modiproduce X AYERWA cstances (Exampl ory e, of X the enzymesinfection and cutin units. layer PLASMODESMATA cuticle is MEMBRANE LAYER PLASMA ULOSE AMELUAE CUTIN CELLAMELAE discovered id,layer oflingin Allen However, in Not of PECTIN CELLULOSE in lauer suberin enzyme are pegdissolving cuticleinvaded and (ii) ofare so Peni cil ium much (1970), cell PATHOLOGY PLANT in Ami l area. that produced by by xclcicuticle n usively Heinen layer. wall plant is Erysi phe is transmethyltheyase, the enzymes knownmechanical leafof and intrra, caused byspinulcutoisum n Chemi pathogen and cally epide id(iii)ermalpresent dodmellea can wood graminis -about by be degrading Linskens (i) rmis. ope otgrowinpathogen pushi it ng which fungaganism term thin : further whirotting is ccll! ch f.sp. from.cutin cutin a causc oxins. metabolites immunity can pathogenesis. have injurious lulases enzymes ing presentthein higher enzyme (b) nourishment. previdedegrading establishment crystalline uponenzymesmajor rusts, tion development pectin enzymes ofBut Somc A move antitoxins. wood methylpectic tin. INTERACTION PATHOGEN HOST Toxins ROLE Hemicellulose: the and toxin and plants. the Cellulose:wilts, (i.e., There and the in to to responsible rotting cellobiase chains.substancEs nces now, carly produced occur enzymes reactiveconstituent group called sub-cellular structure - separation (glycosidases liberated called is IfThese host are OF spaces anthracnose arc the plant host andThey Ci by introduced chemical even TOXINS fungi celulose Pectic from two in cellulose Cellulose pathogens njurious endotoxin, against substances many also are pathologists exotoxin,toxin.the between for These breakconverts to of in by only levels in produced solubilize form the enzymes of pectin main degradation (a) pathogen, mode substances, low saprophytic up enzyme and cclls and groups after are and cell in enzymes into th e th e reactive of Pectin easily. concentrations have cellobiose the leaf along transeliminases), play to of when when th e complex hydrolytically wall, bigher (Gaumann, its cellulose he tmajor by acts insoluble spot form of ction lysis.) bacteria, decisive the esterases, including produced secreted lo host The usuallyw and of celulose enzymes are cell cellulose.uponTherediseases.order line pectic and toxins in molecular hcmicellulose and into not small parasitic microfibrils polysaccharide 1954) of heterogenous walfungi, l clcave native are glucose such ofrole responsible acid,which eral ncluded or are pathogen and into The enzymes, under intracellularly barrier two middle which in dos, micro soluble nematodes cellulose as bringing included excreted antigenic weights play to Cx and cellobiose. groups fruit hydrolyse rties een a are of for units. endo lamella)catalye (b) for among toxinimportant origin, organisms the that rots, by poBysaccharides called giucose and out all and, in cell penetration andgluconases The of chain degradation a can occurs storage the toxins the the inside microor therefore, nature which degrade the Finallycellulotytic andsphtting and hemicel wall. parasiticcellulose jurious develop role incud units disease macera splittingremove as The rots, 65 be- the and are to and act its the of in of  etc.). are tissues fromtoxins mas, manner. 66 the diseasemain but the nonsolani disease.Pathooxins toxinsLuke of antibiotics ionship ment. in copper s' expressingproduced ispigeonmanyusuallypurified hogenFusari um Examples a byclassification Classification toxins toxinsof injurious enzymes and There but patpathogen not speciic 3. species disease d 2. in parasit 1. in(1963) to Similarly, Pathotpxins non-specific. inpea, characteristics d Vivotoxins potato Phytotoxins athemselves nplant They in are affectenzymes. the 3 or by are seems of isa broad toxiclethal stating etc.sympt ofoms host characterized but phytotoxin and/or whi ch phyto pat ogical lot symptoms These between fungus The and () holtoxins. to the the of Fusarium cells : non-specific : of only Buddenhagen to that : well should initiate its These tomato may categories These beconfusion toxins metabolism gical These Examples, of lycopersici, if host and to toxins toxins the Pyriofcularia andknown a Lycomarasmine or much However, macro-organisms the introduced not the are its are microorganisms differ are alteringcausingchemicallyvivotoxin which the plants and may convincing and do are be di_ease ro le the literature. and production (iü) not () the from innot origin. disease the effect wilt (a) present functiontoxisuffering c in have injurious controversies a Kelman host toxinsoryzae cell Fusaric in ; are Alternaric be Phytotoxins, subtle attack in of and (Dimond disease no classification antibiotics (plants xampl es a causing diseases fusaric heal th y 0 able ch whiMoreover, permeabi lity. in substancesproduced in produced (fungi, the specific, of susceptiblewhich acid. (ii) It the frelationship rom chemical to (1964) is (pervasive and structural PATHOLOGY PLANT blast acid in Itmnust and healthy mustdevel opment acid produce (iigiven )) regarding in pathotoxins play It host production early These tomato,is plant. has be Waggoner, produced by Vivotoxinshere.giventhere bacteria, the animals)differentiated important disease (b) host_ ; blight substancesproduced) with by the or senseintegrity is host. chelation beenproduce isolated symptoms are t istomato They Wheeler no mysterious) TherePiricularin of potato,Vivotoxins isolated ofin doubtful. byAl pathogenesis, disease. temari a terminology whereas mycoplas that and a It the th e and clearcut of regarded causal rice. of few must from1953). divided toxins is iron cotton, disease host of the they the diseast a It wilt the (ii ) and closs rol, - and from are orbethe The al by is I continues uccina mildews by the disease (auxin) regulators regulators such pathogen of substancesregarded regarded theinhibitors. plant protoplasmic accumulate toxins ipcreased, protoplasm, It and bytoxin chlorosis Phytophthora plant (C) causes monasproduced ofcausal pathogen Auxins as corrclative fungus root Japanese INTERACTION PATHOGEN HOST Growth fails Toxins(Efect increases of ROLE kill Victorin O minis to of organs, leaf causing as as loss rot produced tabaci, organism in maize curls, inand arc The to Periconia byAltemaria incrcase. banana : excess growth growth perform enzyme salts the inactivates Itetc. produced thu_ actions regulators OF proteins, other invariably of plant diseases. ofseedings pear; infestans, and inhaswitche's phytohormones toxins the tritici, a GROWTH andwater of caused the are disturb of discase inhibitors. metabolic system cells by causal Example bajra been promoters functioning. normal ) other circinata of Victoria on Alternaria Produced hosts caused. normal of growth and di_rupt cucumber, kikuchiana, ) the smut by include by host Tabtoxin wdery causcd byobserved broom, the thethese in substances.is altering organism enzyme suffering requirement electrolytes on blight' Fusarium of of normal host The REGULATORS blocked processes tissues: regulators. plantitself, whereas - both regulatory the Sorghum tenuis, by such by maize galls, cotton or plant normal auxins, the cell of thefungus wild disease mildew oxidaseIAA- Sclerospora that growth discases from tumours, growth. due Due permeability tobacco causal caused get from permeability and the fire oxysponim the abscissic gitbberellins causing of - of may Usually but growth system to to disturbed. Helninthosponum causal of level the Due also it promoters disturbed the citrus toxin organismn wheat are bylate cankers, coagulation wild oats sp., plant has seedling acid is cells : that -thesoUstilago. produce to been the of organism fire - ;) wheat etc. I. blight ofproduction plants affected of of produced of caused indole-3-acetic sp. acid some Respiration saltplasma so host PericoninPhytoalternarin In of stuntingroot, club observed groh and and as blight, disease black cubense, maydis, Panama or that rust some potatoabnormalities some ethylenes cytokinins is well and balance hydrolysis tissues. of bylevel of regulated membranes. they spotvictonae, caused regulating as variegated crown produced ; by of the (v ysiphe discases caused growth ofthat growth rate infail Some Pseudo disease downy these 67 IAA host the rot Ten the by the byare are of is to