Mechanism of Host and Non Host Resistance found in plants. Application of Specific and Non-Specific Resistance for crop improvement in agriculture.

1. :A Brief Insight
Host-Resistance
Versus
Non-Host Resistance in Plants
Submitted To:
Dr.Anirudh Kumar
Assistant Professor,
Department Of Botany,
Faculty Of Science,
Indira Gandhi National Tribal University
Submitted By:
Garaneshwar Shiv Durai
Enroll. No. 2017000248
MSc.Botany-1st Semester
Department Of Botany
Indira Gandhi National Tribal University

2. Introduction
• Plants face several challenges by both biotic and abiotic components of environment during their life
time. Generally plants have certain physical adapations to counter the affect of external abiotic
stresses.
• Similarly, plants possess a dynamic, innate, natural immune system that efficiently detects potential
pathogens and initiates a resistance response in the form of basal resistance and/or resistance (R)-
gene-mediated defense, which is often associated with a hypersensitive response.
Depending upon the nature of plant–pathogen interactions, plants generally have two main resistance
mechanisms;
(•) Host Resistance : It is generally controlled by single R genes and is less durable ,when compared
with non-host resistance.
(•) Non-Host Resistance : It is believed to be a multi-gene trait & is more durable than the host
resistance.
In the succeeding slides, the mechanisms of host and non-host resistance against fungal and bacterial
plant pathogens will be discussed and a comparative analysis will also be drawn ,to decipher their

3. Host Resistance
It is governed by a single gene or a small number of related genes, which encode proteins capable of altering the outcome of
an otherwise compatible plant-pathogen interaction.
Such genes, conditioning host-pathogen specificity, are found in particular sub-populations of the pathogen, plant host or
both the interacting organisms.
On that basis, host resistance can be further sub-divided into 3 major categories :-
(a) Race-Specific Resistance:
It is induced in response to only a particular race of pathogen, but occurs in all cultivars of the host plant. This type of specific
disease resistance is dependent upon genetic variation within the pathogen species, and the production of proteins, capable of
altering the outcome of an otherwise compatible plant-pathogen interaction in only certain pathogen races.
(b) Cultivar–Specific Resistance:
It is activated only in a specific host plant cultivar, but in reaction to all races of a pathogen species. It is also called as species-
specific resistance in a few plant-pathogen systems where non-specific resistance limits the host range of the pathogen to a
plant genus; this type of resistance thus occurs at the level of the host plant species.
It relies upon genetic variation within the host plant species or genus, and the production of proteins capable of altering the
outcome of an otherwise compatible plant-pathogen interaction in only certain plant cultivars or species.

4. (c) Race-cultivar-specific (gene-for-gene) resistance :
Race-cultivar-specific resistance, when both pathogen and host specificity are involved since it results only from the interaction of a particular pathogen race with a particular cultivar of the
host plant. This type of resistance is also referred to as gene-for-gene resistance, because in most cases it requires the presence of both a race-specific avirulence (avr) gene in the
pathogen and one or more corresponding cultivar-specific resistance (R) genes in the host plant (Figure 1).
Avirulence and resistance genes are usually dominant genes, which may exist within multigene families, and undergo a high rate of mutation in response to the presence of each other.
Maintenance of detrimental avirulence genes is thought to be due to a small, additive, pleiotropic pathogenicity role in the pathogen. In a small number of cases of race-cultivar-specific
resistance that involve the production of host-selective toxins, Race-cultivar-specific resistance relies upon the absence of either a race-specific gene conditioning toxin production and a
cultivar-specific gene governing toxin sensitivity (Figure 2).
Figure1: Figure 2: Interactions involving
Gene-for-gene interactions toxin-production genes and toxin- sensitivity
specify race-cultivar-specific genes specify race-cultivar-specific
plant disease resistance disease resistance due to host-selective toxins
Resistance is only induced when a plant cultivar in possession of a specific resistance Disease only occurs in interactions involving a pathogen race in possession of
(R) gene recognises a pathogen race that contains the corresponding avirulence ( avr) gene (a). a toxin-production (TP) gene and a plant cultivar that contains the corresponding toxin-sensitivity ( TS) gene (a).
The absense of either the avirulence gene (b), the resistance gene (c) or both (d) The absence of either the toxin-production gene (b), the toxin-sensitivity gene (c) or both (d), result in plant disease
from the interacting organisms leads to lack of recognition by the host plant and the onset of disease resistance.
Both types of race-cultivar-specific resistance are dependent upon genetic variation within both the
pathogen and host species, and the production of proteins by only particular pathogen races and host cultivars,
that are capable of acting in combination to alter the outcome of a plant-pathogen interaction. An otherwise
compatible interaction results in resistance due to the presence of both avirulence and resistance genes,
whereas genes conditioning toxin production and toxin sensitivity cause disease in an otherwise incompatible
interaction.

5. MECHANİSMS UNDERLYİNG HOST RESİSTANCE
IN PLANTS
q The biochemical mechanisms responsible for the induction of
specific resistance in plant-pathogen interactions are generally
poorly understood, but are likely to vary with both the type of
specific resistance and the plant-pathogen system involved.
q The three most common mechanisms underlying specific
resistance appear to be;
I. Race-specific elicitors,
II. Host-selective toxins,
III. Race-specific suppressors,
but others, as yet unknown, may also exist.

6. (a) Race-specific elicitors
The majority of cases of race-specific resistance appears to be resulted from the generation by a
pathogen of race-specific elicitors of active plant defences, and the recognition of these by the plant
host. Resistance with this biochemical basis is often also cultivar-specific (and thus gene-for-gene),
since the elicitor interacts with a corresponding plant receptor that is usually unique to a particular
cultivar of the host plant. The recognition of the elicitor by its receptor is proposed to occur at the
plant plasma membrane for most fungal pathogens, and within the plant cell for bacterial and viral
pathogens. In bacterial biotrophs such as Xanthomonas and Pseudomonas, which are extracellular
plant pathogens, this event is dependent upon a bacterial membrane transport protein that delivers the
elicitor into the plant cell, and is encoded by the hrp-gene complex. Interaction of the elicitor and
receptor activates a complex signal transduction pathway resulting in the induction of plant defences
against pathogen races harbouring the elicitor. The elicitor is generally the protein that is encoded by
the avirulence gene, however in some plant-pathogen interactions the elicitor has been found to be the
product of a reaction catalysed by this protein. Resistance genes in some cases directly encode cultivar
-specific receptors of race-specific elicitors, and in these cases a direct physical interaction between
avirulence and resistance gene products may occur. However resistance proteins are more likely to
function by registering interactions between the elicitor and an unknown target protein, or act as
unique links in the signalling pathway leading to active plant defences.

7. (b) Host-selective toxins
Race-cultivar-specific pathogen resistance can also occur due to the
production of compounds that are toxic to plants. These host-selective
toxins (HSTs) are generated in a race-specific manner, mainly by
necrotrophic species of the fungal genera Alternaria and Cochliobolus. A
few of the approximately twenty known host-selective toxins are
proteins or peptides that are directly encoded by race-specific pathogen
genes. However, most are non-protein compounds of low molecular
weight that are synthesised in reactions catalysed by proteinaceous race
-specific gene products. Following transport into the host plant cell via
a highly coordinated delivery system, host-selective toxins cause
cellular damage, but only in toxin-sensitive cultivars that harbour a
single gene conditioning toxin sensitivity. The mode of action of host-
selective toxins is highly variable, but appears to always involve either
activation or inhibition of a cultivar-specific protein. For example, T-
toxin, produced by C. heterostrophus, serves to activate a cultivar-
specific protein capable of forming destructive membrane pores,
whereas HC-toxin from C. carbonum inhibits a cultivar-specific version
of an enzyme that modifies DNA-bound proteins to cause disturbances
in gene expression.

8. (c) Race-specific suppressors
Race-specific resistance can also result from pathogen production of
race-specific suppressors that inhibit a non-specific resistance
response. To date, race-specific suppressors have been described for
only a few species of biotrophic plant-pathogenic fungi, including
Phytophthora infestans. In contrast to race-specific elicitors, they are
proposed to interfere with elicitor binding, signal transduction, gene
expression or plant defences to suppress the non-specific resistance
response towards races that harbour them. Race-specific suppressors
may be proteins directly encoded by pathogen genes governing race-
specificity, or may be non-protein compounds produced by reactions
catalysed by these proteins. Plant disease resistance in cases involving
race-specific suppressors may or may not also be cultivar-specific (and
thus gene-for-gene), depending on whether or not the actual
mechanism of suppression involves a cultivar-specific plant molecule.

9. Non-Host Specific Resistance
Non-specific plant disease resistance is multi-component, relying upon a foundation of passive plant defences,
and usually also involving the activation of active defences by non-specific elicitors of biotic origin. The
combination of defences involved in this type of resistance is highly coordinated and similar for all plant-
pathogen interactions. However, substantial variation in both the timing and degree of the active component of
plant defence and in environmental factors have been shown to be critical to its success. Whilst stronger, more
timely non-specific defence responses are responsible for many incompatible plant-pathogen interactions,
weaker non-specific defence responses are often overcome by the pathogen in compatible interactions, and
have also been observed in symbiotic relationships with endophytic fungi.
The genetic basis underlying non-specific plant disease resistance is complex, and involves multiple genes that
encode proteins with a diversity of functions in both partners of the plant-pathogen interaction. These can be
divided into pathogenicity genes that determine the ability of the pathogen to cause disease and defence-
related genes that enable the plant host to execute defence responses. Both classes of genes contain
members that are expressed in a constitutive manner, in addition to genes that are only expressed in response
to the interaction of plant and pathogen. Pathogen genes that govern pathogenicity usually encode proteins that
have a negative impact on disease resistance. The majority of pathogenicity genes in plant pathogens condition
the ability to establish infection, and these include genes that encode proteins with specific roles in adhesion to
the plant surface, the formation of penetration structures, cell wall degradation, and the synthesis of toxic
compounds. However, a number of pathogenicity genes instead govern the ability of the pathogen to defeat
plant defences, such as those encoding proteins involved in the detoxification of phytoalexins. Plant defence-
related genes encode proteins that enable the detection of non-specific elicitors and the activation of an
intracellular signalling pathway leading to plant defences, as well as those themselves involved in passive and
active plant defences, to Passive Defenses and Active Defenses.

10. MECHANISMS UNDERLYING NON-HOST RESISTANCE
• Host resistance and nonhost resistance are most commonly differentiated based on pathogen adaptation to a particular species (host) and lack of
adaptation to other species (nonhost). Both host and nonhost resistances are the outcomes of the plant immune response. 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.
Basal defense in plants is initiated with the perception of evolutionarily conserved microbial- or pathogen-associated molecular patterns (MAMPs
or PAMPs) such as flagellin and EF-Tu by plant extracellular pathogen recognition receptors (PRRs) such as leucine-rich repeat kinases.Such
responses are referred to as PAMP-triggered immunity (PTI). 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. Initiation of plant defense responses
and the counter attack of pathogen are well explained by the widely accepted zig-zag model proposed by Jones and Dangl (2006). According to
this model, there are numerous PRRs in plants to recognize PAMPs and to initiate basal defense responses, but some well-adapted pathogens
secrete effectors to evade recognition by plant PRRs and to promote pathogen growth and virulence. Suppression of PTI by pathogen effectors
leads to effector-triggered susceptibility (ETS). Nonhost resistance is not pathogen-race-specific and is a broad spectrum resistance exhibited by
the whole plant species against a particular pathogen (Heath 2000). Nonhost resistance is often multi-tiered, with several obstacles depending
upon a particular host to stop the colonization by a potential pathogen. 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 barriers such as cell wall, cuticle,
phytoanticipins, etc.; and induced defense responses such as lignin accumulation, production of antimicrobials like phytoalexins, HR response,
induction of pathogenesis-related (PR) proteins, etcq. Depending upon the presence or absence of visual symptoms, nonhost resistance is again
divided into type I and type II nonhost resistance . Type I nonhost resistance does not produce any visual symptoms, whereas type II nonhost
resistance is associated with visual necrosis/cell death due to HR . Type I nonhost resistance typically involves passive or preformed barriers
and/or active defense mechanisms that are induced in response to general elicitors of pathogens such as PAMPs . Type I nonhost resistance
resembles PTI, whereas type II nonhost resistance involves HR and is triggered in response to pathogen elicitor/effector recognition and is similar
to ETI . For example, recognition of pathogen effectors by nonhost plant species has been reported previously when AvrA and AvrD from
Pseudomonas syringae pv. tomato were recognized by R genes Rpg2 and Rpg4, respectively, of the nonhost plant soybean. In addition, AvrRxo1
from Xanthomonas oryzae pv. oryzae was recognized by the R gene Rxo1 of the nonhost plant maize . Despite the fact that there are some
overlaps between host and nonhost resistance, nonhost resistance is more complex and the mechanism of resistance may vary, depending upon
the nature of pathogen (virus, bacteria, and fungi) and the plant species.

11. EVOLUTIONARY PERSPECTIVE OF HOST AND
NONHOST RESISTANCE
The concept of host and nonhost resistance is derived from the fact that not all pathogens can infect all plant species. Host and nonhost interactions between plants
and pathogens are dynamic and greatly influenced by evolution. 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 . Within host species, the variation of resistance among cultivars and
accessions is mainly defined by a large repertoire of R genes that continuously evolve due to gene duplication/deletion, recombination, mutations, and selection
pressure for resistance against pathogens . On the other hand, pathogens also evolve their effector proteins to maintain virulence on host species. Co-evolution of
host and pathogen is also the basis of the zig-zag model that has been developed for plant immunity against pathogens . In some instances, the host plant evolves
and acquires a nonhost status by one-sided evolution of the plant while the pathogen is specialized to a particular host and does not counter evolve . Generally,
durability of nonhost resistance increases against a specialized pathogen when the nonhost species is evolutionarily divergent from the source host species (Fig. 1).
On the contrary, highly evolving pathogens have the potential to overcome the defense exhibited by nonhost species evolutionarily divergent from their source host
(Fig. 1). In general, an increase in genetic distance of nonhost from adapted host increases the durability of nonhost resistance because of the presence of several
mechanisms to block the pathogen infection . Additionally, pathogens which keep evolving generally have a large host range. Several factors which influence genetic
structure and evolutionary trajectory of a pathogen population include the host range, mode of reproduction, transmission and dispersal, life-cycle complexity and
epidemiology, and host longevity . A good example of a pathogen with a large host range, long-distance transmission, sexual and asexual modes of reproduction, and
a complex life cycle including an alternate host is Puccinia spp. The Puccinia spp. cause rust diseases in monocots and cause economically significant damage on
several crop plants in the United States . The host range of Puccinia graminis alone is very large and covers 365 species in 54 genera (Anikster 1984). Another
example is Puccinia coronata var. hordei, also has a broad host range and infects Hordeum, Bromus, Agropyron, Aegilops, Phalaris, and Secale genera . It can be
presumed that such pathogens have a large repertoire of effectors compared to a specialized pathogen . Recently, a new race (Ug99) of Puccinia graminis f. sp. tritici
emerged in Uganda in 1998 which is virulent on most wheat cultivars grown all over the world . Sexual reproduction and long distance dispersal of windborne spores
are the major contributing factors for emergence of new races and rust epidemics. Intercontinental long-distance dispersal of Puccinia graminis f. sp. tritici has been
reported previously . Puccinia graminis f. sp. tritici overwinters and completes its sexual cycle on the alternate host barberry (Berberis vulgaris), and the presence of
barberries increases genetic diversity and infectivity of rust . Therefore, a barberry eradication program was conducted from 1918 to 1980 in the United States to
reduce wheat stem rust epidemics.
Apart from co-evolution, which largely determines host−pathogen interactions, co-speciation, host-shift speciation, and host jump play a role in the adaptation of
pathogens to new plant species (Fig. 1) . Co-speciation happens when both host and pathogen undergo speciation simultaneously to maintain their interactions. The
presence of co-speciation has been experimentally proven by comparing phylogenetic trees of rodents and their ectoparasites, which showed a high degree of
concordance . Host-shift happens when pathogens usually shift from their natural host to related nonhost species. For example, Blumeria graminis that causes
powdery mildew disease on barley underwent host-shift from barley to the related nonhost species, wheat . Similarly, rice blast pathogen Magnaporthe oryzae also
shifted host to cause wheat blast in the mid-1980s . On the other hand, host jump involves adaption of the 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 hosts indicating a cross kingdom jump in the
past . A very good example of host jump is related to Phytophthora infestans that was responsible for the famous 19th century Irish potato famine. Phytophthora
infestans that infect several Solanum species evolved through host jump from Phytophthora mirabilis that infect the four o’clock plant (Mirabilis Jalapa,) Recent
findings suggest that the host specialization followed by host jump is dependent on reciprocal amino acid changes in effector proteins such as a single amino acid
change in one of the effector protein that binds and inhibits a plant’s protease defense . Horizontal gene transfer of pathogenicity genes between pathogen species
beyond reproductive barriers also helps bacterial and fungal pathogens to shift their hosts and infect nonhosts . Interspecific horizontal gene transfer has been
reported for the ToxA gene that was transferred from Phaeosphaeria nodorum to Pyrenophora tritici-repentis, which causes tan spot disease of wheat

12. A, Host resistance is primarily controlled by R-AVR
recognition. A micro-evolution creates diversity within host
species for resistance/susceptibility and also within
pathogen to develop new races with diverse suite of
effectors. Red, yellow, and green indicate host variations for
susceptibility, partial resistance/susceptibility, and
resistance, respectively.
B, Outcomes of nonhost interactions vary with genetic
distance from host species and the pathogen’s ability to
evolve. A rapidly evolving pathogen due to co-speciation,
host shift, and host jump has better capability to adapt to
new nonhost species by breaking the nonhost barriers.
Durability of nonhost resistance with respect to genetic
distance is depicted as a gradient from red to green, where
red is less durable and green is more durable. The
contribution of PAMP-triggered immunity and effector-
triggered immunity also increases and decreases,
respectively, with the increase in genetic distance from host
to nonhost (based on information from Schulze-Lefert and
Panstruga 2011).Evolution of host and Non-host resistance.

13. HOST VERSUS NONHOST RESISTANCE:
PRACTICAL APPLICATION FOR CROP
IMPROVEMENT Compared with host resistance, nonhost resistance is considered more durable; but at the same time, nonhost resistance is more complicated and difficult
to apply in crop breeding. Availability of both susceptible and resistant individuals in host populations against a particular pathogen makes it easier to
identify underlying genetic factors responsible for resistance by employing genetic and quantitative trait loci mapping. Contrarily, a nonhost plant
population generally lacks susceptible individuals, especially if the nonhost is distantly related to the susceptible host. Under these circumstances,
inheritance of nonhost resistance can be achieved by employing three different strategies: crossing host × nonhost where cross species hybridization is
possible; crossing nonhost × nonhost if there are variations in resistance; and crossing rare susceptible and common resistant individuals in marginal host
species (Niks and Marcel 2009). Marginal host species are those which are mostly nonhost to a pathogen species, but rarely individuals with lower
susceptibility than host species still exist (Niks and Marcel 2009). Lack of natural variation for resistance in host and nonhost species can be overcome by
generating variations using mutagenesis and gene silencing. Several genes involved in nonhost resistance of M. truncatula against Phakopsora pachyrhizi
were identified by screening a large Tnt1 insertion mutagenized population of M. truncatula (Tadege et al. 2008; Uppalapati et al. 2012). In addition, PEN
genes were identified and characterized in nonhost Arabidopsis by screening a mutant population upon infection with Blumeria graminis f. sp. hordei
(Collins et al. 2003; Lipka et al. 2005; Stein et al. 2006). In another approach, virus-induced gene silencing (VIGS)-based forward genetics screening was
utilized to identify the role of genes such as SQUALENE SYNTHASE (SQS), GOX, ORNITHINE DELTA-AMINOTRANSFERASE (δOAT), and PROLINE
DEHYDROGENASE (ProDH) in nonhost resistance of N. benthamiana against several bacterial pathogens (Rojas et al. 2012; Senthil-Kumar and Mysore
2012; Wang et al. 2012).
 The next step after identification of genes involved in nonhost resistance is to successfully transfer them to susceptible host species. Genes involved in
nonhost resistance are often difficult to transfer compared with host resistance genes, since they need either wide hybridization or transgenic approaches.
Wide hybridization has been successfully employed in the past to transfer sources of resistance against multiple diseases in wheat by transferring
individual rye chromosomes to wheat (Riley and Macer 1966). More recently, a barley leaf rust resistance gene, Rph22, was successfully transferred from
nonhost species Hordeum bulbosum to Hordeum vulgare (cultivated barley) (Johnston et al. 2013). Similarly, a transgenic approach has also been
implemented successfully in the past in which a nonhost resistance gene, Rxo1, from maize was transferred to rice and imparted resistance against the
bacterial streak pathogen Xanthomonas oryzae pv. oryzicola (Zhao et al. 2005). Recently, another Arabidopsis gene involved in nonhost resistance,
PHYTOPHTHORA SOJAE SUSCEPTIBLE 1 (PSS1), was identified in the Arabidopsis pen1-1 mutant background which is required for both pre- and post
-penetration nonhost resistance against the hemibiotrophic oomycete fungal pathogen Phytophthora sojae and necrotrophic fungal pathogen Fusarium
virguliforme (Sumit et al. 2012). PSS1 encodes a glycine-rich protein (GRP), and expression of AtGRP1 in soybean cultivar Williams-82 led to enhanced
resistance against Phytophthora sojae and F. virguliforme (Sumit 2013).

14. Concluding Remarks
Plant disease resistance is a complex phenomenon that most commonly occurs in a non-specific manner, as a result of multiple
genes conditioning the ability of the pathogen to cause disease and enabling the plant host to mount an effective defence
response. However, plant disease resistance can also be induced only in response to particular pathogen races (race-specific
resistance), only in particular host plant cultivars (cultivar-specific resistance), or only when both a specific pathogen race and
plant cultivar interact (race-cultivar-specific or gene-for-gene resistance). This host-pathogen specificity can be attributed to a
single gene or a small number of related genes enabling the production of race-specific elicitors, host-selective toxins, or race-
specific suppressors in different host-pathogen systems. Specific plant disease resistance resulting from race-specific elicitors is
probably superimposed upon a non-specific resistance response that has been overcome in the host range of the pathogen. In
contrast, host-selective toxins and race-specific suppressors most likely achieve host-pathogen specificity in disease resistance
through the modification or negation of an otherwise successful non-specific resistance response.
Host resistance has been studied extensively, but nonhost resistance is only beginning to be understood. Host resistance is mainly
controlled by gene-for-gene resistance, whereas nonhost resistance is usually more complicated due to the involvement of
multiple pathways. Due to the durability of nonhost resistance over host resistance, nonhost resistance holds great promise for
agriculture. Based on the available information on host and nonhost resistance, we compared these two forms of resistance.
Despite their classification into two classes, host and nonhost resistance share more similarities than differences in their
mechanisms and resistance process. Due to similarities in downstream mechanisms, genes involved in nonhost resistance have
been successfully transferred from nonhost to host species (Johnston et al. 2013; Sumit 2013; Zhao et al. 2005). But identification
and utilization of sources of nonhost resistance in crop improvement are still challenging. We speculate that with the aid of the
latest molecular biology and genomics tools, such as improved transformation methods, advanced tissue culture techniques,
mutagenesis, genome editing, VIGS, and genome sequencing, more novel sources of nonhost resistance will be identified and
effectively utilized in future plant breeding.

15. Thanks For Your Patience !!