This document discusses different types of plant resistance to pathogens. It describes true resistance, which includes partial/quantitative/polygenic resistance controlled by multiple genes (horizontal resistance) and R-gene/monogenic resistance controlled by single genes (vertical resistance). It also discusses the genetics of virulence in pathogens and resistance in host plants using the gene-for-gene concept. Specifically, it explains how avirulence genes in pathogens interact with resistance genes in plants to determine compatibility.

1. Barakat, M. I. E.
2017
Types of Plant Resistance to
Pathogens

2. Types of Plant Resistance to
Pathogens
 True Resistance:
 Partial, Quantitative, Polygenic, or Horizontal
Resistance —
 R-Gene Resistance, Monogenic, or Vertical
Resistance Apparent Resistance Disease Escape;
Tolerance to Disease
 Genetics of Virulence in Pathogens and of
Resistance in Host Plants
 The Nature of Resistance to Disease
Pathogenicity Genes in Plant Pathogens, Genes
Involved in Pathogenesis and Virulence by Pathogens
Pathogenicity Genes of Fungi controlling: Production of
Infection Structures, Degradation of Cuticle and Cell
Wall Secondary Metabolites Fungal Toxins,
Pathogenicity Signaling Systems, Pathogenicity Genes

3. True Resistance
 The genetic information of all organisms, i.e., the
information that determines what an organism can
be and can do, is encoded in its deoxyribose
nucleic acid (DNA). In RNA viruses, of course, it is
encoded in their ribose nucleic acid (RNA).
 In all organisms, most DNA is present in the
chromosome(s). In prokaryotes, such as bacteria
and mollicutes, which lack an organized,
membrane-bound nucleus, there is only one
chromosome and it is present in the cytoplasm,
whereas in eukaryotes, i.e., all other organisms
except viruses, there are several chromosomes
and they are present in the nucleus.

4. GENES AND DISEASE
 When different plants, such as tomato, apple, or
wheat, become diseased as a result of infection
by a pathogen, the pathogen is generally different
for each kind of host plant. Moreover, the
pathogen is often specific for that particular host
plant. Thus, the fungus Fusarium oxysporum f.
sp. lycopersici, which causes tomato wilt, attacks
only tomato and has absolutely no effect on
apple, wheat, or any other plant.
 Similarly, the fungus Venturia inaequalis, which
causes apple scab, affects only apple, whereas
the fungus Puccinia graminis f. sp. tritici, which
causes stem rust of wheat, attacks only wheat.

7. VARIABILITY IN ORGANISMS
 This is true oomycetes and of fungi produced
from sexual spores such as oospores,
ascospores, and basidiospores; of parasitic
higher plants produced from seeds; and of
nematodes produced from fertilized eggs, as
well as of cultivated plants produced from
seeds.
 Even bacteria have mechanisms for the
transfer of genetic information. When
individuals are produced asexually, the
frequency and degree of variability among the
progeny are reduced greatly, but even then
certain individuals among the progeny will
show different characteristics.

8.  Because of the astronomical number of
individuals produced by microorganisms
asexually, the total amount of variability
produced by at least some microorganisms is
probably as great and possibly greater than the
total variability found in microorganisms
reproducing sexually.
 This is the case in the overwhelmingly asexual
reproduction of fungi by means of conidia,
zoospores, sclerotia, and uredospores, and in
bacteria, mollicutes, and viruses.

9. MECHANISMS OF
VARIABILITY
 In host plants and in pathogens, such as most
fungi, parasitic higher plants, and nematodes,
which can, and usually do, reproduce by means
of a sexual process, variation in the progeny
is introduced primarily through segregation
and recombination of genes during the
meiotic division of the zygote.
 Bacteria too, and even viruses, exhibit variation
that seems to be the result of asexual process.
 In many fungi, heteroploidy and certain
parasexual processes lead to variation.

12. General Mechanisms of Variability
 Mutation
‫الطفرات‬
 Recombination
‫االتحادات‬
 Gene and Genotype Flow among Plant
Pathogens
 Population Genetics, Genetic Drift, and Selection

13. Specialized Mechanisms of Variability
in Pathogens
 Sexual-like Processes in Fungi
‫الطرق‬‫الشبيهه‬‫الجنسي‬ ‫بالتكاثر‬
Heterokaryosis
Parasexualism
‫الذاتي‬ ‫التزاوج‬
Vegetative Incompatibility
Heteroploidy
‫تباين‬‫النوايات‬‫واختالفها‬
 Sexual-like Processes in Bacteria and Horizontal
Gene Transfer(Conjugation – Transformation –
Transduction)
Genetic Recombination in Viruses

14. TYPES OF PLANT RESISTANCE
TO PATHOGENS
 True Resistance
**Partial, Quantitative, Polygenic,
or Horizontal Resistance
**R Gene Resistance, Race-Specific,
Monogenic,
or Vertical Resistance

15. Horizontal resistance (polygenic)
 In genetics, the term horizontal resistance was
first used by J.E. Vanderplank(1963) to describe
many-gene resistance, which is sometimes also
called generalized resistance.
 This contrasts with the term vertical resistance
which was used to describe single-gene
resistance. Raoul A. Robinson(1967) further
refined the definition of horizontal resistance.
Unlike vertical resistance and parasitic ability,
horizontal resistance and horizontal parasitic
ability are entirely independent of each other in
genetic terms.

18.  In the first round of breeding for horizontal resistance,
plants are exposed to pathogens and selected for
partial resistance. Those with no resistance die, and
plants unaffected by the pathogen have vertical
resistance and are removed. The remaining plants
have partial resistance and their seed is stored and
bred back up to sufficient volume for further testing.
The hope is that in these remaining plants are multiple
types of partial-resistance genes, and by
crossbreeding this pool back on itself, multiple partial
resistance genes will come together and provide
resistance to a larger variety of pathogens.
 Successive rounds of breeding for horizontal
resistance proceed in a more traditional fashion,
selecting plants for disease resistance as measured
by yield. These plants are exposed to native regional
pathogens, and given minimal assistance in fighting

19. R Gene Resistance, Race-Specific,
Monogenic, or Vertical Resistance
 Many plant varieties are quite resistant to some races
of a pathogen while they are susceptible to other races
of the same pathogen. In other words, depending on
the race of the pathogen used to infect a variety, the
variety may appear strongly resistant to one pathogen
race and susceptible to another race (race specific)
under a variety of environmental conditions. Such
resistance differentiates clearly between races of a
pathogen, as it is effective against specific races of the
pathogen and ineffective against others.
 Such resistance is sometimes called strong, major,
race-specific, qualitative, or differential resistance, but
it was more commonly referred to in the past as
vertical resistance.

20.  Race-specific resistance is always controlled by one
or a few genes (thereby the names monogenic or
oligogenic resistance).
 These genes, referred to as R genes, control a major
step in the recognition of the pathogen by the host
plant and therefore play a major role in the expression
of resistance. In the presence of race-specific
resistance, the host and pathogen appear
incompatible.
 The host may respond with a hypersensitive reaction,
may appear immune, or may inhibit pathogen
reproduction. Often, race-specific resistance inhibits
the initial establishment of pathogens that arrive at a
field from host plants that lack, or have different,
major genes for resistance.

21. GENETICS OF VIRULENCE IN PATHOGENS
AND OF RESISTANCE IN HOST PLANTS
 The Gene-for-Gene Concept
The gene-for-gene relationship was discovered by the late
Harold Henry Flo(1942).
who was working with rust (Melampsora lini) of flax (Linum
usitatissimum).
Flor showed that the inheritance of both resistance in the host
and parasite ability to cause disease is controlled by pairs of
matching genes.
A. One is a plant gene called the resistance (R) gene.
B. The other is a parasite gene called the a virulence (Avr)
gene.
Plants producing a specific R gene product are resistant
towards a pathogen that produces the corresponding Avr gene
product. Gene-for-gene relationships are a widespread and
very important aspect of plant disease resistance. An example
can be seen with Lactuca serriola.

26. Resistance genes
 Classes of resistance gene
There are several different classes of R Genes. The major
classes are the NBS-LRR genes[7] and the cell surface
pattern recognition receptors (PRR).[8] The protein products
of the NBS-LRR R genes contain a nucleotide binding site
(NBS) and a leucine rich repeat (LRR). The protein products
of the PRRs contain extracellular, juxta membrane, trans
membrane and intracellular non-RD kinase domains.[8][9]
Within the NBS-LRR class of R genes are two subclasses
One subclass has an amino-terminal Toll/Interleukin 1
receptor homology region (TIR). This includes the N
resistance gene of tobacco against tobacco mosaic virus
(TMV).
The other subclass does not contain a TIR and instead has a
leucine zipper region at its amino terminal.

27.  The protein products encoded by this class of
resistance gene are located within the plant cell
cytoplasm.
 The PRR class of R genes includes the rice XA21
resistance gene that recognizes the ax21 peptide [10]
and the Arabidopsis FLS2 peptide that recognizes the
flg22 peptide from flagellin.
 There are other classes of R genes, such as the
extracellular LRR class of R genes; examples include
rice Xa21D [11] for resistance against Xanthomonas
and the cf genes of tomato that confer resistance
against Cladosporium fulvum.
 The Pseudomonas tomato resistance gene (Pto)
belongs to a class of its own. It encodes a Ser/Thr
kinase but has no LRR. It requires the presence of a
linked NBS-LRR gene, prf, for activity.

28. Specificity of resistance genes
 R gene specificity (recognising certain Avr gene
products) is believed to be conferred by the
leucine rich repeats. LRRs are multiple, serial
repeats of a motif of roughly 24 amino acids in
length, with leucines or other hydrophobic
residues at regular intervals. Some may also
contain regularly spaced prolines and arginines.
 LRRs are involved in protein-protein interactions,
and the greatest variation amongst resistance
genes occurs in the LRR domain. LRR swapping
experiments between resistance genes in flax rust
resulted in the specificity of the resistance gene
for the avirulence gene changing.

29. Avirulence genes
 The term “avirulence gene” remains useful as a
broad term that indicates a gene that encodes any
determinant of the specificity of the interaction
with the host. Thus, this term can encompass
some conserved microbial signatures (also called
pathogen or microbe associated molecular
patterns (PAMPs or MAMPs)) and pathogen
effectors (e.g. bacterial type III effectors and
oomycete effectors) as well as any genes that
control variation in the activity of those
molecules.
 There is no common structure between avirulence
gene products. Because there would be no
evolutionary advantage to a pathogen keeping a
protein that only serves to have it recognised by
the plant, it is believed that the products of Avr
genes play an important role in virulence in
genetically susceptible hosts.

30.  Example: AvrPto is a small triple-helix protein
that, like several other effectors, is targeted to the
plasma membrane by N-myristoylationAvrPto is
an inhibitor of PRR kinase domains. PRRs signal
plants to induce immunity when PAMPs are
detected. The ability to target receptor kinases is
required for the virulence function of AvrPto in
plants. However, Pto is a resistant gene that can
detect AvrPto and induce immunity as well.
AvrPto is an ancient effector that is conserved in
many P. syringae strains, whereas Pto R gene is
only found in a few wild tomato species. This
suggests recent evolution of the Pto R gene and
the pressure to evolve to target AvrPto, turning a
virulence effector to an avirulence effector.

31.  Unlike the MAMP or PAMP class of avr genes that
are recognized by the host PRRs, the targets of
bacterial effector avr proteins appear to be
proteins involved in plant innate immunity
signaling, as homologues of Avr genes in animal
pathogens have been shown to do this. For
example, the AvrBs3 family of proteins possess
DNA binding domains, nuclear localisation signals
and acidic activation domains and are believed to
function by altering host cell transcription.

32. The Nature of Resistance to
Disease
 A microorganism is pathogenic, i.e.,
 it is a pathogen, because it has the genetic
ability to infect another organism and to
cause disease.
 Either a plant is immune to a pathogen, i.e.,
 it is not attacked by the pathogen even under
the most favorable conditions,
 or it may show various degrees of resistance
ranging from near immunity to complete
susceptibility.

33.  Resistance may be conditioned by a number of
internal and external factors that operate to reduce
the chance and degree of infection.
 The first step in any infection is recognition of the
host by the pathogen and perhaps the opposite,
some type of recognition of the pathogen by the
host.
 Therefore, absence of a recognition factor(s) in the
host could help it avoid infection by a particular
pathogen.
 Generally, any heritable characteristic of the plant
that contributes to localization and isolation of the
pathogen at the points of entry, to reduction of the
harmful effects of toxic substances produced by
the pathogen, or to inhibition of the reproduction
and, thereby, further spread of the pathogen,