pathogenesis

2. .
Doctoral Seminar II
On
Role of Toxins in Plant Pathogenesis
Major Advisor
Dr.Dayaram
Univ.Prof.
Deptt. Of Plant
Pathology
Speaker
Mukesh Kumar
Ph.D Scholar
Department of Plant Pathology
Dr. Rajendra Prasad Central Agricultural University Pusa,
Samastipur, 848185 (Bihar) India

3. INTRODUCTION

4. .
Toxin hypothesis

5. Target sites of Toxin in Plant cell

6. 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)

7. A. Pathotoxins
.
1. 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.
2. Most of these toxins are produced by pathogens
during pathogenesis.
Ex: Victorin: Cochliobolus victoriae
(Helminthosporium victoriae), the causal agent of
Victoria blight of oats. This is a host specific toxin.

8. B. Phytotoxins
1.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.
2.These are the products of parasites which induce few or none of
the symptoms caused by the living pathogen.
3.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)

9. 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)

10. Classification based on specificity of toxins
1.
1. 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.
2. 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)

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

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

13. Effect of toxins on host tissues
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)
1. Changes in cell wall permeability:

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

15. 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.
. (Singh,
2001)
3. Other mechanisms:-

16. 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.

17. 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.

18.  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:

19. 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.

20.  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

21. 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)

22.  The eyespot disease caused by Helminthosporium sacchari is
especially severe in seedling of certain sugarcane cultivars.
 The host specific toxin produced by the fungus induces reddish
brown strip when injected into susceptible leaves.
The toxin brings about changes in chloroplast and cell wall
permeability .
HS- toxin or Helminthosporium sacchari

24.  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:

25. Host-specific Toxins in Relation to Pathogenesis and Disease
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

26.  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:

28.  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
Non-specific/Non-selective toxin:

29. 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.

30. 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

32.  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:

33. 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.

34. Effect of toxin from Alternaria citri on a leaf of the host plant. Top leaf: 2 days after
a 50 µg drop containing 0.05 µg of toxin was placed on each side of the midrib,
near the leaf center. Control leaf is shown below. (Kohmoto, 1999).

35. 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 O2); the activated
O2 destroy the host membrane and provide nutrients to pathogen,

36. 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)

37. Mode of action of Cercosporin

38. Ergot alkaloid
 The most prominent member of this group is Claviceps
purpurea.
This fungus grows on rye and related plants and produces
alkaloids.
Cause ergotisms in humans and other mammals who consume
grains contaminated with its fruiting structure called ergot
Sclerotium.

40. Aflatoxin
 Aspergillus flavus, Aspergillus nomius 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).

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

43. 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.
 Careful management plants should be developed so that
consumption of the toxic plant parts are avoided.