Non-host resistance is a broad-spectrum plant defense that provides immunity to all members of a plant species against all isolates of a microorganism that is pathogenic to other plant species.

1. Presented by-
Akanksha Shukla
Ph.D. 1st year
Dept. of Plant Pathology

3. NON-HOST RESISTANCE
Plant Innate Immunity/ Species Resistance/ Durable resistance/ Basal defense/ Non-specific
resistance
• A broad-spectrum plant defense that provides immunity to all members of a plant species against
all isolates of a microorganism that is pathogenic to other plant species is called Non-host
resistance (NHR), a term that was introduced by Michele Heath to scientific literature in the late
1970s.
• The intrinsic property to resist pathogen virulence displayed by organisms without triggering
canonical resistance (R) genes has been termed nonhost resistance (NHR).
• Potentially phytopathogenic micro-organisms incapable of infecting any cultivar of a given plant
species are referred to as heterologous pathogens or non-host pathogen, while plants that are
resistant to all isolates of a given pathogen species are called non-host plants.
• NHR results in reduced penetration or proliferation of a potential pathogen in a non-host plant.
• Unlike R-gene mediated resistance, which is often genetically controlled by a single gene, most
non-host resistance is expected to be governed by a broad range of protective mechanisms that are
regulated by multiple genes and an interplay of both constitutive barriers and inducible reactions.

4. • Non-host resistance is often multi-tiered, with several obstacles depending upon a particular host to stop the
colonization by a potential pathogen. Plants have a multitude of antimicrobial features, both constitutive and
inducible, that could potentially confer disease resistance. These obstacles include, but are not limited to, the
presence/absence of signals from plants, such as surface topology features that are required to initiate pathogen
growth; preformed physical barriers such as wax layers, rigid cell wall and cuticle, preformed chemical barriers
like phytoanticipins, etc. that initially stop establishment of infection structures.; and induced defense
responses such as lignin accumulation, production of antimicrobials like phytoalexins, HR response, induction
of pathogenesis-related (PR) proteins.
• Although there are common themes of defense among all plants, there are also differences between species,
and sometimes between genotypes within species, in the structure, biochemical nature, and the eliciting
features of these defenses.

5. MECHANISMS UNDERLYING NON-HOST RESISTANCE
• Host resistance and non-host resistance are most commonly differentiated based on pathogen adaptation to a
particular species (host) and lack of adaptation to other species (non-host).
• Among several components of the plant immune response, basal defense is the first line of defense and is
initiated during the early phases of pathogen detection.
Pathogen recognition by non-host plants
• Recognition of non-self is the key to the activation of innate defense mechanisms in plants in response to
microbial attacks.
• Plants resist pathogen invasion by deploying various defense responses that are activated by two main
branches of their immune system.
• The first branch consists of transmembrane Pattern recognition receptors (PRRs) that activate basal defense
responses by recognizing extracellular Pathogen associated molecular patterns (PAMPs) common to many
classes of microbes. A successful pathogen defeats this first line of defense with effectors that enhance their
virulence.
• Pathogen effectors (virulence factors) are specifically recognized by corresponding resistance (R) genes in the
second branch of the plant immune system.

6. PAMPs triggered receptor-mediated defense responses
• When a potential pathogen overcomes the constitutive defense layers of a non-host plant, it is recognized at the PM of plant
cells.
• Pathogen recognition in non-host plants is brought about by PAMPs, also known as general or exogenous elicitors.
zig-zag model proposed by Jones and Dangl (2006).
• Recognition of PAMPs by cognate PRRs in non-host induces
multiple defense responses referred to as PAMP-triggered
immunity (PTI) leading to basal resistance or NHR in plants.
• PAMP perception triggers activation of signaling cascade and
transcriptional changes. Early events in the cascade involve
ion fluxes, protein phosphorylation, enhanced cytosolic Ca2+
concentrations, Ca2+-dependent protein kinases, mitogen-
activated protein kinase (MAPK), extracellular adenosine
triphosphate (eATP) and reactive oxygen species (ROS)
accumulation.
At the molecular level, depending upon the genetic distance
from the host species, host resistance is predominantly regulated
by ETI, whereas nonhost resistance is regulated by
PTI and/or ETI. So, There are also some overlaps between basal
defense and nonhost resistance because it is possible that both
host and nonhost plants may recognize similar factors to initiate a
defense response.

7. TYPES OF NHR
Plants have evolved to defend themselves against most phytopathogens by recognizing them and
triggering an array of defense responses. An incompatible interaction of a pathogen and a non-host
plant often induces several different defense signaling cascades, including generation of active oxygen
species, programmed cell death or HR in infected cells, and induction of PR genes. HR is commonly
used as a visual marker for incompatible plant–pathogen interactions.
Non-host resistance against bacteria, fungi and oomycetes be classified into two types:
TYPE I
Does not produce any visible symptoms (necrosis)
The pathogen does not get past the first or the second
obstacle, and the multiplication and penetration into the
plant cell will be completely arrested.
Plants recognize general elicitors from pathogens in a
nonspecific manner to activate defense responses.
TYPE II
Always associated with rapid localized necrosis (HR).
Pathogen may conquer early obstacles by producing
detoxifying enzymes to overcome the preformed
constitutive barriers.
Plants have evolved to recognize specific pathogen
elicitors, either in the plant cytoplasm or at the plant cell
membrane, which trigger a defense mechanism that will
often lead to HR.

8. (b) During type II non-host resistance the non-host
pathogen is able to overcome preformed and general
elicitor-induced plant defense responses, probably by
producing detoxifying enzymes. Specific pathogen
elicitors are then recognized by the plant surveillance
system and this triggers plant defense leading to a
hypersensitive response (HR). PR gene expression and
SAR are also induced during type II nonhost resistance.
A model for type I and type II non-host resistance
(a) During type I non-host resistance the non-host pathogen
is not able to overcome the preformed barriers and general
elicitor-induced plant defense responses such as cell wall
thickening, phytoalexin accumulation, other plant secondary
metabolites and papilla formation. Pathogenesis-related (PR)
gene expression as a component of systemic acquired
resistance (SAR) can be induced by general elicitors of the
non-host pathogen.
Fungal/ oomycete
non-host pathogen
Bacterial non-host
pathogen
NP
NP
Mysore et al., 2004

9. Plant cells possess a variety of membrane receptors that perceive exogenous signals (e.g. PAMP, represented as stars), which can be either peptides
or oligosaccharides. A given ligand activates a specific receptor that initiates downstream signaling events. Penetration of a non-host pathogen is
restricted at the cell wall by callose deposits, cytoskeleton reorganization and polarization of secretory components. Actin microfilaments (horizontal
lines below the PM) become focused at the penetration site. A PEN1-mediated and vesicle-based secretion system delivers cargo molecules to the
penetration site. PEN3- encoded ABC transporters deposit antimicrobial compounds at the pathogen invasion site, synthesized in peroxisomes in a
PEN2-mediated pathway. Defense gene expression is induced by general elicitors of the non-host pathogen leading to type I non-host resistance
without any associated cell death.
Mysore et al., 2013

10. The non-host pathogen is able to overcome preformed and general elicitor induced plant defense responses, probably by producing detoxifying
enzymes. Specific pathogen elicitors are then recognized by the plant’s surveillance system, and this triggers plant defense reactions leading to cell
death. H2O2 produced during electron transport in chloroplasts has been shown to be involved in the restriction of haustoria. Cell death regulators like
BI-1 (Bax inhibitor 1), caspases and NbCD1 also play a role in triggering cell death during type II non-host resistance
Mysore et al., 2013

11. Pathogen Strain Non-host plant(s) Visible
symptoms
Type I non-host resistance
Pseudomonas syringae pv. phaseolicola NPS3121 Arabidopsis None
Xanthomas campestris pv. campestris 8004 Nicotiana benthamiana None
Gaeumannomyces graminis var. tritici T5 Avena strigosa None
Puccinia graminis f. sp.tritici ANZ Oat None
P. infestans 88069 N. clevelandii None
Type II non host resistance
X. campestris pv. glycines 8ra Pepper, tomato HR
Alternaria brassicicola MUCL20297 Arabidopsis HR
Blumeria graminis f. sp. tritici bgtA95 Barley HR
Fusarium solani f. sp. phaseoli W-8 Pea HR
X. citri 3213 Cotton, bean HR

12. • The type of non-host resistance triggered in a non-host plant is dependent on both the plant species
and the pathogen species, such that a non-host plant species can show type I non-host resistance
against one pathogen species and type II resistance against another pathogen species.
• For example, N. benthamiana exhibits type I non-host resistance against Xanthomonas campestris
pv. campestris and type II non-host resistance against P. syringae pv. tomato.
• A single pathogen species can trigger both type I and type II non host resistances on different plant
species.
• For example, P. syringae pv. phaseolicola triggers type I non-host resistance in Arabidopsis and
type II non-host resistance in tobacco.

13. Components of non-host resistance
1. Preformed or passive defense mechanism
2. Inducible plant defense mechanisms
3. Plant defense signalling
4. Broad-spectrum disease resistance genes

14. • Preformed defense is the first obstacle a pathogen faces before invading the plant.
• They include both physical restriction and chemical inhibition of pathogens.
• Some structural defense are present in the plant even before the pathogen comes in contact with the
plant. Such structure include the amount and quality of wax and cuticle that cover the epidermal
cells, the structure of the epidermal cell walls, the size, location and shapes of stomata and
lenticels.
• The presence of tissues made of thick walled cells that hinder the advance of pathogen on the plant.
• A thick mat of hairs on a plant surface may also exert a similar water-repelling effect and may
reduce infection.
• The plant cytoskeleton provides a physical barrier against most invading plant pathogens.
• Plant actin microfilaments playing a role in defense against fungal penetration, and their disruption
leads to the loss of non-host resistance against several non-host fungi
1. Preformed or passive defense mechanism

15. • Plants constitutively produce a plethora of secondary compounds like phenolic compounds,
tannins, and some fatty acid-like compounds such as dienes during defense against
microorganisms.
• Phytoanticipins are major secondary metabolites present in their active form in plants before
pathogen infection. Fragarin, a phytoanticipin isolated from the cytosolic fraction of strawberry
(Fragaria ananassa) leaf tissues, inhibits the growth of many bacterial pathogens.
• Saponins are constitutively produced in many plants and can also be induced as a result of a
pathogen infection. The root infecting fungus Gaeumannomyces graminis var. tritici is a wheat
pathogen and is unable to infect oats; it produces the root-specific avenacins, a class of triterpene
saponin.
• In Brassicaceae, sulfur- and nitrogen-containing secondary metabolite compounds called
glucosinolates and their derivatives are known to play a role in plant defense against a wide range
of pathogens

16. 2. Inducible plant defense mechanisms
• The second obstacle an invading pathogen has to face is the inducible plant defense mechanisms.
• These defense responses arrest nonhost-pathogen growth by producing structural barriers, inducing de novo
biosynthesis of antimicrobial chemicals and/or proteins, and activating several defense pathways at the molecular
level.
• Cell wall reinforcement by callose, lignin, and suberin deposition is widely known to be induced after recognition
of nonhost pathogens.

17. • Apart from the induced physical barriers, several chemical compounds are synthesized de novo or
converted from nontoxic to toxic compounds and act as antimicrobial agents.
• Phytoalexins are low molecular weight antimicrobial compounds that are synthesized de novo in
response to pathogen attacks.
• Lettuce produces hydroxyproline-rich glycoproteins, phenolic compounds, and a phytoalexin
(lettucenin A) as defense against nonhost pathogens.
• Another phytoalexin, camalexin, which is known to disrupt bacterial membranes, is shown to
accumulate in Arabidopsis plants inoculated with the non-host pathogen P. syringae pv. syringae, a
causal agent of bacterial brown spot in beans.
• Organosulfur compounds, such as sulforaphane, are known to be synthesized in Arabidopsis and
released into the apoplast to arrest the growth of non-host P. syringae pathovars.

18. 3. Plant defense signalling
Several plant signaling components are involved during the induction of plant defense. During nonhost-pathogen
invasion, plants perceive nonhost-pathogen cues and activate several defense pathways at the molecular level.
Efficient signal perception and robustness of individual pathogen recognition events are characteristics of non-
host resistance. An invading pathogen has to bypass many of these signaling components to cause disease
successfully in plants.
• Classical defense-pathway-related genes, such as phytoalexin-deficient 4 (PAD4) and pathogenesis-related 1
(PR1), have also been shown to be highly induced in Arabidopsis upon nonhost-pathogen inoculation.
• Salicylic acid is one of the key signaling molecules that activate plant defense responses against invading
pathogens. For example, Arabidopsis is a non-host for cowpea rust fungus (Uromyces vignae) and hence
restricts the growth of this fungus. The Arabidopsis mutant sid2, defective in an enzyme that synthesizes
salicylic acid, and Arabidopsis NahG plants (which express salicylate hydroxylase that can degrade salicylic
acid) support growth of U. vignae indicating that the salicylic acid pathway is required for non-host resistance
against the rust fungus in Arabidopsis.

19. • Ethylene perception is often required for basal resistance against pathogens and it can also induce
disease resistance in plants. For example, Transgenic tobacco plants expressing the Arabidopsis etr1-1
gene (which causes loss of ethylene perception) were unable to support induction of basic PR genes
upon tobacco mosaic virus (TMV) infection.
• Heat-shock proteins (Hsps) are highly conserved proteins that are induced during various forms of
environmental stress. For example, silencing of Hsp70 and Hsp90, a cytosolic protein in N.
benthamiana individually compromise non-host resistance by allowing the multiplication and growth of
the non-host pathogen P. cichorii when compared to the wildtype N. benthamiana plants. Silenced
plants did not produce non-host HR after inoculation with P. cichorii or P. infestans INF1 elicitor.
• Wound-induced protein kinase (WIPK) and salicylic acid-induced protein kinase (SIPK) have been
previously implicated as signaling components of plant defense reactions. A recent report shows that
silencing of WIPK and SIPK in Nicotiana benthamiana compromises nonhost resistance against
Pseudomonas cichorii by allowing multiplication and growth of this non-host pathogen.

20. Complex sensory, signalling and executive mechanisms constitute the basis for plant non-host resistance to heterologous pathogens. Recognition of pathogen associated
molecular patterns (PAMPs) through specific receptors at the plant cell surface is thought to mediate activation of inducible defence responses in non-host plants. Mechanical
stimulation of plant defence may also occur during attempted microbial invasion (Gus-Mayer et al., 1998; Schmelzer, 2002). PAMP receptors initiates signalling cascades and,
subsequently, inducible defences. Homologous virulent pathogens employ effector proteins that may suppress activation of plant species resistance at various stages (red lines).
White boxes indicate the sensory and signalling elements implicated in the activation of inducible plant defence in non-host plants. Blue boxes indicate preformed barriers and
inducible responses that together constitute a multilayered defence arsenal of non-host plants to attempted microbial infection. sensory, signalling and executive mechanisms
may only be partially conserved in non-host plants, and may be differentially efficient in various plant–microbe interactions. Abbreviations: FLS2, flagellin sensing 2; MPK6,
mitogen-activated protein kinase 6; SGT1, suppressor of G2 allele of Skp1; HSP, heat shock protein; PAD3, phytoalexin deficient 3; NHO1, non-host resistance 1; PEN,
penetration.

21. 4. Broad-spectrum disease resistance genes
Gene/protein Function in non-host resistance (NHR) Reference
PAMPs involved in NHR
Pep-13 Induces defense responses in non-host plants like potato Nurnberger et al. (1994)
Harpin (Hrp Z) Elicits HR-like cell death and defense responses in various plants
Avirulennce (avr) genes These genes from bacterial pathogens are recognized by previously unidentified
R-genes in non-host plants.
Kobayashi et al. (1989)
and Arnold et al., 2001
Genes involved in NHR
PEN1(PENETRATION
1)/ROR2
This gene is involved in timely deposition of papillae during non-host
interactions.
Collins et al. (2003)
PEN2 Encodes myrosinase involved in hydrolysis of indole glucosinolates to release
potential antimicrobial components at the site of non-host interaction.
Lipka et al. (2005) and
Bednarek et al. (2009)
PEN3/PDR8 May be involved in exporting toxic materials to the site of non-host pathogen
interaction and intracellular accumulation of toxins.
Stein et al. (2006)
ETR1-1 Ethylene insensitive (etr1-1) tobacco plants lost resistance against many non-host
pathogens; but N-gene-mediated gene-for-gene resistance against TMV was not
compromised.
Knoester et al. (1998)
NHO1 Required for NHR of Arabidopsis against Pseudomonas syringae pv.
phaseolicola.)
Kang et al. (2003)

22. R-gene mediated genes involved in NHR
EDS1 This gene is necessary for R-gene-mediated resistance to many pathogens in
Arabidopsis and also involved in execution of NHR against isolates of
Peronospora parasitica and Albugo candida.
Parker et al. (1996)
SGT1 Silencing of SGT1 in N. benthamiana compromises NHR against P. syringae
pv. maculicola and Xanthomonas axonopodis pv. vesicatoria
Peart et al. (2002)
Heat-shock proteins
(Hsps)
Silencing of Hsp90 and Hsp70 in N. benthamiana individually compromised
NHR against P. cichorii.
Kanzaki et al. (2003)
WIPK and SIPK In N. benthamiana virus-induced gene silencing of NbSIPK and NbWIPK
allowed multiplication of non-host bacterium P. cichorii.
Sharma et al. (2003)
PAD4/SAG101 Pad4 and sag101 single mutation have little effect on the frequency of Bgh
haustoria formation in Arabidopsis. But along with pen mutation (pen2
sag101pad4) NHR was compromised.
Lipka et al. (2005) and
Stein et al. (2006)

23. Relative contribution of defense components to non-host resistance (NHR) may vary depending on the pathogen species. Various pathogens cease to
grow in non-host plants due to maldifferentiation of infection structures during preinvasion. In addition, nonhost pattern-recognition receptors (PRRs)
trigger defense response via pathogen-associated molecular pattern (PAMP) recognition, which terminates pathogen infection. Conversely, non-
adapted pathogens could have not evolved effectors to modulate defense response or non-host plants could not have effector targets utilized as host
factors. Effector-triggered immunity is also a major component of NHR and several evidences support multiple resistance (R) protein–effector
interactions. Although NHR largely shares defense signaling components with host resistance, chemical barriers such as phytoalexin have evolved in a
speciesspecific manner and play a pivotal role as determinants of host range.
Mode of action in plant nonhost resistance
Lee et al., (2007)

24. Different layers of non-host resistance of plants against bacterial
pathogens. Upon landing on the plant surface, potential bacterial
host pathogens enter into the mesophyll apoplast via stomatal or
wound openings. After gaining access to the apoplastic fluid, a
successful pathogen manipulates plant cells to release more
nutrients so that it can multiply and eventually cause disease.
However, because of the existence of nonhost resistance, not all
pathogens can complete the above-described steps. The first
layer of plant defense on the leaf surface and in the apoplast
involves the presence of preformed or induced structural
barriers, such as wax, and defense by chemical molecules, such
as antibacterial compounds. Inducible defense responses occur
first due to pathogen-associated molecular pattern (PAMP)
perception, and, in the advanced stages, by recognition of
bacterial effector molecules. The direct interaction between
pathogen and plant cell usually initiates either the hypersensitive
response (HR) or other defense pathways, leading to an arrest of
pathogen growth. Some of the recently identified genes
contributing to nonhost resistance are shown.
Cyp710A1, cytochrome p450 family 710 subfamily A
polypeptide 1; EDS1, enhanced disease susceptible 1; GOX,
glycolate oxidase; MAPK, mitogen-activated protein kinase;
NHO1, nonhost 1; OAT, ornithine-δ-aminotransferase; ProDH,
proline dehydrogenase; ROS, reactive oxygen species; RPL,
ribosomal protein L; SGT1, suppressor of G2 allele of SKP1;
SQS, squalene synthase.
Senthil-Kumar, M., & Mysore, K. S. (2013)

25. Schematic Representation of Arabidopsis Non-host Resistance to Bgh
After germination of spores (Sp), formation of appressoria (Ap), and breaching of the host cell wall (CW) by the fungal penetration peg (Pp), ;90% of penetrations
are stopped in cell wall extensions called papillae (Pa). This resistance is dependent on unidentified cargo molecules (green circles) delivered by a PEN1-mediated
vesicle (Ves)–based secretion system and on postulated toxin(s) (dark blue circles) synthesized in peroxisomes (Per) in a PEN2-mediated pathway and delivered by a
PEN3-encoded ABC transporter in the plasma membrane (PM) to the apoplast and pathogen invasion site. These events are components of pre-haustorial resistance.
The activation of the dynamic pre-haustorial resistance, dependent on cytoskeleton function, may be induced by mechanical or chemical signals resulting from cell
wall penetration and/ or PAMPs (yellow circles) produced by the pathogen and detected by host PAMP receptors (PAMP-R). Approximately 10% of infections
(increased to ;30 to 90% in pen1, pen2, and pen3 single and double mutants) form haustoria (H) and are stopped (post-haustorial resistance) by basal resistance
possibly contributed to by PEN2 pathway products (dark blue circles) and hypersensitive host cell death (HR) dependent on EDS1, SAG101, and PAD4. Because
these genes and the HR are also associated with gene-for-gene R genes, it is possible that R proteins could also function to perceive effector molecules (light blue
circles) secreted by Bgh haustoria.
Ellis, J. (2006).

26. The term NHR was first coined to describe the resistance displayed by some plants against rust
fungus during the pre-invasive stage of infection before the fungal feeding structure, the haustoria, is
formed.
We can generally describe NHR in two steps:
NHR
Pre-invasive resistance
Pre-invasive NHR can be either passive or active and usually
occurs without detection of the pathogen or the activation of
plant immune response but rather from physical or chemical
barriers already present in the plant leading to an incompatible
interaction. In some instances, pre-invasive NHR also involves
active defense response wherein a barrier is formed (eg.,
stomatal closure) in response to pathogen attack.
Post-invasive resistance
In post-invasive NHR, infection is
followed by symptom development
such as HR/cell death, production of
ROS, and induction of post-invasive
plant defense genes to further limit the
penetration and growth of nonhost
pathogens.

27. In pre-invasive NHR, pathogen fails to penetrate apoplast due to passive or active defenses such as physical or chemical barriers. Proteins involved
in pre-invasive NHR are shown (PEN1, PEN2, PEN3, GCN4, NOG1-2, CaM7 and BRT1). Post-invasive defenses consist of a second tier of NHR
that can halt pathogen progression even after colonization of the apoplast or some fungal hyphae penetration. Proteins involved in post-invasive NHR
responses by activation of HR responses such as cell death or ROS accumulation are shown (PAD4, ELO1, ELO2, SQS, NOG1-1, SAG101, ProDH,
PING4, PING5, RPL12, RPL19, GOX and SGR). Some proteins acting in both types of NHR defense are shown such as EDR1, EDS1, RNR8 and
PSS1. Proteins indicated in red color are negative regulators of NHR while proteins in black are positive regulators.
Schematic diagram showing pre- and post-invasive nonhost resistance in plants
Jose Pedro Fonseca, Kirankumar S. Mysore (2018)

28. Conditional NHR

29. Panstruga, R., & Moscou, M. J. (2020). Molecular Plant-Microbe Interactions, 33(11)

30. Evolutionary perspective of host and non-host resistance
• Non-host interactions between plants and pathogens are dynamic and greatly influenced by
evolution at molecular level depending upon the genetic distance from host species.
• Within host species the variation of resistance among cultivars is mainly defined by R genes that
continuously evolve due to gene duplication or deletion, recombination, mutation and selection
pressure for resistance against pathogen on the other hand pathogens also evolve their effector
proteins to maintain virulence on host species.
• One of the evolutionary explanations for NHR is that pathogens become so specialized to cause
virulence on specific hosts that they fail to infect phylogenetically distant species from the host.
• The greater the phylogenetic distance between nonhost and host plants, the higher will be the
number of mechanisms that could block pathogen infection. This is because there is a correlation
between genetic distance and genetic variability
• An example is the spread of the fast-evolving, virulent race Ug99 (also known as TTKSK) of the
fungus Puccinia graminis f. sp. tritici, the causal agent of wheat stem rust disease. Ug99 has
evolved to be virulent against the resistance gene Sr31 from rye (Secale cereale) and many other R
genes from wheat such as Sr38 introduced into wheat from Triticum ventricosum.

31. Gill et al., 2015
susceptibility
partial resistance or susceptibility
Resistance
A) Host variability for-
Gradient of Durability of
nonhost resistance w.r.t
genetic resistance
More durable
Less durable
B)
A) Host resistance is primarily controlled bye R- Avr
recognition. A micro evolution creates diversity within
host species for resistance or susceptibility and also
within pathogen to develop new races with diverse
Effector.
B) Outcomes of non host interactions vary with genetic
distance from host species and the pathogens ability to
evolve. A rapidly evolving pathogen due to Co-
speciation, host shift and host jump has better capability
to adapt to new non host species by breaking the non host
barriers. The contribution of PAMP Triggered immunity,
effector triggered immunity also increases and decreases
respectively with the increase in genetic distance from
host to non-host.

32. Factors that determine the adaptation of pathogens to a new plant species
1. Co-speciation happens when both host and pathogen undergo speciation simultaneously to maintain their
interactions.
2. Host shift happens when pathogens usually shift from their natural host to related non host species. For
example Blumeria graminis that causes powdery mildew disease on barley underwent hosts shift from barley
to the related non host species like wheat. Similarly, the rice blast pathogen Magnaporthe Oryzae Also
shifted host to cause wheat blast in mid 1980s.
3. Host jump involves adaptation of pathogen to a distantly related plant species from their source host or
sometimes even across kingdom. For example, many plant bacterial and fungal pathogens such as
Pseudomonas aeruginosa, Agrobacterium radiobacter, Alternaria spp. and fusarium spp. have a wide plant
host range but are also capable of infecting mammalian host indicating a cross Kingdom jump in the past. A
very good example of host jump is related to Phytophthora infestans that was responsible for famous 19th
century Irish potato famine. Phytophthora infestans that infect several solanum species evolved through host
jump from Phytophthora mirabilis that infect the 4:00 o'clock plant Mirabilis jalapa.

33. Effector and NB-LRR gene evolution during co-speciation and
host jumps.
The evolution of host NB-LRR (colored squares) and pathogen
effector gene (colored circles) repertoires following co-speciation
or host jumps.
In the last common ancestor (A) of two plant species, (B) and (C),
few pathogen effectors match cognate NB-LRR proteins, leading
to pathogen strain- and host accession-dependent immunity or
pathogen colonization.
Shortly after speciation of plants (B) and (C) the last common
pathogen species is still able to colonize both plant species.
Following a period of co-evolution of both new host–parasite pairs,
new complementary NB-LRR gene-effector gene pairs appear.
The emergence of (B) or (C) specific NB-LRR proteins
recognizing conserved effectors and/or the deletion of conserved
effectors drives the pathogen into reproductive isolation by
preventing further cross-infection.
Pathogens can also colonize new phylogenetically distant plant
habitats (D) by ‘host jumps’.
Upon a period of co-evolution, new complementary NBLRR gene-
effector gene pairs emerge also in this scenario.

34. • The plant immune responses can be broadly grouped in two major layers:
• NB-LRR and PRR-triggered immunity contribute to nonhost resistance such that with increasing phylogenetic
divergence time between two plant species the relative effectiveness of PRR-triggered immunity increases
whereas the relative contribution of NB-LRR protein-triggered immunity decreases.
• One mechanistic explanation for this could be that effectors from a given pathogen species fail to effectively
suppress PRR-triggered immunity in nonhosts because their corresponding host cellular targets have diverged
in the nonhost to an extent that impedes effective manipulation by the effector repertoire. Additionally, the
continuous co-evolutionary arms race between host-adapted pathogens and their hosts appears to drive a more
rapid evolution of NB-LRR loci compared to the rest of plant genomes. Thus, the selective advantage of
maintaining a given NB-LRR recognition specificity following evolutionary radiation of plants is expected to
diminish with increasing divergence time between two plant species A and B on the assumption that the
effector gene complement of a pathogen species evolves rapidly
Those triggered by pathogen/microbe-associated
molecular patterns that are conserved between
species of a microbial group (PAMP/ MAMP-
triggered immunity, or PTI/MTI)
PTI/MTI is based on PRRs that serve as receptors
for PAMPs/MAMPs
Those triggered by isolate-specific
pathogen effectors (effector-triggered
immunity, or ETI).
ETI invokes intracellular NB-LRR
proteins that detect either the actions or
structures of pathogen effectors

35. The model is based on two assumptions:
(i) the proportion of pathogen effectors that fail
to ‘find’ corresponding targets raises with
increasing divergence time between host and
non-host, and
(ii) the co-evolutionary arms race in host-
adapted interactions and concomitant changes in
NB-LRR and effector repertoires ‘depletes’ the
capacity of phylogenetically distant nonhosts to
recognize effectors of host-adapted pathogens.
A model of Relative contribution of NB-LRR- and PRR-triggered immunity to nonhost resistance
The relative contribution of NB-LRR triggered immunity (blue) and PRR-triggered (red) immunity to nonhost
resistance against a given pathogen as a function of the evolutionary distance of the authentic host plant species of
that pathogen to an assumed nonhost species

36. NHR outcomes of a hypothetical pathogen on a range of plant taxa.
Pathogen infection scenarios are as follows;
1) Spore germination on a plant phylogenetically very distant to the host
plant. An absence of appropriate plant signals prevents the development
of appropriate pathogen infection structures on the leaf surface (green
line).
2) Appropriate pathogen infection structures are produced post-spore
germination but the attempted infection is unable to overcome epidermal
penetration resistance (orange star) and invade the leaf.
3) An infection site has breached the plant epidermis but is restricted by
additional post penetration NHR mechanisms without hypersensitive
cell
death due to the pathogen’s inability to effectively suppress PTI.
4) An effector (magenta circle) is recognised by the nonhost plant
leading to ETI and hypersensitive cell death (red stars).
5) Significant non- adapted pathogen growth occurs but the pathogen is
incapable of reproduction.
6) Successful infection and reproduction on a fully susceptible host
plant.
7) Resistance to pathogen infection by ETI on a host plant species
containing an appropriate NLR gene.
Increasing compatibility between effectors and plant targets results in
increased pathogen growth, unless an effector is recognised by the plant
(ETI).

38. Quantitavive analysis of NHR to M. oryzae in Arabidopsis mutants
Mean frequency of M. oryzae penetration into A. thaliana
mutants @ 48hpi (Expressed as a total no. of infection sites.) Mean length of infection hyphae measured @48hpi

39. Quantitavive analysis of post penetration resistance to M.
oryzae in Arabidopsis mutants
Microscopic views of infection sites in Arabidopsis mutants
Fluorescence microscopic
view @ 48hpi
Light microscopic
view @ 48hpi
pen2
Pen2 mpk6
In conclusion, MPK6 was involved in penetration and post penetration resistance as a positive regulator to M. oryzae in Arabidopsis
i. Successful penetration without infection hyphae
ii. Successful penetration with short infection hyphae
iii. Successful penetration with long infection hyphae
iv. Successful penetration with branched infection
hyphae

40. Effect of the Xoo inoculum concentration on
HR induction. Xoo at 1×106 , 1×107 and 1×108
cfu mL−1 concentrations was inoculated in
fully expanded N. benthamiana leaves.
Optimization of the Xoo inoculum concentration
for HR induction in N. benthamiana

41. Effect of exogenous H2O2 on Xoo-induced HR.
Leaves were infiltrated first with Xoo and then with
0.1 M H2O2 twice, at 9 and 11 hpi
DAB staining for
H2O2 detection
Effect of exogenous catalase treatment on
Δhpa1-induced HR.
H2O2 H2O2
An exogenous H2O2 supply leads to an earlier and
stronger Xoo-induced HR in N. benthamiana
Elimination of H2O2 by catalase compromises Xoo-
induced HR

42. Conclusion
NHR is a widespread phenomenon resulting from long term co-evolution
between plants and their numerous biotic associates.
The NHR defense responses are predominantly triggered by perception of
pathogen derived MAMPs or effectors, but recognition independent processes
also function to limit non-adapted pathogens.
The genetic and molecular basis of pathogen resistance displayed at the species
level overlaps with that mediating basal resistance to host-adapted pathogens.