Role of Toxins in Pathogenesis: Pl. Path. 111 (Cr. Hrs. 3+1)

Role of toxins in pathogenesis
Pl. Path. 111 (Cr. Hrs. 3+1)
P.N. Sharma
Department of Plant Pathology,
CSK HPKV, Palampur (H.P.)
Toxin in Pathogenesis
 Low mol. weight microbial metabolites that are toxic
to plant or animal
 Exo-toxins (excreted from living cells)
 Endo-toxins ( released from the lysed cell)
 Toxins act directly on living protoplast
 On the basis of their role in pathogenesis- classified as
 Pathotoxins (Wheeler and Luke, 1963)
 Tab-toxin; HMT toxin
 causal role in the disease
 Vivo toxins (Diamond & Waggoner, 1953)
 partial role in disease
 Fusaric acid, pyricularin
 Phytotoxins
 Role is suspected in disease
 Alternaric aid; cochliobolin.
Pathotoxins (Wheeler and Luke, 1963)
Those toxins which plays an important causal role in disease and

are produced by the pathogen or interaction between host and
pathogen
 Criteria for any toxin to be a pathotoxin:

 When applied on a susceptible host in low concconcentration,
should produce all or nearly all symptoms of the disease
 Toxin and the pathogen should have same host range; same
resistance/ susceptibility spectrum
 The pathogenicity of the pathogen should be correlated with its
capacity to produce the toxin.
e.g. Tab-toxin: Pseudomonas tabaci;
HMT toxin: Dreschlera maydis race T
Vivotoxins (Diamond & Waggoner, 1953)
Those toxins produced in the infected plant /host by the

pathogen and/ or its host that function in the production
of the disease
 Criteria/ characteristics of vivotoxins
 Reproducible separation of the toxin from the diseased host
 Purification and chemical characterization and
 Induction of atleast a part of disease syndrome when applied
on healthy plant
 These are generally non-specific
Fusaric acid: Fusarium spp.
Pyricularin: Pyricularia oryzae
Phytotoxins
 Are phytotoxic substances produced by living
organism and whose role in disease is merely
suspected rather than established.
 Role is suspected in disease
 Alternaric acid; cochliobolin.

On the basis of specificity to
host (Scheffer, 1983)
 Host selective/ specific toxins

 Non- host selective/ non-specific toxins
Specific/ selective toxins
 Are those toxins which adversely affect the specific host of
the pathogen
 Are normally essential for pathogenicity
 20 such toxins has been recognized mainly produced by
Alternaria and Cochliobolus spp.
 Victorin
 T-toxin,
 HC-toxin,
 AAL-toxin
Non-Specific/ selective
 Are those toxins that affect the protoplast of

many unrelated plant species in addition to
the main host of the pathogen producing the
toxins
 Tab toxin; phseolotoxin, tentoxib Cercosporin

 These toxins affect virulence of the pathogen
but are not essential for pathogenicity.
Effect of toxins on host tissue
 Changes cell permeability
 Disruption of normal metabolic activity
 Loss of salts from protoplasm increases
 Respiration – tab toxinine
 Uncoupling of oxidative phosphorylation – victorin
 Inhibition of host enzyme - tab toxin inhibit normal
host enzymes
 Affect cellular transport system e.g. H+/K+ exchange
at the cell membrane
 Other mechanisms
 Interfere with growth regulatory system e.g. inhibition of
root growth ( F. moniliforme)
Toxin-producers
 Some bacteria e.g., Pseudomonas,
Burkholderia, Clavibacter, Streptomyces,
Xanthomonas
 A number of fungi: e.g. Alternaria,

Ascochyta, Bipolaris, Botrytis, Cercospora,
Cochliobolus, Colletotrichum, Drechslera,
Fusarium, Phoma
Host selective(specific) toxins
Host-Specific (selective) Toxins
• Produced by fungi
• Almost all are produced by loculoascomycetes
• Alternaria spp. and Cochliobolus spp. primarily
• First toxins characterized – AKT-toxin (Japan 1933),
Victorin (USA,1947), HC-toxin (USA,1965)
• Toxins reproduce all disease symptoms when applied
to a susceptible host
• Scheffer & Nelson – 1960’s – single genetic loci
control toxin production in Cochliobolus spp.
• Cochliobolus heterostrophus – T-toxin – TOX1
• C. carbonum – HC-toxin – TOX2
• C. victoriae – Victorin – TOX3
VICTORIN
 Victoria blight of oats -Cochliobolus victoriae

 A host-specific toxin – victorin: a cyclic
pentapeptides
 Toxin reproduces all disease symptoms when
applied to a susceptible host
 Susceptibility to toxin conferred by dominant allele
at Vb locus
 Victorin causes premature senescence
of leaves
T-toxin
• Produced by Helminthosporium maydis race T
(Cochliobolus heterostrophus race T)
• Southern Corn Leaf Blight
• Toxin is a polyketide
• Toxin causes swelling, uncoupling of oxidative
phosphorylation, stimulation of respiration, leakage of
Ca2+ and NAD in mitochondria
• single genetic locus is involved in toxin production
HC-toxin
• Produced by Cochliobolus carbonum (Helminotsporium
carbonum)– causes Northern Leaf blight of Corn
• Cyclic peptide
• mode of action may be different than T-toxin - inhibiting defense
reactions rather than causing cell death
• Hm1 was the first plant resistance gene to be cloned and
characterized in 1992 by Johal & Briggs Science 258: 985.
• Hm1 encodes a NADPH-dependent reductase enzyme (HC-toxin
reductase - HCTR) that detoxify the toxin
Alternaria toxins
• Produced by closely related Alternaria spp.
Alternaria alternata.
• All are low molecular weight, secondary
metabolites and are structurally similar
• AF, ACT and AKT toxins affects
• Plasma membrane of susceptible hosts
• electrolyte loss, membrane invaginations (Kohmoto et
al. 1993)
•One specific genotype of each host is susceptible to
toxin - very narrow host range
• Tangerine pathotype – ACT-toxin
• Strawberry pathotype – AF-toxin
• Japanese pear pathotype – AKT-toxin
AKT-toxin
AF-toxin
ACT-toxin
Non host selective
(non-specific) toxins
Tab toxin
 Produced by Pseudomonas syringae pv. tabaci causes wild fire disease
in tobacco
 Pathotoxin
 Also by other strains of pv. tabaci in other hosts like bean and soybean,
also by other attacking oat, maize and coffee.
 Toxin producing strains cause necrotic spots on leaves surrounded by
yellow halo.
 Tab toxin is a dipeptide composed of amino acid threonine and
tabtoxinine
 The toxin as such is not toxic but in the cell it get hydrolysed and
release aminoacid tabtoxinine which is toxic
 Act by
 inhibiting / inactivating the enzyme glutamine synthetase
 Uncoupling of phosphorylation and photorespiration,
 destroy the thylakoid membrane of the chloroplast thus causes chlorosis and then
necrosis.
Phseolotoxin
 Produced by P. syringae pv. phaseolicola causes halo blight
of bean
 Toxin causes growth reduction
 Disrupt apical dominance and accumulation of amino
acid ornithine
 Phaseolotoxin is a modified ornithine-alanine -arginine
tripeptide with phosphosulfinyl group.
 Toxin act by
 inhibiting pyrimidine nucleotide biosynthesis, reduce
activity of ribosomes, interfere with lipid synthesis
 Changes cell permeability
Tentoxin
 Produced by Alternaria alternata (A. tenuis)
 causes leaf spots and chlorosis
 It is cyclic tetrapeptide
 that bind to and inactivate the protein
(chloroplast – coupling factor) involved in energy
transfer into chloroplast
 Also inhibits phosphorylation of ADP to ATP
 Leading to disruption of chlorophyll synthesis
Cercosporin
 Produced by Cercospora spp. And other fungi
 Causes leaf spot disease
 This toxin is activated by light and become
toxic to plants by generating activated
species if oxygen (single O); the activated O
destroy the host membrance and provide
nutrients to pathogen,
 It is photosensitizing perylenequinone that
absorb light energy
Fusarium toxins
 Marticin: pathooxin produced by Fusarium
oxysporum f sp. pisi – pea wilt; have
nepthazarin; red pigmented compounds
 Fusric acid: Vivotoxin, chemically 5-n- butyl-
picolinic aacid produced by many spp of
Fusairim: Fusarium oxysporum f sp. Batatis
(sweet potato); cubense (banana); lini
(Linseed); lycopersici (Tomato); vasinfectum
(Cotton)
 Lycomarasmin: Fusarium oxysporum f sp.
lycopersici
Pyricularin
 Pyricularia oryzae – rice blast
 Exist in two froms:
 α-picolinic acid
 pyricularin
 Toxic to conidial germination, however, the
fungus produces a pyricualrin binding protein
(copper oxidase) that binds with pyricularic
and destroy the fungitoxicity but not the
phytotoxicity.
 It affect respiration and growth at low conc.
But inhibit at high concentration.
Other non specific toxins include
 Fumaric acid : Rhizopus spp.

 Oxalic acid: Sclerotinia, Sclerotium spp.
 Alternaric acid: Alternaira spp.
 Ophiobolin: Cochliobolus spp.
 Pyricularin: Magnaporthe grisea
 Lycomarasmin: F. oxysporum in tomato
Acknowledgements
 I gratefully acknowledge the use of some very

important photographs given in text book “Plant
Pathology” by G N Agrios.
 I also acknowledge the scientists who spent
valuable time in generating information on various
aspects of plant pathology and displayed the same
on internet for use by students, teachers and
researchers

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Role of toxins in pathogenesis

Pl. Path. 111 (Cr. Hrs. 3+1)

Those toxins which plays an important causal role in disease and

 Criteria for any toxin to be a pathotoxin:

Those toxins produced in the infected plant /host by the

 Role is suspected in disease

 Alternaric acid; cochliobolin.

 Host selective/ specific toxins

 Are those toxins that affect the protoplast of

 Tab toxin; phseolotoxin, tentoxib Cercosporin

 A number of fungi: e.g. Alternaria,

 Victoria blight of oats -Cochliobolus victoriae

 Fumaric acid : Rhizopus spp.

 I gratefully acknowledge the use of some very

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