This document summarizes a credit seminar presentation on the vivotoxin fusaric acid. Fusaric acid is produced by Fusarium species and is a host-nonselective vivotoxin. It was first identified in 1934 but its toxic properties were recognized in the 1950s. As a vivotoxin, fusaric acid produces disease symptoms but is not the initial causal agent of infection. It causes chlorosis in plants by chelating iron and copper and disturbing cellular ion balance and enzymatic processes. The presentation reviewed the mechanism and harmful effects of fusaric acid as well as methods for detecting its production and impact on plants.
3. Toxins Produced by Plant Pathogens
These are the chemicals that are produce by
the plant pathogenic micro-organisms that cause
disruption in the system of the plant.
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4. Robert Koch (1843- 1910)
According to Koch’s
Postulates a substance to
be called as a toxin,
The compound must be
isolated from the diseased
plant.
It should not be present in
healthy plant.
Compound must be chemically
characterized.
When isolated toxin is
reintroduction to a healthy
host, it should produce the
original symptoms.
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5. 5
On the basis of specificity
Host selective Host non-selective
(Scheffer, 1983)
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Host specific/ Host Selective toxins:
This metabolic compounds are toxic to the
specific susceptible host of the pathogen.
Host non-specific/ Host non-Selactive toxins:
This metabolic compounds do not have any
host specificity and affect many unrelated
plant species that is normally infected by a
pathogen.
8. 8
Pathotoxin:
Plays major role in disease development and
produce most of the symptoms in the plant.
Phytotoxin:
Though they are produced during host plant
interaction they are not necessary to occur a
disease.
Vivotoxin:
It functions in the production of disease, but is
not itself the initial inciting agent of disease.
9. Fusaric acid
Fusaric acid is produced by
Fusarium spp.
It is host-non specific
vivotoxin.
Chemically it is a picolinic
acid (5- Butylpicolinic acid).
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Source: Wikipedia
10. History of Fusaric acid
This secondary metabolite was first reported
in 1934 from Fusarium heterosporum, but
its toxic nature was recognized about two
decades later by Gaumann et al. 1952, who
also reported its occurrence from Fusarium
oxysporum f. sp. lycopersici, Fusarium
oxysporum f. sp. vasinfectum and Gibberella
fujikuroi.
Since then this phytotoxic metabolite has
been detected in various Fusarium formae
specialis of the elegance group which
included Fusarium oxysporum f.sp.
lycopersici, batatis, conglutinans, cubense,
lini, vasinfectum, udum and Fusarium
moniliforme (Gaumann, 1957;
Kalyanasundaram, 1958; Prasad and
Chaudhary, 1974).
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12. Mechanism of Fusaric acid
Picolinic acid resembles as a chelating compound which
is an aromatic ring structure.
Butyl side chain responsible for increasing lipophilicity
of FA and enables it to penetrate cell membranes.
A hydroxyl (OH−) group that acts as a proton donor and
is responsible for the acidic properties of FA.
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Kalyanasudaram and Saraswathi Devi (1955)
13. Why Fusaric acid is vivotoxin?
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Vivotoxin designates a secondary
metabolite produced by the pathogen
and/or its host during infection,
produces disease symptoms, but is not
oneself the initiating causal agent of
the infection.
Out of all, Fusaric acid (FA) is
amongst the oldest identified secondary
metabolites produced by Fusarium species,
known for a long time to display strong
phytotoxicity and moderate toxicity to
plant cells; however, the cellular targets of
FA and its function in fungal pathogenicity
remain unknown (López-Díaz et al. 2018).
Programmed chlorosis of banana leaves after Fusarium
infection. The image was recorded 15 days after
Fusarium infection of the banana seedling.
14. Harmful effect of Fusaric Acid on Plants
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The toxin is active at 20-200mg/kg fresh
weight. Sometimes, another toxin,
dehydrofusaric acid is associated with
fusaric acid which is easily converted into
the latter. The role of fusaric acid in the
plants is said to be of many types -
• It mainly causes interveinal chlorosis.
• It causes chelation of iron and copper in
the host cells and alters the cell wall
permeability.
• This disturbs the ionic balance of the
cell.
• It also affects the enzymatic processes in
the cell.
• By chelating the enzymes or by rendering
respiratory enzymes ineffective, it alters
respiratory pattern of the plant.
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A concomitant increase in ROS production, the down regulation of antioxidative
enzymes activities and upregulation of lipid peroxidation were crucial for the onset of cell
death. These results suggested that FA-induced damage might result from ROS pathways.
Thus, our experiments provide a useful model plant system for research on FA-induced
plant cell death.
Detection of ROS generation in the tomato leaves treated with Fusaric acid
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Three major criteria as the nominal need to set up
vivotoxicity.
These were -
• (a) reproducible segregation from the infected host plant,
• (b) purification, and
• (c) re-production of at least a fraction of the disease
symptoms by allocating the toxin in a same healthy plant.
“Fusaric acid - a vivotoxin is a disease-producing
entity and therefore a pathogenic agent."
Paradoxically,
24. References
Gaumann, E. (1957). Fusaric acid as a wilt toxin. Phytopathology, 47:
342-357.
Gaumann, E., St. Naef-Roth and Kobel, H. (1952). Uber Fusarinasure,
ein zweites Welketoxin des Fusarium lycopersici Sacc. Ibid., 20, 1-38.
Wheeler, H., & Luke, H. H. (1963). Microbial toxins in plant
disease. Annual Reviews in Microbiology, 17(1), 223-242.
Dimond, A.E. and Waggoner, P.E. (1953). On the nature and role of
vivo-toxins in plant disease. Phytopathology, 43: 229-235.
Srivastava, S., Singh, V. P., & Rana, M. (2020). Fusaric Acid: A Potent
Vivotoxin. European Journal of Molecular & Clinical Medicine, 7(07),
2020.
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