Role of toxins and Enzymes in Pathogensis.pptx

Vedasree16 37 views 28 slides Aug 01, 2024
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About This Presentation

this provides information about toxins and enzymes produced by bacteria which plays major role in producing the disease in plants


Slide Content

Role of toxins and Enzymes in Pathogenesis. A . Vedasree 2019515104

Toxins: Toxins are any substances produced by the pathogen which is injurious to the host and it directly and immediately play a crucial role in pathogenesis

Classification of toxins .. According to the source of origin, toxins are divided into 3 broad classes namely. 1. Pathotoxins 2. Phytotoxins 3. Vivotoxins (Wheeler and Luke, 1963)

Pathotoxins : These are the toxins which play a major role in disease production and produce all or most of the symptoms characteristic of the disease in susceptible plants. Most of these toxins are produced by pathogens during pathogenesis. Ex: Tab toxin, phaseolotoxin.

 Phytotoxins: These are the substances produced in the host plant due to host- pathogen interactions for which a causal role in disease is merely suspected rather than established. These are the products of parasites which induce few or none of the symptoms caused by the living pathogen. They are non specific and there is no relationship between toxin production and pathogenicity of disease causing agent.

Vivotoxins : These are the substances produced in the infected host by the pathogen and / or its host which functions in the production of the disease, but is not itself the initial inciting agent of the disease. 

Classification based on specificity of toxins: Host specific / Host selective toxins:- These are the metabolic products of the pathogens which are selectively toxic only to the susceptible host of the pathogen. Non-specific/Non-selective toxin:- These are the metabolic products of the pathogen, but do not have host specificity and affect the protoplasm of many unrelated plant species that are normally not infected by the pathogen. Ex: Tab-toxin,( Scheffer , 1983)

Differentiate :- Host – specific and Non-host specific toxins : Host specific Non-host specific. 1. Selectively toxic only to susceptible host of the pathogen. No host specificity and can also affect the physiology of those plant that are normally not infected by the pathogen. 2. Primary determinants of disease. Secondary determinants of disease. 3. Produce all the essential symptoms of the disease. Produce few or none of the symptoms of the disease. . Ex: Tentoxin, Tabtoxinx

Bacteria generate toxins which can be classified as either  exotoxins  And  endotoxins . Exotoxins are generated and actively secreted; endotoxins remain part of the bacteria. Usually, an endotoxin is part of the bacterial outer membrane , and it is not released until the bacterium is killed by the  immune system .

  Toxins produced by some bacteria:   Tabtoxin or wild fire toxin : Pseudomonas tabaci . Phaseolotoxin: Pseudomonas syringae pv . Phaseolicola . Tagetitoxin : Pseudomonas syringae pv . Tagetis , Rhizobitoxine : Rhizobium japonicum.

Effect of toxins on host tissues: 1. Changes in cell wall permeability: Toxins kill plant cells by altering the permeability of plasma membrane, thus permitting loss of water and electrolytes and also unrestricted entry of substances including toxins. Cellular transport system, especially, H+ / K+ exchange at the cell membrane is affected. (Singh, 2001)

2.Disruption of normal metabolic processes:- Increase in respiration due to disturbed salt balance. Malfunctioning of enzyme system. (Singh, 2001) 3. Other mechanisms:- Interfere with the growth regulatory system of the host plant. Some toxins inhibit root growth. (singh,2001)

Non-specific/Non-selective toxin: Tabtoxin or Wildfire toxin:- Tabtoxin is produced by Pseudomonas syringae pv . tabaci the causal bacterium of tobacco wildfire disease. In tobacco wildfire disease the necrotic lesion on the leaves are surrounded by a yellow halo. Most of the toxins produced by plant pathogens are pleiotropic that is, they have more than one effect on the host cell, but most bacterial toxin, include tabtoxin, are monotropic, having single effect. Tabtoxins is a dipeptide toxin composed of two amino acids: Threonine and tabtoxinine . Tabtoxin as such is not toxic to plants. In the cell, it becomes hydrolysed to release tabtoxinine .

Tabtoxinine inactivates the enzyme glutamine synthase in plants. Inactivation of glutamine synthase leads to depleted glutamine level This results in the accumulation of ammonia in the cells. Accumulated ammonia uncouples the photosynthesis and photorespiration Ammonia also destroys thylakoid membrane of chloroplast leading to chlorosis and eventually necrosis.

Structure of tabtoxin:

Phaseolotoxin: It is a general toxin produced by Pseudomonas syringae pv . Phaseolicola , causes halo blight of bean and some other legumes. The chlorotic halos are accompanied by ornithine accumulation in the tissues. Reduced growth, distruption of apical dominance and accumulation of amino acid ornithine are the effects of phaseolotoxin. Phaseolotoxin is a tripeptide toxin composed of ornithine-alanine-arginine. This tripeptide also carries a phosphor sulf amyl group. The toxin is cleaved by the host enzymes to release alanine, argininine and phospho- sulf amyl ornithine(PSMO)

PSMO is the functional moiety of the toxin. PSMO inactivate the enzyme ornithine carbamoyltransferase (which normally converts ornithine to citrulline, a precursor of arginine). By the action accumulation of ornithine and depleted level of arginine occurs in the cells. Other physiological effects of Phaseolotoxin: Inhibit pyrimidine nucleotide biosynthesis. Reduce the activity of ribosome. Interfere with lipid biosynthesis. Change the permeability of membranes.

Structure of phaseolotoxin:

Tagetitoxin : It is produced by Pseudomonas syringae pv . tagetis . It causes leaf spots, and usually a chlorosis of the apical leaves.

Rhizobitoxine : This toxin is synthesised by certain strains of root nodulating bacteria, Rhizobium japonicum . Causes chlorosis in the developing leaflets of plants having nodules colonized with these strains.

Enzymes: A substance produced by a living organism which acts as a catalyst to bring about a specific biochemical reaction. Enzymes are produced by the pathogen for entry into plant cell. As the plant cell contains cutins , celluloses, pectins , hemicelluloses, proteins, lipids and sugar molecules. Cutinases , Pectinases

Plant cell wall composition:

Cell wall degrading Enzymes Cuticular enzymes : Cutinases ; are the esterases and break the ester linkage between cutin moleculses . These degrade cutin , which is an insoluble polyester of C16–18 hydroxy fatty acids and is the main component of the plant surface. Eg : Streptomyces scabies. Cutin polymer : Fatty acid derivatives (Monomers & oligomers)- Initially small amount of enzyme is produced, after formation of monomers & oligomers, induces more cutinase production These enzymes soften the cuticle Some of the fatty acid present in wax also induces cutinase production Glucose suppresses the expression of the cutinase gene

Pectin degrading Enzymes: Pectin act as a cementing material between cells Enzymes called as pectinases or pectolytic enzymes Produced by bacteria - Pseudomonas solanacearum. Three types of pectinases produced by different pathogen are 1.Pectin esterase (PE) or pectin methyl esterase (PME) 2.Poly galaturonases (PG & PMG) 3.Pectin trans eliminase (PTE)

Pectin esterase (PE) or Pectin methyl esterase (PME) : •These hydrolyze the methyl ester group of the pectinic acid to methyl alcohol and pectinic acids of reduced methoxy contents and finally to pectic acid. •These alter the solubility of pectinic chains so that they may be attacked by chain splitting enzymes i.e. PGs. •PME produced by Erwinia sp., Xanthomonas campestris.

Pectin transeliminase or Pectate lyases : Pectin is also broken down by these enzymes, by - elimination of water molecules rather than hydrolysis. Produced only by Erwinia carotovora causing soft rot of carrot and X. campestris The pectolytic enzymes causes liquification of the pectic substances which hold the cell together and lead to maceration of tissues thus facilitate the pathogen entry into host

Poly galaturonases (PG & PMG): These enzymes splits pectin chain to shorter chains (one or few molecules of galacturonic acid) Galacturanan monomers triggers pectinase production in the pathogen. Monomer units absorbed by the pathogen act as the inducer for the mass production of pectin.