ACHARYA N.G.

RANGA AGRICULTURAL
UNIVERSITY

AGRICULTURAL COLLEGE
BAPATLA

Department
Course of Plant Pathology
In – Charge

COURSE NO. : PL PATH 505

COURSE TITLE : PRINCIPLES OF PLANT PATHOLOGY
TOPIC : GENETICS AND MOLECULAR BASIS OF HOST
PATHOGEN INTERACTION

Course In - Charge
DR SK ABDUL SALAM,
ASSISTANT PROFESSOR,
DEPARTMENT OF PLANT PATHOLOGY.
Submitted by
CHARUBALA B,
BAM/24 – 065,
 M. Sc 1st YEAR, DEPARTMENT OF PLANT
PATHOLOGY.
GENETICS OF HOST PATHOGEN INTERATION
Herold Henry Flor showed correlation between inheritance of pathogenicity
and resistance to linseed rust caused by Melampsora lini which is now
commonly known as gene -for -gene hypothesis.
Flor that for each gene conditioning rust reaction in the host there is a
specific gene conditioning pathogenicity in the parasite .
For each resistance gene in the host there is a corresponding gene for
avirulence in the pathogen conferring resistance and viceversa. (Flor,1942)
He states that during their evolution host and parasite developed
complementary genic systems
GENE-FOR-GENE HYPOTHESIS

GENE-FOR-GENE HYPOTHESIS ILLUSTRATED FOR TWO

MATCHING AVR/R GENE PAIRS
 -
- NO DISEASE
+ DISEASE
CRITERIA FOR GENE FOR GENE TYPE OF RELATIONSHIP
It is most common in specialized or obligate parasites and totally absent in
non specialized ( facultative )pathogens .
According to Vander Plank (1973) gene for gene type of relationship can
exist only in those host – parasite systems where both the components are
living for a certain critical period of time in order to let their nuclei
transcribe, translate and subsequently exchange genetic information .
The genes-for-gene systems thus involve biotrophy.
But the converse is not necessarily true. For example, Plamodiophora
brassicae , the cause of club root of crucifers, is biotrophic but no evidence
has yet been presented in the literature to suggest that host pathogen
interaction in them is based on a gene-for – gene systems
MOLECULAR BASIS OF HOST PATHOGEN INTERACTION
ELICITOR MOLECULES, THE INITIATORS OF THE DEFENSE
CASCADE
Elicitor molecules do not have a signature structure and are made up of
molecules such as oligosaccharides, peptides, lipids, and proteins.
They include molecules released from or produced by pathogens that provide
information for plants to perceive and recognize signal from pathogens by
cell surface-localized receptors, resulting in the activation of plant immunity
Elicitors in pathogens can be categorized into two categories: general
elicitors and race-specific elicitors
Elicitors that are capable of triggering defense in both non-host and host
plants through the perceived presence of potential pathogens are known as
general elicitors
β-glucan elicitors from Phytophthora sojae are able to activate defense
responses in rice, soybean, and other non-hosts.
Race-specific elicitors play essential roles as virulence determinants.
These virulence determinants include harpins and avr gene products.
This cultivar-specific (gene-for-gene) resistance can be determined by the
pair of genes that complement each other between pathogen races and
specific host cultivars .
The absence of either one of these genes in the interaction can result in
disease.
BACTERIAL ELICITORS
FUNGAL ELICITORS

NON-PATHOGENIC ELICITOR MOLECULES: INDUCERS OF

SYSTEMIC RESISTANCE
Flagellin from the beneficial Pseudomonas putida WCS358 has been
reported to induce systemic resistance against P. syringae in Arabidopsis.
Similarly, the LPS of certain Gram-negative bacteria have also been
reported to induce systemic resistance.
Linear hepta-β-glucoside laminarin produced by brown algae elicits a
defense in various plants species including rice and soybean .
RECEPTOR MOLECULES: PERCEPTION AND ACTIVATION
The perception of elicitors involves surface-based receptors or intracellular
receptors in plants that will detect the pathogenic patterns.
Receptor-like proteins (RLPs), receptor-like kinases (RLKs), and
extracellular binding proteins constitute surface level multicomponent
recognition complexes
With one receptor, a plant can recognize a complete taxonomic group that
features a particular PAMP
For example, flagellin receptor FLS2 (flg22) enables the plant to recognize
all mobile flagellated bacteria.
 Ve1 is an example of a plant receptor molecule in tomato, which binds to the
Ave1 elicitor molecule from fungi. Ve1 can also be introduced as the PRR or
R protein where the Ave1 peptide is referred to as the effector acting as
MAMP

Schematic representation of plant receptor-like protein kinases (RLKs) possibly

associated with elicitor perception. All the RLK identified contain a serine-
threonine kinase domain and their extracellular domains exhibit similarity to
diverse sequence motifs. (A) Xa21 from rice contains leucine-rich repeats
(LRR) (B) Ath LecRK1 from Arabidopsis contains lectin-like motifs. (C) PR5K
from Arabidopsis exhibits similarity to the PR protein thaumatin . (D) CHRK1
from tobacco shows similarity to the PR protein chitinase . (E) WAK1 from
Arabidopsis contains epidermal growth factor-like (EGF) repeats. (F) LRK10
from wheat do not exhibit homology to a particular established sequence motif.
(G) StPRKs from potato exhibit a novel bimodular cysteine motif
TWO FORMS OF IMMUNITY IN PLANTS
In classic textbooks, these two forms have been called
1)Basal or horizontal disease resistance and
2)Resistance (R) gene-based or vertical disease resistance
These two forms are now defined as
1)PAMP-triggered immunity (PTI) and
2)Effector-triggered immunity (ETI) in a new terminology.
PTI (formerly called basal or horizontal resistance) is based on the PRR
mediated recognition of MAMPs and DAMPs, the so-called general
elicitors.
ETI (formerly called R-gene-based or vertical resistance) is based on the
highly specific, direct or indirect interaction of pathogen effectors and the
products of plant R genes according to the gene-for-gene theory.
PLANT INNATE IMMUNITY :PAMP - TRIGGERED IMMUNITY
(PTI)
PAMPs are pathogen-derived molecules that constitute portions of fungal
cell walls, structural components of pathogens, or flagellum .
PAMP( Pathogen associated molecular patterns ), Herbivory-associated
molecular patterns (HAMPs), and Damage-associated molecular patterns
(DAMPs) MAMPs ( Microbe associated molecular patterns ) are referred as
general elicitors
These molecules are perceived and recognized by by pattern recognition
receptors (PRRs) in plants and activates innate immunity (non host
resistance)
In the case of non-host resistance, a particular plant can be resistant to
different kinds of pathogens .

The recognition of elicitors at the molecular level results in PAMP-triggered

immunity (PTI), which causes reactive oxygen species (ROS) production,
 the activation of mitogen-activated protein kinases (MAPK), Ca 2+ signaling,
and ultimately transcriptional reprogramming .
In the first phase of plant innate immunity, PTI stops the colonization of
pathogens after their PAMPs are recognized by PRRs in plants.
PLANT-INDUCED IMMUNITY: EFFECTOR ACTIVATED SYSTEM
In contrast to PTI, ETI involves effector molecules instead of PAMPs, and it
is different from PAMPs, where effectors act as indicators of potential
pathogens.
Virulence factors from the pathogens are secreted into the plants and act as
effector molecules .
R proteins in the plants will identify the effectors to activate ETI .
An example of the effector–R gene model in plant pathogen interaction can
be seen in the interaction between coiled-coil, nucleotide binding site and
leucine rich repeats (CC-NBS-LRR) of the Pi-ta receptor in rice and with the
AvrPita effector of Magnaporthe grisea
The initiation of ETI results in the death of cells in the infected area and thus
prevents infection from spreading to other parts of the plant, causing
hypersensitive response (HR) , which results in programmed cell death
(PCD)
When the plant survives the infection in one site, it often develops increased
resistance to subsequent attacks throughout the plant and enjoys protection
against a wide range of pathogenic species.
This phenomenon is known as systemic acquired resistance (SAR)
It is transmitted through the phloem to other parts of the plant via signal
molecules, resulting in increased resistance throughout the plant
Examples of signaling molecules that are induced by pathogenic infection
include SA, methyl salicylate, jasmonate (JA), and ethylene (ET)
EX : Fu et al. (2012) state that when SA is elevated at the area of infection, it
will bind to the low-affinity binding receptor NPR3 (Non expressor of PR
Genes 3) and cause the degeneration of cell-death suppressor NPR1, which
subsequently results in HR
Elicitors may be categorized in two classe A: General (or non-specific) elicitors
do not significantly differ in their effect on different cultivars within a plant
species and are involved in primary innate immunity. They include chemicals,
Microbes-Associated Molecular Patterns (MAMPs) from non-pathogenic
microorganisms, Damage-Associated Molecular Patterns (DAMPs) from plant
surfaces resulting from the action of the invading agent and Pathogen-
Associated Molecular Patterns (PAMPs) from pathogenic microorganisms.
Specific elicitors (or effectors) are formed by specialized pathogens and
function only in plant cultivars carrying the corresponding disease resistance
gene. Effectors typically lead to the secondary innate immunity after an
intracellular receptor-mediated perception
MODELS OF INTERACTION BETWEEN EFFECTOR AND R GENES
IN PLANT IMMUNITY
DIRECT INTERACTION
ELICITOR RECEPTOR MODEL
The elicitor-receptor model states that elicitor protein encoded by avirulence
gene (Avr) of a plant pathogen interacts with the receptor molecule encoded
 by the complementary resistance (R) gene of the host plant (Agrios 1969;
Vander Biezen and Jones 1998).
Elicitors encoded by Avr genes can be general and race-specific elicitors.
The general elicitors induce defense both in the host and nonhost plants
whereas the race specific elicitors are able to trigger defense response only in
specific host cultivars which lead to disease resistance in them

Direct interactions between host resistance (R)/susceptibility (r) alleles and

pathogen avirulence (A)/virulence (a) alleles
EX : The Pto gene in tomato confers resistance against races of Pseudomonas
syringae pv. tomato that carries the avirulence gene avrPto (Martin et al. 1993)
INDIRECT INTERACTION OF R–AVR GENES
The guard model
The decoy model
Zig zag model
 Multi component model
GUARD MODEL
This model was given by Vander Biezen and Jones in the year 1998
This model suggests that the R proteins are present in association with a
protein known as the guardee.
When the effector/Avr gene product interferes with the guardee protein, it
activates resistance
Ex : The targeting of the RIN4 protein by the AvrRpm1 and Avrpt2 effectors,
which cleaves the RIN4 in Arabidopsis, leading to its recognition by the R
protein

DECOY PROTEIN MODEL

The “decoy protein” hypothesis is built on the concept that this decoy protein
is able to mimic the pathogen effector target and restrict infection but has no
direct role in immunity
A good example for this model would be the decoying method of
extracellular Protein-6 (Ecp6) produced by Cladosporium fulvum while
infecting tomato that mimics the chitin-binding capacity of the receptor to
supress chitin recognition by the host .
ZIG ZAG MODEL

The zigzag model describes four phases:

Phase 1 (PAMPs detected by PRRs)
Phase 2 (Pathogens deliver effectors to interfere with PTI)
Phase 3 (Effectors recognized by NB-LRRs, ETI)
Phase 4 (Loss/gain of effectors over evolutionary time).
MULTI COMPONENT MODEL

The model schematically shows the key points of activation and modulation
of plant immunity.
Plant resistance mechanism of an incompatible interaction might be divided
into three phases:
(1) Interaction
(2) Activation/modulation
(3) Effective resistance (immunity)
During the interaction stage, two principal effects are detected
(A) modifications of virulence factor targets and
(B) specific alterations of primary plant metabolism.
In the activation stage: The modifications of virulence factor targets induce
the Nibblers Triggered Signaling (NTS) or PPRs Triggered Signaling (PTS),
mediated by R-genes activation.
These metabolic alterations induce a feedback regulation of primary
metabolic pathways resulting in a Hormone Tempered Resistance (HTR).
 In the effective resistance stage, the NTS/PTS, and the HTR converge to
confer a resistance specific to the lifestyle of pathogen (Pathogen lifestyle-
Specific Resistance, PSR)
THE PLANT DEFENSE RESPONSE: THE PLAYERS AND PATHWAYS
INVOLVED

Pathogen-associated molecular patterns (PAMP)-triggered immunity (PTI)

and effector-triggered immunity (ETI) for different types of molecular
patterns produced by pathogenic and non-pathogenic microorganisms and
insects (microbe-associated molecular patterns (MAMPs), damage-
associated molecular patterns (DAMPs), and herbivore-associated molecular
patterns (HAMPs).
The well-established elicitor–receptor model for pathogenic fungus and
bacteria, insects and non-pathogenic microbes are chitin elicitor binding
protein/chitin elicitor receptor kinase (CEBIP/CERK), chitin, FLAGELLIN
SENSITIVE2/BRI1-associated kinase (FLS2/BAK1), flg22, PEP receptor
1/2 (PEPR1/2), peptides (Pep), Lysin motif protein ½ (LYM1/LYM2), LPS,
and hydrophobin-like elicitor (SM1)
REFERENCES :
Andolfo, Giuseppe & Ercolano, Maria. (2015). Plant Innate Immunity
Multicomponent Model. Frontiers in Plant Science.
Guillaume Henry, Philippe Thonart & Marc Ongena, «PAMPs, MAMPs,
DAMPs and others: an update on the diversity of plant immunity
elicitors», BASE [En ligne], volume 16 (2012), numéro 2, 257-268
Hoorn, Renier & Kamoun, Sophien. (2008). From Guard to Decoy: A New
Model for Perception of Plant Pathogen Effectors. The Plant cell. 20.
2009-17.
Lauge, Richard & De Wit, Pierre. (1998). Fungal Avirulence Genes:
Structure and Possible Functions. Fungal genetics and biology : FG &
B. 24. 285-97.
Lin, Min & Lillemo, Morten. (2021). Advances in genetic mapping of
Septoria nodorum blotch resistance in wheat and applications in
resistance breeding.
Malik, Abdul & Kumar, & Nadarajah, Kalaivani. (2020). Elicitor and
Receptor Molecules: Orchestrators of Plant Defense and Immunity.
International Journal of Molecular Sciences. 21. 963.
Zvereva, Anna & Pooggin, Mikhail. (2012). Silencing and Innate Immunity
in Plant Defense Against Viral and Non-Viral Pathogens. Viruses. 4.
2578-97.