Pathogen-derived molecules : Enzymes
Other molecules? Pathogen-derived molecules Pathogen-derived molecules : Pathogen-derived molecules Pathogens possess avirulence genes whose products are involved with determining host specificity.
Pathogens may possess hrp genes whose products are associated with induction of the hypersensitive response in plants. Pathogen-derived molecules : Necrotrophic pathogens produce a wide range of extracellular enzymes enabling them to enter plant cells by degrading plant cell wall polymers. Many of these extracellular enzymes exist as isozymes. Microbial proteases may degrade plant cell wall proteins associated with resistance.
Biotrophic pathogens produce very little extracellular enzymes in comparison to necrotrophs Pathogen-derived molecules Pathogen-derived molecules : Pathogenic fungi possess cutinases enabling them to penetrate cutin on the surface of plants. Plant pathogenic bacteria do not possess cutinases and can only enter plants through natural openings, e.g. stomata, or wounds.
Some pathogens produce phytotoxins which kill plant cells, preventing them from responding in a co - ordinated manner to resist infection. Phytotoxins can be specific (affecting the host range of the pathogen) or may be non-specific (affect plants outwit the host range of the pathogen). Pathogen-derived molecules Pathogen-derived molecules : Pathogen-derived molecules Fungal pathogens are generally able to rapidly degrade phytoalexins produced by the host plant whereas degradation of phytoalexins from non-host plants is very slow. There is little evidence of phytoalexin degradation by bacteria Toxins : Exotoxins
Toxins very low concentration are directly toxic to the cells of the suscepts.
In plant pathology toxins are the products of pathogen, its host, or host – pathogen interactions. Toxins Toxins : Toxins Phytotoxins
Vivotoxins Phytotoxins : Phytotoxins Substances for which a causal role in disease is merely suspected, rather than established can be called phytotoxins.
These are product of parasite which induce a part or none of the symptoms caused by the living pathogen.
Non-specific and no relationships between symptoms/virulence/and amount of/ toxins produced by the pathogen.
Alternaric acid by Alternaria solani. Pathotoxins : Pathotoxins The toxin will produce all symptoms characteristics of the disease.
Sensitivity to toxin will be correlated with the susceptibility of the host to the pathogen.
The toxin produced by the pathogen will be directly correlated with its ability to cause disease (Wheeler and Luke, 1963).
Victorin by Cochliobolus (Helminthosporium) victoriae. Is the only one to fulfill these requirements. Vivotoxins : Vivotoxins Vivotoxin is a substance 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 (Dimond and Waggoner, 1953)
Three criteria were suggested for a vivotoxin;
(1) Reproducible separation of the toxin from sick plant, Vivotoxins : (2) Purification or chemical characterization,
(3) Induction of at least a portion of the disease syndrome by placing the toxin in a healthy plant.
(4) Production by the causal organism of the disease ( Graniti, 1972)
Vivotoxins are nonspecific.
Fusaric acid, Lycomarasmin, and Piricularin. Vivotoxins Ecological roles for toxins : Ecological roles for toxins Effects on plant
contributory to virulence
debilitating plant cells?
altering plant gene expression to prevent defense response? Slide 17: contribution to pathogen fitness
promoting nutrient leakage
altering plant metabolism
staking out the food source
antiherbivore activities against mammals, insects, nematodes, other fungi, etc.
may sometimes be a dual role with virulence or pathogenicity determination Possible roles in disease : Possible roles in disease Necrotrophic fungi, e.g. Cercosporella spp.:
cause necrosis/cell death
suppress defense response Possible roles in disease : Hemibiotrophic fungi, e.g. Cochliobolus carbonum (and other Cochliobolus spp.?):
prevent cell death?!
suppress defense response Possible roles in disease Possible roles in disease : Biotrophic fungi
Known pathotoxins are not generally associated with strictly biotrophic fungi.
However, this doesn't indicate a lack of such toxins, since these are the less tractable systems for experimentation. Possible roles in disease Possible roles in disease : suppressors of resistance?
elicitors of race-specific resistance?
evidence: rust resistance gene, Pc-2, at toxin (victorin) sensitivity gene locus, Vb
Mutagenesis results suggest these are the same gene. Possible roles in disease Biotrophic fungi Genetic interactions of Avena sativa and Cochliobolus victoriae : Genetic interactions of Avena sativa and Cochliobolus victoriae Toxin characteristics (the following roles are not mutually exclusive) : Toxin characteristics (the following roles are not mutually exclusive) host selective vs. nonselective or nonspecific
causing programmed cell death or:
preventing cell death or hypersensitive response (e.g. HC-toxin)
Often require active cell metabolism for function (e.g. victorin).
indicating what? Chemical classes of phytotoxins : Chemical classes of phytotoxins Polyketides
synthesis related to that of fatty acids
e.g. T-toxin (Yang et al. 1996) Chemical classes of phytotoxins : Terpenoids
prenyltransferases in biosynthesis
e.g. gibberellic acid
e.g. fusicoccin (glycosylated diterpene) Chemical classes of phytotoxins Chemical classes of phytotoxins : Peptides, nonribosomally - synthesized (mostly cyclic oligopeptides)
peptide synthases in biosynthesis
e.g. HC-toxin (Panaccione et al. 1992; Walton 1996)
e.g. victorin (Wolpert et al. 1985)
one of the few known metabolites to be chlorinated Chemical classes of phytotoxins Chemical classes of phytotoxins : Proteins, ribosomally -synthesized
e.g. Ptr toxin (Ciuffetti et al. 1997)
More complex pathways
e.g. ergot alkaloids
prenylated & methylated tryptophan linked to cyclic peptide derivative
e.g. oxalic acid (HOOC-COOH) (Dutton & Evans 1996) Chemical classes of phytotoxins Mode of Action : Mode of Action Change in cell permeability:- Lycomarasmin, Fusaric acid, Picolinic acid, and Victorin etc.
Disruption of normal metabolic processes:- (a) obstruction of metabolism of methionine by tabtotoxine. (b) Inhibition of Polyphenol oxidase by piricularin. (c) Formation of chelate - ring complexes with heavy metals e.g. Fusaric acid and Picolinic acid. Mechanisms of action : Mechanisms of action AAL toxin and fumonisin: inhibition of sphingosine lipid biosynthesis (Wang et al. 1996)
These may trigger programmed cell death (apoptosis).
HC toxin: inhibition of histone deacetylase (Brosch et al. 1995; Ransom and Walton 1997)
suppressing resistance response?
preventing programmed cell death? Mechanisms of action : T-toxin: uncoupling chemiosmotic gradient in mitochondria
T-Urf-13 protein in maize mitochondria (Dewey et al. 1988); evidence:
genetic linkage, maternally inherited sensitivity
mutants with reduced sensitivity Mechanisms of action Mechanisms of action : Victorin: inhibition of glycine decarboxylase, which is:
involved in activating single-carbon (methylene) groups in biosynthesis
involved in photorespiration Mechanisms of action Mechanisms of action : Cercosporin (Jenns et al. 1995)
light activation => triplet oxygen => singlet oxygen => lipid peroxidation Mechanisms of action Mechanisms of action : Fusicoccin
from Fusicoccum amygdali, a wilt pathogen of Prunus spp.
activates plasmalemma H+-ATPase
perhaps mediated by interaction with a regulatory 14-3-3 proteins
Recall the activities of lipodepsipeptide toxins from Pseudomonas syringae and the XR. How is fusicoccin different or similar in activity? Mechanisms of action Basis for host resistance : Basis for host resistance HC-toxin: detoxification (Johal & Briggs 1992; Meeley et al. 1992)
T-toxin: absence of site (Wise et al. 1987)
AAL toxin, cercosporin, Ptr toxin, etc.: unknown Wilting toxin. : Wilting toxin. Fusicoccum amygdali that belongs to the Fungi imperfecti secretes a terpenoid (fusicoccin) that increases the influx of potassium into the cells of the stomata and induces thereby a permanent opening of the stomata. The consequent high loss of water causes finally the perishing of the plant. Fusicoccin is therefore also known as a wilting toxin. Helminthosporium maydis : Helminthosporium maydis The toxins ( –cyclic peptides –) of Helminthosporium maydis have an exactly reversed effect. H. maydis is the causative agent of a corn disease that effects mainly corn of the genotype Texas male sterility cytoplasm – CMS. It brought about one of the worst epidemics ever caused by fungi in the United States in 1970. Its toxins inhibit the light-induced potassium-uptake through the stomata. This lowers transpiration and consequently also the activity of photosynthesis (C. J. ARNTZEN et al., 1973). Self protection : Self protection As in bacterial systems, the pathogen may lack the site of action, have a resistant form of the target, fail to take up the active toxin, or detoxify
Some host selective toxins simply don't affect non-target organisms, including the pathogen
e.g. T- toxin Self protection : Other host selective toxins are either not taken up or detoxified by most organisms
e.g. HC-toxin, which has a nonselective activity against histone deacetylase, but is detoxified by most grasses
Non-selective toxins need to be detoxified or avoided
e.g.: In Cercospora nicotianae the SOR1 and CRG1 genes are necessary for resistance to cercosporin (Chung et al. 1999; Ehrenshaft et al. 1999)
mechanism(s) unknown Self protection