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Types of pathogens

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Gamete types (male & female): 1R : 1r. Progeny genotypes: 1R/R : 2R/r : 1r/r ... gametes from first parent. AB Ab aB ab. AB A/A,B/B A/A,B/b A/a,B/B A/a,B/b ... – PowerPoint PPT presentation

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Title: Types of pathogens


1
Types of pathogens diseases (taxonomic groups)
  • Diseases
  • Anthracnose
  • Leaf Spots
  • Stem canker
  • Fruit Blotch
  • Blights
  • Damping-off
  • Rusts
  • Smuts
  • Rots
  • Mildew
  • Mosaics
  • Wilts
  • Cankers
  • Stunts
  • Galls
  • Pathogens (major types)
  • Fungi Oomycetes
  • Bacteria (including phytoplasmas)
  • Viruses ( Viroids)
  • Nematodes
  • Parasitic plants

2
Types of pathogens (methods of pathogenicity)
Different pathogens can be classified as to
whether they feed off living cells or cells they
have killed Many pathogens lie somewhere on a
continuum between the two extremes, with
differences between infection stages.
Biotrophic Necrotrophic
rusts, smuts, downy powdery mildews, viruses
Toxin-producing fungi, bacteria
They may infect healthy cells early in the
interaction but grow and reproduce on dead tissue.
Live off healthy cells. In early stages of
compatible interactions they avoid detection by
the host, they may be able to inhibit defense
responses once they are established.
Kill cells and live off them. Saprophytes toxins
may be very host specific (even cultivar
specific) or they may be very nonspecific.
3
Biotrophic fungi penetrate living plant cells
with haustoria
4
Types of pathogens diseases (specificity or
host specialization)
Highly specific Some pathogens or parasites
cause disease only on specific genotypes of a
host plant species. Nonspecific (broad host
range) Some pathogens or parasites will attack
many different plant species.
5
Types of resistance (one classification based on
inheritance gene number and effect)
  • Qualitative, or simply inherited
  • Genes often race-specific and often follow
    gene-for-gene model
  • Often called R genes or major genes, sometimes
    vertical resistance genes.
  • Often condition a hypersensitive response (HR).
  • Quantitatively inherited resistance
  • Controlled by multiple genes with smaller
    effects.
  • Often assumed to be race-nonspecific but not
    clear to what extent these resistances are
    controlled by the same types of genes as the
    simply inherited resistances.
  • May be called partial resistance or minor gene or
    polygenic resistance or horizontal resistance.

6
Types of resistance (Host vs. Nonhost)
Non-host resistance The entire plant species is
resistant to a specific pathogen or parasite
(Heath 2000 Curr. Op. Plant Biol. 3315-) -Very
common -Often under complex genetic control Host
(cultivar) resistance Some genotypes of the
species are resistant, some are not. -Usually
pathogen/parasite specific -Often controlled by R
genes
7
Types of resistance (based on phenotype)
  • Immunity
  • No successful infection and no visible damage to
    the plant, not even HR
  • Tolerance
  • The host becomes infected yet suffers less damage
    than susceptible plants under the same degree of
    parasitism.
  • Possible manifestations of quantitative
    resistance
  • Fewer lesions
  • Smaller lesions
  • Slower disease progress, including latent period
  • Longer green leaf retention
  • Less stunting, wilting or deformation
  • Greater yield in presence of disease (tolerance)

8
Types of resistance (based on mechanism)
Passive resistance Based on compounds and
structures that are preformed (present before the
pathogen/parasite infects) -Examples protease
inhibitors, antimicrobial compounds like saponins
and phenolics, antimicrobial peptides, cuticular
wax. -Many forms are fairly nonspecific e.g.
some protease inhibitors can affect insect
herbivory and fungal pathogenesis. Active
resistance based on induction of defenses after
the pathogen/parasite attacks. -Probably now
receiving most focus scientifically. -Plants
recognize the presence of the pathogen by
detecting elicitors (things that elicit defense
responses). -Elicitors can be specific or
nonspecific. -Defenses induced after pathogen
recognition are numerous and many are
nonspecific. -Response is often very localized,
but can be expressed as systemic acquired
resistance (SAR).
9
Basis of gene for gene resistance
Resistant Plant Cell
Resistance genes
Avirulent Pathogen
Transcription factor activation
Avirulence genes
Defense responses PR/SAR protein Wall
reinforcement Phytoalexin ROS Cell death
Formation of more signal molecules
10
Features of R gene recognition defense
signaling
  • Interact with Avr gene products directly or
    indirectly
  • Interact with Avr gene products inside or outside
    cell
  • -R genes typically expressed before pathogen
    challenge
  • -Some defense responses can occur within minutes,
    others take longer
  • -Different plants have different responses, may
    depend on R gene
  • -Many defense responses are very localized, some
    systemic
  • -R genes do not act alone, other gene products
    are required

11
Quadratic Check for Gene-for-Gene Interactions
Host Genotype RR or Rr rr
Pathogen Genotype Avr avr
Susceptibility (disease)
Resistance (no disease)
Susceptibility (disease)
Susceptibility (disease)
  • Other general rules
  • Only R genes matched by Avr genes cause
    resistance
  • Susceptible alleles at R genes cause no
    resistance
  • R genes act independently (with exceptions). One
    R gene matching its Avr gene will cause
    resistance.

12
Molecular Interpretation for Quadratic Check
Host Genotype RR or Rr rr
Pathogen Genotype Avr avr
Resistance
Disease
Disease
Disease
13
Interactions considering two resistance genes
14
Review Single gene segregation ratios
Dominant R gene in a test cross   R/R X
r/r ? R/r X r/r   Gametes from
heterozygote 1R 1r Progeny genotypes
1R/r 1r/r Progeny phenotypes 1
Res. 1 Susc. (same as genotypes in a test
cross)
15
Review Single gene segregation ratios.
Dominant R gene in a F2   R/R X r/r
? R/r ? or (self
fertilized, or sib mated) Gamete types (male
female) 1R 1r Progeny genotypes 1R/R
2R/r 1r/r Progeny phenotypes 3 Res.
1 Susc. (When in doubt, draw a Punnett square)
16
Two gene ratios independent segregation
 1) test cross A/a B/b X a/a b/b   Gametes
from heterozygote 1A B 1 A b 1a B 1a
b   Progeny genotypes   gametes from first
parent gametes A B A b
a B a b from 2nd P. a b A/a, B/b A/a,
b/b a/a, B/b a/a, b/b Genotypic ratios
phenotypic ratios gametic ratios
(1111) Ratio of resistance if either gene
provides resistance 31 (resistant
susceptible)
17
Two gene segregation ratios independent
segregation
2) F2 A/a B/b ? or (self fertilized, or
sib mated) Progeny genotypes   gametes
from first parent AB Ab
aB ab AB A/A,B/B A/A,B/b
A/a,B/B A/a,B/b from Ab A/A,B/b A/A,b/b
A/a,B/b A/a,b/b 2nd P aB A/a,B/B A/a,B/b
a/a,B/B a/a,B/b ab A/a,B/b A/a,b/b
a/a,B/b a/a,b/b Genotypic ratios 9 possible
genotypes (112242211) Phenotypic ratio
with dominant genes 9 A-,B- 3 A-,b/b 3 a/a,
B- 1a/a,,b/b Ratio of resistance if either gene
provides resistance 151 (RS)
18
Segregation ratios for two dominant R genes
19
More Terminology
Isolates (collected individuals) of a given
pathogen with a specific combination of
avirulence genes are often considered to be
members of the same race (pathotype, biotype).
Interactions where the host is resistant and the
pathogen is avirulent are incompatible
interactions, while those where the host is
susceptible to the race are called compatible
interactions. By definition, different races of
a pathogen are differentiated by their ability to
attack different plant lines carrying different
resistance genes (differential cultivars). At
the same time, however, these races are used to
determine which resistance genes various plant
lines carry.
20
Constructing a gene-for-gene model
General rule geneticists do not give
designations to genes until they have
demonstrated that it is not a previously named
gene. More specific rules 1) If you can
explain the resistance in a plant line with a
single gene, do not postulate more than one gene.
2) If you can explain the resistance of a
line without postulating new genes, dont
postulate new genes. 3) If the resistances
of two plant lines look identical to all races,
tentatively assume they have the same resistance
genes. 4) Test your resistance gene model with
segregation data.
21
Example of a model construction
Plant Pathogen isolate
Simplify your data set.
22
Plant Pathotype
Model construction
Start with the cultivars that are resistant to
the fewest pathotypes. Assume (for now) that
Line A carries a single gene, R1. On the basis
of a gene-for-gene interaction, race 1 then
carries Avr1. Also, races 2 - 5 must not carry
Avr1.   Line B is resistant to two races that
line A is not so it definitely carries a
different resistance gene. Also, it is
susceptible to race 1, so it does not carry R1.
We have no reason to believe the resistance to
race 2 is controlled by anything different than
the resistance to race 4 so we will assume the
same gene is controlling resistance to both. We
will call this gene R2 and assume that races 2
and 4 both carry Avr2.
23
Plant Pathogen race
Line C is resistant to one race that neither
Line A or Line B are resistant two so must carry
a different gene. Also, it is susceptible to
races 1 and 2 and therefore does not carry R1 or
R2. We will assume the same gene is controlling
resistance to both race 3 and race 4. We will
call this gene R3 and assume that races 3 and 4
both carry Avr3.   Line D is not resistant to
any races that none of the previously considered
lines are resistant to. It does have resistance
to a unique combination of resistances though.
It might carry R1, because it is resistant to all
the races that Line A is resistant to. It
might carry R2, because it is resistant to all
the races that Line B is resistant to. It does
not carry R3 because it is susceptible to race 3
if it carried R3 it would be resistant. We can
explain the resistance in line D by tentatively
assuming it carries both R1 and R2 and we do not
need to postulate any new genes for this line.
24
Plant Pathogen race
Line E is resistant to one race that none of the
other lines is resistant to and therefore must
carry a novel resistance gene. We will call this
R4 and assume that race 5 carries Avr4. Line E
does not carry R1 or it would be resistant to
race 1, it does not carry R2 or it would be
resistant to race 2. It could carry R3 because
it is resistant to both races that this gene
confers resistance to. Line E may, or may not,
carry R3 in addition to R4, and races three and
four may or may not carry Avr4.   Notice that
for each plant line we are asking two questions
Does the line have resistance that is different
than all of the other lines? And, could that
resistance be explained by a combination of the
resistance genes we have already postulated.
25
Plant Pathogen race
Our model stands as above until we test it by
genetic analysis. One test is to determine
how many independently segregating genes control
resistance in each of the lines to each of the
races. This can be done by crossing each of the
lines to a universally susceptible line, making
F2 or test cross populations of each of these
crosses, and testing the segregation of each
cross with each of the races that are avirulent
on that line. For example, if you inoculated an
F2 of the Line A x Line U (universal suscept)
with race 1 and saw single gene segregation, you
would not have to modify your model, but if you
saw 2 gene segregation your model might need a
major overhaul.
26
Homework 1, prediction of segregation ratios
for resistance.  1A) What are the expected
segregation ratios from progeny of test cross
families (crossed to a universal suscept) made
from F1 crosses between the two host genotypes
given, when challenged with the pathogen genotype
given. Assume resistance and avirulence are
completely dominant at each locus and, as
predicted by the gene-for-gene model, any
resistance gene that is matched by an avirulence
gene conditions resistance.
27
1B) What are the expected segregation ratios from
progeny of F2 families made from F1 crosses
between the two host genotypes given, when
challenged with the pathogen genotype given.
Again, assume resistance and avirulence are
completely dominant at each locus and, as
predicted by the gene-for-gene model, any
resistance gene that is matched by an avirulence
gene conditions resistance.
28
Homework 2 Constructing a gene-for-gene
model Make a model for the genetics of
resistance in the lines below. In your model,
state which gene each of the lines carries.
Postulate no more resistance genes than is
absolutely necessary. The crop you are working
on has two well characterized genes which control
resistance to mildew. Your line 1 has gene R1
and your line 2 has gene R2. Both genes have
been used by yourself and other breeders to
develop mildew resistant cultivars. Over the
past few years, shifts in the pathogen population
has occurred and neither gene consistently
provides resistance to the disease. To identify
and characterize new sources of resistance you do
two things 1) you make a new collection of
pathogen isolates to add to the three races you
have used over the years to distinguish lines
carrying R1 and R2 and 2) you screen lots of
cultivars and plant introductions to identify new
sources of resistance. After testing a large
number of mildew isolates with lots of germplasm,
you find that you have two new races and six new
sources of resistance that do not seem to have
just R1 or R2. Make a model for the genetics of
resistance in these lines. The table below shows
the reactions of the four mildew races on the
different lines you have identified.
29
Homework 2 worksheet
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