Role of Plant toxin

Role of Plant toxin. Collected by Zahid

1. . Role of Toxins in Plant Pathogenesis

2. INTRODUCTION Definition Toxin is a poisonous substance that is a specific product of the metabolic activities of a living organism and is usually very unstable , notably toxic when introduced into the tissues, and typically capable of inducing antibody formation.

3. Target sites of Toxin in Plant cell

4. Classification of toxins . . A c co rdi n g to t he s ou r c e of o r i gin, t oxi n s a re d i vided into 3 broad classes namely. Pathotoxins Phytotoxins Vivotoxins ( Wheeler and Luke, 1963)

5. A. 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 : V i c to r i n : C oc h liob o lus victoriae ( H e l m int h os p ori u m v i c t o r iae ) , the causa l agen t of Victoria blight of oats. This is a host specific toxin.

6. B. 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. Ex: Alternaric acid – Alternaria solani. Piricularin- Pyricularia oryzae. (Wheeler and Luke, 1963)

7. C. Vivotoxins 1.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. Ex :-Fusaric acid – Wilt causing Fusarium sp . (Dimond and Waggoner, 1953)

8. 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. Ex:- Victorin, T-toxin, Phyto-alternarin, Amylovorin. 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: Ten-toxin, Tab-toxin, Fusaric acid, Piricularin, Lycomarasmin and Alternaric acid (Scheffer, 1983)

9. Differentiate host – specific and non-host specific toxins Host specific Non-host specific Host specific. toxic h o st 1. Selectively s us ce p t i b le pathogen. d eterm i n a n ts of 2. Primary disease. 3. P r o d u ce all t h e ess e n t ial symptoms of the disease. Ex: Victorin, T- toxin Non-host specific . o n ly to 1. N o ho s t s p e c i fici t y a n d can of the also affect the physiology of those plant that are normally not infected by the pathogen. 2. S eco n d ary d eterm i n a n ts of disease. 3. P r o du ce few or n one of t h e symptoms of the disease. Ex: Tentoxin, Tabtoxin

10. Host specific:- T-toxin: Helminthosporium maydis HC-toxin: Helminthosporium carbonum. HS- toxin: Helminthosporium sacchari. Phytoalternarin: Alternaria kikuchiana PC- toxin: Periconia circinata Non-host specific:- Tentoxin: Alternaria tenuis. Tabtoxin or wild fire toxin: Pseudomonas tabaci. Phaseolotoxin: Pseudomonas syringae pv . Phaseolicola.

11. Effect of toxins on host tissues . (Singh, 2001) 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.

12.  Increase in respiration due to disturbed salt balance.  Malfunctioning of enzyme system (Singh, 2001) 2.Disruption of normal metabolic processes:-

13.  Interfere with the growth regulatory system of the host plant.  Some toxins inhibit root growth. Ex:- Fusarium moniliforme produces a thermostable toxin even in soil around the root which causes browning of the root and their restricted development. . ( S i n g h , 2001) 3. Other mechanisms:-

14. The selective (Host-specific) Toxins T-toxin or Helminthosporium maydis race T-toxin (HMT-toxin) Is produced by the fungus Helminthosporium maydis ( Cochiobolus heterostrophus ). The pathogen cause leaf blight of maize. T-toxin is the disrupting the function of the mitochondria of Tcms maize. T-toxin bind to inner mitochondrial membrane protein (URF-13), the product of the T-URF 13, gene to create a pore on the membrane, cause leakage of small molecules, and subsequently inhibit ATP synthesis, resulting in cell death.

15. The Effect of T-toxin From Cochliobolus heterostrophus on T-cms maize  T-toxin bind to inner mitochondrial membrane protein (URF-13), the product of the T-URF 13, gene to create a pore on the membrane, cause leakage of small molecules, and subsequently inhibit ATP synthesis, resulting in cell death.

16. Is one of the most impotent and selective Pathotoxins. it is the first- well documented and widely recognised host-specific toxin. This toxin is produced by Cochliobolus victoriae, the fungus that causes victoria blight of oat. The disease is characterised by necrosis of the root and stem base and blighting of leaves. It is highly mobile in the plant. Victorin or HV-toxin:

17. The current model of victorin-induced cellular responses. (Tada et al., 2005) The current model of victorin-induced cellular responses. Victorin-sensitive cells. (A) Victorin may interact with an extracellular mediator( s) in Vb/Pc-2 oats and stimulates ion fluxes across the plasma membrane, followed by the activation of defense responses and rapid cell death. After cell death, victorin may permeate cells and is distributed in the mitochondria, inducing a senescence-like response. (B) Victorin-insensitive cells. Victorin neither induces cell death nor enters the resistant cells.

18.  The fungus causes leaf spot of maize. The fungus species has tow races, 1 and 2 . only race 1 produces the HC-toxin.  Race 1 is also weak pathogenic on most lines but is highly virulent on maize that is homozygous recessive at the Mendelian loci Hm1 and Hm2. HC- toxin or Helminthosporium carbonum toxin

19. Infection of maize by Cochliobolus carbonum race 1 (HC-toxin-producing). The plants in the foreground are genotype hm1/hm1 hm2/hm2 (susceptible). A few plants were inoculated by spraying conidia and the other plants became infected by natural spread. The plants in the background are genotype Hm1/- (resistant). (Baidyaroy et al ., 2001)

20. T h e e y es p o t d i s ease c a used by Hel m i n tho s pori u m sac c h a r i is especially severe in seedling of certain sugarcane cultivars . The h o s t s p e cific tox i n p r o d u c ed by the f u n g u s indu c es r e dd ish brown strip when injected into susceptible leaves .  T he toxin b rings about changes in chlo r opla s t and cell w all permeability . HS- toxin or Helminthosporium sacchari

21.  Milo disease or periconia blight caused by periconia circinata attacks only milo type of grain sorghum. The pathogen is soil-borne and invade the root and lower internodes of the plant. The toxin causes rapid loss of potassium ions and other materials through leakage of the plasma membrane of susceptible but not resistance tissues. PC-toxin or periconia toxin:

22. to Pathogenesis and Disease H o s t -s p eci f i c T oxins in Re l a t ion Resistance R.P. SCHEFFER Effect of Periconia circinata toxin on susceptible and resistant sorghum seedlings. Equal amounts of toxin were added to the nutrient solution of the susceptible (center) and resistant (right) seedlings three days before this picture was taken. The untreated control is on the left

23.  This host specific toxin is produced by Alternaria kikuchiana , the fungus causing black spot of japanese pear .  Three Phytoalternarin A, B and C have been obtained from culture filtrates of the fungus.  There is direct damage to the plasma membrane leading to a rapid loss of electrolytes. AK-toxin Phytoalternarin:

24.  T a b t o x i n or W i l d fi r e toxi n :- T a b t oxin is P s e udo m o n as s yri n gae p v . tabaci the causal p r o d uc e d b y b a c t e r ium 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 Non-specific/Non-selective toxin:

25. Disease development on transgenic tobacco leaves inoculated with P. syringae pv . tabaci . Tobacco plants were inoculated at two points per leaf with P. syringae pv . Tabaci (109bacteria/ml) by the multiple needle method and kept for 6 days in a humid box to develop the disease. Control tobacco (left) shows the chlorotic symptoms of pathogen attack, whereas the transgenic tobacco TAB7 (right ) exhibits no symptoms at the inoculation sites of P. syringae pv . tabaci.

26. Phaseolotoxin: Pseudomonas syringae pv . Phaseolicola , causes halo blight of bean and some other legumes.  The chlorotic halos are accompanied by ornithine accumulation in the tissues.  Both race 1 and race 2 of P . phaseolicola can produce phaseolotoxin, but they differ in host range, suggesting that the toxin is not involved in host specificity. Phaseolotoxin

27. Is Produced by Alternaria alternata. causes leaf spots . That bind to inactivate the protein. Also inhibits phosphorylation of ADP to ATP. Leading to disruption of chlorophyll synthesis Tentoxin:

28. Toxicity of AK-toxin produced by the Japanese pear pathotype of Alternaria alternata . The culture filtrate of the Japanese pear pathotype was dropped on slightly wounded points of left-half leaves. Right-half leaves were spray inoculated with a conidial suspension. Leaves were incubated for 24 h.

29. Cercosporin Produced by Cercospora sp . Causes leaf spot disease of groundnut This toxin is activated by light and become toxic to plants by generating activated species if oxygen (single O 2 ); the activated O 2 destroy the host membrane and provide nutrients to pathogen,

30. Cercosporin production and mode of action. Cercosporin is produced by the fungus in response to environmental cues, primarily light. Once produced and excreted by the fungus, the cercosporin molecule is activated by light to generate activated oxygen species. The activated oxygen species, in turn, cause peroxidation of the plant host membrane lipids, leading to membrane damage and cell death. Membrane damage allows for leakage of nutrients from the host leaf cells into the leaf intercellular spaces, and is hypothesized to be the mechanism that provides these intercellular pathogens with the nutrients required for growth and sporulation in host tissues. (Ehrenshaft et al ., 2000)

31. Mode of action of Cercosporin

32. Aflatoxin  Aspergillus flavus, Aspergillus n o m i u s and Aspergillus parasiticus. There are four kinds of Aflatoxins such as Aflatoxin B1, B2, G1 and G2, in which Aflatoxin B1 (AFB1) is highly toxic and carcinogenic (Leontopoulos et al., 2003) . Aflatoxins are known to be carcinogenic agents that are serious hazards to human and animal health (Sidhu et al., 2009). In addition, Aflatoxin also has an impact on agricultural economy through the loss of crop production (Wu, 2004).

33. Aspergillus Ear Rot (Charles et al ., 2011)

34. Conclusions Plant toxins confer a competitive advantage to the plant, and especially protect it from insect attack or plant pathogens. Poisoning of livestock is coincidental to this function. Since plant toxins seem specifically targeted on insects, either by concentration in a particular plant part or by production at concentrations sufficient to intoxicate the insect, livestock poisonings may be avoidable. so that  C are f ul m anage m e nt p lants should be developed consumption of the toxic plant parts are avoided.