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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 raceT
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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Lect. 6a Pl Path 111- Toxins.pdf

  • 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.)
  • 2. 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.
  • 3. 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 raceT
  • 4. 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
  • 5. 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.
  • 6. On the basis of specificity to host (Scheffer, 1983)  Host selective/ specific toxins  Non- host selective/ non-specific toxins
  • 7. 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
  • 8. 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.
  • 9. 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)
  • 10. 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
  • 12. 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
  • 13. 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
  • 14. 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
  • 15. 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
  • 16. 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
  • 19. 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.
  • 20. 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
  • 21. 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
  • 22. 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
  • 23. 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
  • 24. 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.
  • 25. 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
  • 26. 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