Indian Journal of Experimental Biology
Vol. 42. March 2004. pp.244-252
Review Article
Plant immunization
I L Kothari* & Miral Patel
Department of Biosciences. Sardar Patel University. Vallabh Vidyanagar 388 120. India
Plant immunization is the process of activating natural defense system present in plant induced by biotic or abiotic
factors. Plants are pre-treated with inducing agents stimulate plant defense responses that form chemical or physical barriers
that are used against the pathogen invasion. Inducers used usually give the signals to rouse the plant defense genes
ultimately resulting into induced systemic resistance. In many plant-pathogen interactions. R-Avr gene interactions results in
localized acquired resistance or hypersensitive response and at distal ends of plant. a broad spectrum resistance is induced
known as systemic acquired resistance (SAR). Various biotic or abiotic factors induce systemic resistance in plants that is
phenotypically similar to pathogen-induced systemic acquired resistance (SAR). Some of the biotic or abiotic determinants
induce systemic resistance in plants through salicylic acid (SA) dependent SAR pathway. other·, require jasmonic acid (JA)
or ethylene. Host plant remains in induced condition for a period of time. and upon challenge inoculation. resistance
responses are accelerated and enhanced. Induced systemic resistance (ISR) is effective under field conditions and offers a
natural mechanism for biological control of plant disease.
Keywords: Hypersensitive response. Induced systemic resistance. Plant immunization. Systemic acquired resistance
Plants possess constitutive and inductive defense
mechanisms against pathogen attack.
These
mechanisms fail when the plant is infected by a
virulent pathogen because the pathogen avoids
, triggering or represses resistance reactions, or evades
the effects of activated defenses 1.2.3.4. If defense
mechanisms are triggered by a stimulus prior to
infection by a plant pathogen, disease can be reduced.
Induced resistance is a state of enhanced defensive
capacity developed by a plant when appropriately
stimulated 5.6. Induced resistance is not the conception
of resistance where there is none, but the activation of
dormant resistance mechanisms that are expressed
upon subsequent, so-called challenge inocul<ition with
a pathogen 7• Induced resistance occurs naturally as a
result of limited infection by a pathogen, particularly
when the plant \....:velops a hypersensitive reaction.
Although, tissue neclOsis contributes to the level of
induced resistance attained, activation of defense
mechanisms that limit a primary infection appears
sufficient to elicit induced resistances. Induced
resistance can be triggered by certain chemicals, nonpathogens, avirulent forms of pathogens, incompatible
races of pathogens, or by virulent pathogens under
circumstances where infection is held up owing to
environmental
conditions.
Generally,
induced
resistance is systemic, because the defensive capacity
is increased not only in the primary infected plant
parts. but also in non-infected, spatially separated
*Correspondent author : Email - [email protected]
Phone: + 912692226883 ext. 212; Fax: +91 2692236475
tissues. Because of this systemic character, induced
resistance is commonly referred to as systemic
acquired resistance (SAR)9-12. However, induced
resistance is not always expressed systemically .
Localized acquired resistance (LAR) occurs when
only those tissues exposed to the primary invader
become more resistant lO •
Activation of systemic acquired resistance (SAR) is
a mechanism whereby plan ~ cells can be stimulated to
turn on their defenses to fight invasion by biotic /
abiotic factors . This activation is essentially a form of
'plant immunization' and can be compared to
immunization against disease in mammals. Plants are
treated with activating agents to stimulate plant
defense responses that form chemical or physical
barriers that are used by the plant to ward off diseases.
Inducing agents include pathogens, biocontrol agents,
certain types of composts, and plant activating
compounds. SAR and LAR are similar in that they are
effective against various types of pathogens. A signal
that promulgates the enhanced defensive capacity
throughout the plant in SAR appears to be lacking in
,LAR. SAR is characterized by an accumulation of
salicylic acid (SA) and pathogenesis-related proteins
(PR)II-14. Accumulation of SA occurs both locally
and. at lower levels. systemically. concomitant with
the development of SAR. Exogenous application of
SA also induces SAR in several plant species 11.15.16.
SAR was originally described using weak pathogens
as activators of plant defense responses. However, the
utility of this form of plant inoculation is limited in
the field because of the likelihood of pathogen spread
KOTHARI & PATEL: PLANT IMMUNIZATION
following application. The discovery that certain
biocontrol agents and specific plant activators could
induce resistance has made the use of SAR as a
disease control strategy an achievable goal. In nature,
immunization can occur when plants come into
contact with a necrotizing pathogen. Immunization
takes place not only at the primary infection site, but
also in distant (systemic) parts of the plant.
Necrotizing agents and chemicals are not the only
way to immunize plants against pathogens. Plantgrowth-promoting rhizobacteria have also been shown
to induce systemic resistance in plants. For example,
Pseudomonas fluorescens strains can induce
resistance against viruses, bacteria and fungi.
However, little is known about the underlying
mechanisms and the molecular basis involved.
Mechanism
Plant immunization in plants is usually associated
with the activation of a wide variety of defense
responses that serve to prevent pathogen replication
andlor movement.
In
some plant-pathogen
interactions, the ability of the host plant to recognize
the pathogen and activate these responses is regulated
in a gene-for-gene specific manner by the direct or
indirect interaction between the products of a plant
resistance (R) gene and a pathogen avirulence (Avr)
gene I7.18. When either the plant or the pathogen lacks
its cognate gene, activation of the plant's defense
. responses either fails or it is delayed sufficiently so
that pathogen colonization ensues l 9 .
After avirulent pathogen or some inducer
compound has generated a defense-eliciting signal
and the plant has perceived it, what are the
downstream events that are stimulated ? Gene-forgene interaction can induce signaling responses, such
as activation of protein-kinases, stimulation of an
oxidative burst, and induction of ion fluxes across the
cellular membrane20,22. These and other events, in turn
activate defense responses, such as cell wall crosslinking and the expression of defense-related
genesIJ .23.24. One downstream component of defense
signal transduction that deserves particular emphasis
is salicylic acid. Salicylic acid is a key signaling
intermediary that triggers systemic acquired resistance
(SAR). The earliest responses activated after host
. plant recognition of an Avr protein or a non-host
specific elicitor is the oxidative burst, in which levels
of reactive oxygen species (ROS) rapidly increase I8.25 .
These ROS are predominantly the superoxide anion
(02') and hydrogen peroxide (H 20 2) which arise from
successive one electron reductions of molecular
245
oxygen. ROS generation appears to occur irrespective
of the type of eliciting pathogen (bacterial, fungal, or
viral). ROS generation is localised to the point of
infection and appears to occur primarily in the
apoplasm even if an intracellular pathogen is
involved26 . A eicosionid pathway is particularly
associated with the inflammatory response of the
mammalian immune system. This pathway results in a
series of inter- and intracellular signals derived from
arachidonic acid (liberated from membrane
phospholipids by activated phospholipase A2)' Two
major branches of the pathway exist. One branch,
leading to the synthesis of prostaglandins,
prostacyclins and thromboxanes, is regulated by
cyclooxygenase (more correctly prostaglandin
endoperoxide synthase), whilst the other route, via a
family of lipoxygenases, results in the formation of
acid
(nn-hydroxy-eicosa-5,8, 10, 14-tetraenoic
HETE) , leukotrienes and lipoxins. A variety of antiinflammatory drugs, including indomethacin and
aspirin, inhibit cyclooxygenase. Aspirin exerts this
effect via acetylation of an amino acid in the active
site27 . A common feature of many plant-pathogen
interactions is the rapid production of active oxygen
species (AOS). Superoxide (02') and H20 2 are the
species most commonly measured, but their
accumulation undoubtedly results in a plethora of
other species, some of which (e.g. the hydroxyl
radical) are extremely damaging. While a rapid
biphasic production of AOS has been observed in a
number of systems 24.28 , the source of this oxidative
burst remains a subject of debate. One theory is that
salicylate inhibits catalase, ascorbate peroxidase or
other enzymes in the anti-oxidant armoury (thus
allowing H20 2 to accumulate/9 . This hypothesis
suffers from a number of problems like nonphysiologically high concentration of SA required to
effect inhibition. The activation of lipoxygenase
(yielding O2'), could also supply the burst, however,
most of the available evidence suggests that AOS
production is extracellular. AOS could be produced
by an unusual pH-dependent reaction of cell wall
peroxidases 3o, and this may represent the principal
source of AOS in some plants or during some
interactions. Most attention has, however, focussed on
a system similar to that which generates the oxidative
burst in mammalian macrophages, In this model , an
electron is transferred from an intracellular donor
(NADH) across the plasma membrane (by the action
of NADPH oxidase) to molecular oxygen, yielding
O2'. Homologues of the individual components of the
mammalian NADH oxidase assembly have been
246
INDIAN J EXP mOL, MARCH 2004
identified in plants, and, in some cases, the plant
oxidative burst exhibits similar inhibitor sensitivity to
the mammalian system3J .
Resistant plants often develop a hypersensitive
response (HR), in which a necrotic lesions forms at
the site(s) of pathogen or elicitor activitl 2.33 . The
localized cell death associated with HR resembles
animal programmed cell death, and it may help to
prevent the pathogen from spreading to uninfected
tissues. Just before or concomitant with the
appearance of a HR is the increased synthesis of
several families of pathogenesis-related (PR) proteins
in the inoculated leaves 34 . Many of these proteins
have been shown to exhibit antimicrobial activity
either in vitro or in vivo. PR-proteins are subsequently
expressed in the uninoculated portions of the plant,
concurrent with the development of a long lasting,
broad spectrum resistance known as systemic
acquired resistance (SAR)J J. Because of the
correlation, increased PR gene expression is
frequently used as a marker for SAR. The upstream
regulatory region of the PR-l gene has been
characterized in details 35 . Two positive regulatory
elements within the region, both of which are required
for induction of PR-l by salicylic acid, manifest
consensus sequences for recognition by transcription
factors. The first of these elements corresponds to the
cognate sequence of bZIP proteins, a class of
transcription factors common to fungi, plants, and
animals. bZIP factors are active as dimers, each
protomer of which is defined by two domains, one is a
basic domain that interacts with specific DNA
sequences, and the second is characterized by a
leucine zipper that is required for dimerization. One
category of plant bZIP factor that deserves particular
mention is the family of TGA proteins. In
Arabidopsis, six distinct g,enes have been, therefore,
allocated to TGA famill . An ortholog of TGA 1 has
been first recognized in tobacco for its ability to bind
with high specificity to the pentanucleotide element
(TGACG) within 35S promoter of the cauliflower
mosaic virus33. Specific protein-DNA interactions that
involve this consensus sequence are typical of all the
TGA proteins. Significantly, this pentanucleotide
exists within the first of the two elements that are
35
necessary for salicylic acid induction of PR-l gene .
The second of the two elements within the PR-l
promoter appears to correlate not to the specificity of
TGA protein, but rather to the recognition element of
NF-kB, a vertebrate transcription factor of the ReI
famill 8. NF-kB has been extensively studied because
it functions within various contexts of mammalian
signal transduction pathways that lead to the
transcription of genes involved in apoptosis, cell
growth and differentiation, and immune functions. In
addition, NF-kB represents an important model
transcription factor because its molecular relationship
to higher orders of regulatory control in transduction
pathways has been elucidated. Specifically, the ability
of NF- kB to activate transcription is controlled in
that it remains sequestered in the cytoplasm by an
inhibitory factor, IkB, to which it is bound. This
inhibitory function, in turn, is regulated by a specific
kinase that phosphorylates kB so as to tag it for
ubiquitinmediated degradation, thereby freeing NFkB to enter the nucleus and activate the transcription
of its target genes 39 . One protein that proves to be
crucial to SAR is the product of the NPRlgene (for
NONEXPRESSER OF PR-l; also known as NIMl [for
NONINDUCIBLE IMMUNITYl t°.4J.
An extensive research indicates that salicylic acid
(SA) is a critical signaling molecule in the pathway(s)
leading to local and systemic disease resistance, as
well as PR expression42 .43. In addition, recent studies
have demonstrated that ethylene and jasmonic acid
(JA) mediate the activation of various defense
responses and resistance to certain pathogens44 ,45. JA
signaling can be induced by a ran~e of abiotic
stresses, including osmotic stress46 .4, wounding,
drought, and exposure to "elicitors," which include
chitins, oligosaccharides, oligogalacturonides48 , and
extracts from yeast. A mitogen-activated protein
kinases named WIPK is transcribed minutes after
tobacco is wounded49 , and the WIPK protein product
is activated50. Jasmonic acid and its methyl ester
accumulate in wounded tobacco plants, but do not
accumulate in wounded transgenic plants, in which
expression of WIPK is genetically suppressed. This
indicates that expression of WIPK is required for
wound-induced JA biosynthesis. However, the
wounded transgenic plants accumulated SA and
transcripts of the gene pathogenesis related protein 1
( PRl ), indicating that suppression of JA pathway
permits wound induction of the SA pathway49 .. More
significantly,
transgenic
tobacco
plants
overexpressing WIPK accumulate JA and proteinase
inhibitor 2 (PIN2) transcripts5o.5J
Apparently
therefore, the wound-induced transcription of WIPK
and activation of the protein product activates JA
biosynthesis and suppresses SA-dependent signaling.
Other than SA, JA and ethylene as signal molecules,
nitric oxide (NO) has been implicated in the
activation of plant defenses 52 . This compound has
previously been shown to serve as a key redox-active
KOTHARI & PATEL: PLANT IMMUNIZATION
signal for the activation of various mammalian
defense responses, including the inflammatory and
innate immune responses 53 .54 . Till date, atleast in three
NO
is
different
plant-pathogen
interaction,
documented as signal for activation of plant defense
responses.
Inducers
SAR has been demonstrated to occur in many
plants including cereals, vegetable, and nursery and
tree crops, can provide protection against pathogens
for which there is no effective disease control
measure currently available. There is a low risk of
pathogen populations developing resistance to SAR
since that would entail overcoming an array of plant
defense mechanisms. Finally, the use of biocontrol
agents as inducing agents can provide other
advantages to the plant such as plant growth
promotion, which is often associated with certain
types of biocontrol agents. Growth enhancement has
also been reported for a plant activator.
The necrosis-related immunization process seems
to follow a salicylic acid (SA)-dependent pathway.
Strong support for the implication of SA in this
pathway comes from experiments with transgenic
plants (expressing the NahG gene for salicylate
hydroxylase) unable to accumulate SA. Such plants
become susceptible to avirulent pathogens and cannot
be immunized. Treatment of plants with SA or
chemicals such as benzo (1 ,2,3) thiadiazole-7carbothioic acid S-methyl ester (BTH) and 2,6dichloroisonicotinic acid (INA) also leads to
subsequent immunization. Benzothiadiazole, induces
systemic resistance in wheat, which is one of the
novel class of inducers of systemic acquired
resistance 55 . The expression analysis of genes induced
in barley after chemical activation reveals distinct
disease resistance pathways 56.
Two products are available to immunize plants
from some fungal diseases. These two products are
Messenger™, from Eden Bioscience57 ,58 and Elexa™,
from Safe Science. Their main target is powdery
mildew in vegetable crops and grapes, and they fall
into the Environmental Protection Agency's Plant
Defense Booster (PDB) category, which classifies
them as "low risk biochemical pesticides". Messenger
has an active ingredient called harpin Ea, which is a
protein produced by bacteria. First, bacteria are
filtered out of the protein product. The protein is
harvested by culturing and applying heat to destroy
the bacteria. When Messenger is applied to the
foliage, the plant's defensive biochemical pathways
247
are activated within 5-10 min 59 •60 . Besides the benefits
of disease prevention, plant growth response is
positively increasing plant biomass, flowering and
early maturing, and crop yield and quality . Elexa's
active ingredient, chitosan, is obtained from the shells
of shrimp and crabs. The cell wall of fungal spores
that attack plants are comprised of chitin. When
chitosan is applied, the plant believes that fungal
spores have arrived. The plant then triggers the
production of a protein called chitinase, which attacks
the fungal chitin skin, loosening its cell walls and
causing potential cell wall disintegration. Messenger
and Elexa represent the genesis of a new plant
immunization technology that allows the plant to
protect itself from disease.
One of the advantages of using biocontrol agents,
composts, or plant activating compounds to stimulate
SAR is that they will not cause disease. A key
advantage to SAR is that the plant, once immunized,
has its activity until flowering, thereby limiting the
number of applications necessary for defense
mechanisms turned on for an extended period of time,
usual effective disease control61 • Immunization is
generally broad spectrum, effective against an array
of different pathogens and pathogen types (i.e. fungi,
nematodes, viruses and bacteria). Studies on
suppression of fusarium wilt of carnation and radish,
caused by Fusarium oxysporum f.sp. dianthi (Fod)
and F. oxysporum f.sp. raphani (For), respectively,
established competition for iron as the mechanism of
disease reduction by P. putida strain WCS358 62 -64 •
Under iron-limiting conditions in the rhizosphere,
WCS358 secretes a pyoverdin-type siderophore
(pseudobactin 358) that chelates the scarcely available
ferric ion as a ferric-siderophore complex that can be
transported specifically into the bacterial cell.
Siderophores released by Fod or For under these
circumstances are less efficient iron-chelators than
pseudobactin 358, so iron available to the pathogens
can become limiting in the presence of WCS358. Due
to iron deficiency, fungal spore germination is
inhibited and hyphal growth restrained, effectively
lowering the chance that the plants become infected,
and disease incidence and severity are reduced. The
plant, in contrast, does not appear to suffer from iron
shortage65 -66 . A bacterial mutant generated by Tn5
transposon mutagenesis and unable to produce
pseudobactin 358 (WCS358 Side) did not reduce
disease incidence67 • A different bacterial strain,
Pseudomonas fluorescens WCS417, was about twice
as effective as WCS358 in suppressing fusarium wilt
in carnation. However, a Side mutant of this strain was
248
INDIAN J EXP BIOL, MARCH 2004
as effective as the wild type in suppressing the
65
disease . Clearly, a mechanism other than common
procedures to accomplish induced resistance are
pouring a suspension of the bacteria on, or mixing it
with, autoc1aved soil; dipping the roots of seedlings in
a bacterial suspension at transplanting; or coating
seeds with high numbers of bacteria before sowing 68 .
Subsequently, seedlings are challenged with a
pathogen. Because rhizobacteria are present on the
roots, systemic protection against root pathogens must
be demonstrated by applying the inducing bacteria to
one part of the root system and the challenging
pathogen to another part, for instance by making use
of split-root systems. Testing for protection against
foliar pathogens is easier, because the pathogens are
naturally separated from the rhizobacteria. However,
rhizobacteria applied to seeds, or to soil into which
seeds are sown or seedlings are transplanted, can
move into the interior of aerial plant tissues and
maintain themselves to some extent on the exterior of
aerial surfaces 69 . The stems, petioles, cotyledons
and/or leaf extracts of tested plant were free from , or
contained negligible quantity of inducing bacteria
implying involvement of ISR. Some of the strains of
PGPR has successfully induced resistance against the
pathogen viz., P. aeruginosa 7NSK2-induced
'
.
. b
resIstance
111
ean aga111st
gray mo Id 70 , P. jl uorescells
WCS417 -mediated protection of carnation against
fusarium wilt 71 and resi stance in cucumber against
anthracnose 72 . When spontaneous rifampicin-resistant
mutants were used for treating seeds, some strains
were recovered from inside surface disinfested roots.
However, none of the inducing strains was found in
leaves used for challenge. Upon injection of
cucumber cotyledons P. fJutida 89B-27 and Serratia
marcescens 90-166 multiplied in the tissue but were
not recovered from stems 1 or 2 cm above or below
the cotyledons73 . While some bacteria that induce
systemic resi stance colonize internal tissues, they do
not appear to establish themselves on challenged
leaves, suggesting that neither competition nor
antibiosis is involved in disease suppression 72.74
Certain Pseudomonas produce salicylic acid that is
d eterm1l1ant
"
'
SAR45 .75 .
.
an Important
1I1VO Ive d III
Salicylic acid is known to activate plant defense
responses and is thought to function as a signal
molecule within the plant after the onset of resistance.
However, bacterial salicylic acid production is not the
only determinant of SAR since there are examples of
biocontrol agents that can activate resistance but do
not produce salicylic acid . It is thought that some
biocontrol agents activate resistance at low iron
concentrations through the production of ironscavenging
compounds
called
siderophores.
Additionally,
certain
plant
growth-promoting
biocontrol agents have demonstrated altered insect
feeding patterns in cucumber, making treated plants
less susceptible to predation than non-treated plants
and limiting the spread of pathogens that are vectored
by the insects. Field experiments with several of these
biocontrol agents have demonstrated that SAR is a
viable disease control strateg/ 6 .
P. syringae pathovars syringae and phaseoliCola
elicit a non-host hypersensitive response (HR) when
injected into the leaves of tobacc0 57 .77 • This HR is
dependent upon the ability of the bacteria to assemble
an hrp (for HR and pathogenesis) pilus (a kind of
biological microinjection system) utilised to introduce
avr gene products into the plant cells 58 . Assembly of
the pilus and transfer of the avr gene products is
required to elicit HR. Mutant bacteria (such as the
hrpL strain used in this study) fail to produce the pilus
and do not induce HR. Neither syringae nor
phaseolicola are pathogens of tDbacco (hence ' nonhost' HR), and in this respect are not as ideal as
tobacco mosaic virus (TMV) which is a pathogen of
tobacco and which causes disease or elicits HR
depending upon absence or presence of a single gene
(the N gene) in a given tobacco cultivar's genotype.
Expression and introduction of avr gene products into
a plant cell would seem to be uniquely
counterproductive as far as a pathogen is concerned,
since it is these very products that elicit defense
responses such as HR78. This is tme of the response of
resistant plants (incompatible interaction) that have the
necessary gene or genes required to recognize the A vr
gene product. However, A vr genes are actually part of
the pathogen's colonisation mechanism when in contact
with a susceptible host (compatible interaction), and are,
thus, necessary for pathogen survival in a suitable host
plant. One good example of this involves the interaction
between tobacco mosaic virus (TMV) and tobacco
plants. In susceptible tobacco plants (those lacking N
resistance gene) the virally-encoded replicase is an
integral part of the vims's replication machinery .
However, it is the same replicase that is recognised in
resistant plants (by N gene product), and that results in
the characteristic hypersensitive response. However,
TMV strains in which replicase has been mutated to
produce an enzyme that is still active, but has lost the
recognition sequence, will be able to avoid the defense
response even in tobacco plants possessing N gene. This
is the basis for the so-called 'evolutionary arms race'
between plants and pathogens.
KOTHARI & PATEL: PLANT IMMUNIZATION
In recent years the maJonty of pathogenesis
research has focussed on defense responses dependent
upon AvrlR gene interactions. This is quite natural
that such systems are highly tractable to a genetic
approach, offer the opportunity for an enter into the
molecular biology of defense signal transduction, and
AvrlR interactions are often a feature of the most
aggressive and economically important diseases. In
fact, the aggressive nature of such 'pathogens is
probably the driving force of the 'evolutionary arms
race' that underlies avrlR-dependent responses (Avr
gene products are actually agents of pathogenesis in
susceptible plants; resistant plants have acquired the
ability to recognize these products and turn the
pathogen's own weapon against it).
Observations :nade in rice emphasize the
complexity of interactions between signals. 2,6,dichloroisonicotinic acid (INA), an inducer of
systemic acquired resistance (SAR) and putative SA
. . 31
. ,
•
mumc " protects nce agamst the nce blast pathogen
(Magnaporthe grisea) , Wasternack et al. 79 have also
reported induction of thionin, a antifungal protein in
barley by INA. In tobacco; INA induces expression of
a set of genes associated with SA-dependent SAR sO
and homologues of these are expressed in rice
following INA application. However, contrary to the
standard antagonism model, not only does INA
induce endogenous JA accumulation in rice, but
exogenous JA application enhances INA-mediated
resistance and potentiates INA-induced defense gene
expression si .
Pathologists describe two different types of disease
suppression in compost and soil. General suppression
is due to many different organisms that either
compete with pathogens for nutrients and/or produce
general antibiotics that reduce pathogen survival and
growth. This type of suppression is effective on those
pathogens that have small propagule size, resulting in
small nutrient reserves and the need to rely on
external carbon sources. Thus, an active microflora in
the soil or compost will often prevent disease since
the pathogens are outcompeted. Examples of this
mechanism are suppression of damping off and root
rot diseases caused by Pythium species and
Phytophthora species s2 . Specific suppression, on the
other hand, is usually explained by one or a few
organisms. They exert hyperparasitism on the
pathogen or induce systemic resistance in the plant to
specific pathogens, much like a vaccination. With
specific suppression, the causal agent can be clearly
transferred from one soil to another. Pathogens such
as Rhizoctollia solani and Sclerotium rolfsii are
249
examples where specific suppression may work but
general suppression does not work. This is because
these organisms have large propagules that are less
reliant on external energy and nutrients and thus less
susceptible to microbial competition. Specific
hyperparasites such as Trichoderma species will
colonize the propagules and reduce disease potential.
Methyl bromide is found to be harmful chemical for
animals and humanbeings. In substitution to methyl
bromide, composts and biocontrol a§ents are used in
biological control of plant diseases s . To control the
disease incidence and increase production of tomato,
compost amendments were exploited by conventional
and organic production systems S4 . Some species of
rhizobacteria are known to induce systemic resistance
in plants. Screening assay for this type of bacteria has
been developed by Han et al S5 . Trichoderma hamatum
382 and Flavobacterium balustinum 299 have been
identified as effective biocontrol agents in compostamended substrates 86•87• They consistently induce
suppression of diseases caused by a broad spectrum of
soilborne plant pathogens if inoculated into compost
3fter
peak
heating
but
before
substantial
recolonization with mesophilic microorganisms has
occurred88 • The presence of significant populations of
T. hamatum 382 and F. balustinum 299 in fortified
commercial mixes is one of several factors crucial to
efficacy 86. Compost and compost-water extract were
also used to induce systemic resistance in cucumber
and Arabidopsis 89. Suppression of plant diseases
caused by Pythium and Phytophthora species were
controlled to an extent by using compost90 . Foliar
diseases of ornamental plants were also suppressed by
use of compost and T. hamatum 38291 •92 •
Concluding remarks
Understanding the evolution of induced defense
will be advanced by applying our knowledge of
quantitative genetic variation in induced resistance to
fitness consequences for the plant. Such experiments
should be conducted in environments with and
without plant attackers. More researches on signal
transducers and their downstream components are in
progress for elucidation of biochemical aspect of
resistance in plants. With isolation of some of the
genes like Nim 1, NPR 1 or P1N 2, immense
opportunities have been unfolded for protein
biochemists, biologists, physiologists and geneticists
alike to elucidate how these gene products function
and the gene families evolve. The concept of this
induced resistance has been tried on plants like
arabidospis, tobacco, tomato, cereal, pearl millet,
250
INDIAN J EXP BIOL, MARCH 2004
barley, but there are yet many economically important
crops left which are destroyed due to devastating
pathogens. Biotic factors like P. syringea or some
strains of PGPR and abiotic factors like salicylic acid,
acetlysalicylate, benzothiadozole should be marked as
low risk factor like MESSENGER and EDEN. Field
trials with such inducers should be encouraged and
should be provided to the farmers.
References
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