This document discusses the protein-protein concept and gene-for-gene hypothesis in plant-pathogen interactions. It contains the following key points:
1. The protein-protein concept provides a biochemical explanation for the gene-for-gene hypothesis, where the mutual recognition between a host and pathogen is due to interactions between their encoded proteins, not the genes themselves.
2. In compatible/susceptible interactions, the pathogen produces a protein that can interact with and activate the host's complementary protein, inducing susceptibility. In incompatible/resistant interactions, the pathogen's protein is not recognized by the host.
3. Studies have found greater antigenic/protein similarity between hosts and pathogens leads to susceptibility, while resistance
Integrated disease management (IDM), which combines biological, cultural, physical, mechanical, legislative and chemical control strategies in a holistic way rather than using a single component strategy proved to be more effective and sustainable.
The power point presentation includes information regarding various methods and concepts involved in fungi bacteria and virus with some suitable examples
The concept of gene for gene hypothesis was first developed by Flor in 1956 based on his studies of host pathogen interaction in flax, for rust caused by Melampsora lini. The gene for gene hypothesis states that for each gene controlling resistance in the host, there is corresponding gene controlling pathogenicity in the pathogen. The resistance of host is governed by dominant genes and virulence of pathogen by recessive genes. The genotype of host and pathogen determine the disease reaction. When genes in host and pathogen match for all loci, then only the host will show susceptible reaction. If some gene loci remain unmatched, the host will show resistant reaction. Now gene – for –gene relationship has been reported in several other crops like potato, sorghum, wheat, etc. The gene for gene hypothesis is also known as “Flor Hypothesis.”
"In field molecular diagnostics as an aid to disease management"EMPHASIS PROJECT
Insights about isothermal Polymerase Chain Reaction (PCR) assays and how they can be used to diagnose the presence of latent diseases in the field, including those which are especially difficult to identify. They will show how assays are developed, and how they may be used to improve disease management choices.
The target audience are researchers, agri-business and forestry experts, farmers and foresters and any other interested in plant health.
Do not hesitate to contact EMPHASIS project through Facebook, Twitter, email (emphasisproject@gmail.com) or through their website (http://www.emphasisproject.eu/) if you want to be updated on webinars dates and content and book a ticket.
To watch on Youtube: https://youtu.be/yFEG9uTEhdc
plant pathogen interaction
different types of pathogens
gene for gene hypothesis
direct receptor model
Elicitor receptor model
suppersor repressor model
gaurd hypothesis
Integrated disease management (IDM), which combines biological, cultural, physical, mechanical, legislative and chemical control strategies in a holistic way rather than using a single component strategy proved to be more effective and sustainable.
The power point presentation includes information regarding various methods and concepts involved in fungi bacteria and virus with some suitable examples
The concept of gene for gene hypothesis was first developed by Flor in 1956 based on his studies of host pathogen interaction in flax, for rust caused by Melampsora lini. The gene for gene hypothesis states that for each gene controlling resistance in the host, there is corresponding gene controlling pathogenicity in the pathogen. The resistance of host is governed by dominant genes and virulence of pathogen by recessive genes. The genotype of host and pathogen determine the disease reaction. When genes in host and pathogen match for all loci, then only the host will show susceptible reaction. If some gene loci remain unmatched, the host will show resistant reaction. Now gene – for –gene relationship has been reported in several other crops like potato, sorghum, wheat, etc. The gene for gene hypothesis is also known as “Flor Hypothesis.”
"In field molecular diagnostics as an aid to disease management"EMPHASIS PROJECT
Insights about isothermal Polymerase Chain Reaction (PCR) assays and how they can be used to diagnose the presence of latent diseases in the field, including those which are especially difficult to identify. They will show how assays are developed, and how they may be used to improve disease management choices.
The target audience are researchers, agri-business and forestry experts, farmers and foresters and any other interested in plant health.
Do not hesitate to contact EMPHASIS project through Facebook, Twitter, email (emphasisproject@gmail.com) or through their website (http://www.emphasisproject.eu/) if you want to be updated on webinars dates and content and book a ticket.
To watch on Youtube: https://youtu.be/yFEG9uTEhdc
plant pathogen interaction
different types of pathogens
gene for gene hypothesis
direct receptor model
Elicitor receptor model
suppersor repressor model
gaurd hypothesis
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Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
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2. • Protein for protein hypothesis –biochemical
explanation of gene for gene hypothesis
• These concepts explain how a host (plant) recognize
their pathogen and suppress its further growth
• (H. Flor, 1942) - For each resistance gene in the host
there is a corresponding gene for avirulence in the
pathogen conferring resistance and viceversa
• “Avr” genes present in pathogen helps the host plant to
trigger its defensive mechanisms
3. Recognition between host and
pathogen
• When a pathogen comes in contact with host cell
, an early event takes place, triggers a rapid
response, either allows or prevent growth of
pathogen and development of disease
• “Early events “ - biochemical substance,
structures & pathogen elicitor molecule , these
components induce specific actions or formation
of specific products by other organisms
4. Pathogen genotype Host genotype
R r
A — A R + A r
a + a R + a r
A - pathogen with dominant a-virulent gene- produce elicitor
molecule
a- recessive a-virulent gene
R – host with dominant resistant gene – produce receptor
molecule
r - host with recessive resistant gene
+ compatible reaction
— incompatible reaction
5. Explanation of G-G hypothesis
• Pathogen has gen: pathogencity gene & specific Avr gene A
or a
• A a
Produce no elicitor
an elicitor
Host with Rgene
Produce
a receptor
Host receptor
recognize pathogen elicitor and
Triggers defense reaction receptor find no
elicitor ,so no defence
Host resistant reaction Host
AR susceptible (aR)
Pathogen
Host Host
6. Contd……..
• A a
Produce no elicitor
an elicitor
Host with rgene
Produce host with rgene
no receptor
Lack receptor
No defence mechanism triggered
Host lacks resistance to this pathogen’s virulence genes
no receptor ,so no
host defence mechanism triggered
Host susceptible Host
Ar susceptible (ar)
Pathogen
Host Host
7. Biochemical explanation for G-G
concept –Protein –protein concept
• There are two explanation for P-P concept
• According to first specificity in gene for gene
systems lies in susceptibility (Van der Plank,
1978)
• whereas to other specificity lies in resistance
(Ellingboe, 1981).
8. • According to Van der Plank (1978), specificity in gene –
for- gene relationships lies in susceptibility.
• He explains it with the help of interactions of five host
and five pathogens attacking them specifically.
• Suppose there are five host varieties with five different
R genes; R1, R2, R3----------R5.
• A plant with resistance gene R1 is attacked by a
pathogen having virulence gene a1 and not to
pathogen without this particular resistance gene
irrespective of how many the virulence genes it may
have.
9. Pathogen plant
R1 R1 R2 R2 R3 R3 R4 R4 R5 R5
a1 a1 S
a2 a2 S
a3 a3 S
a4 a4 S
a5 a5 S
10. • Resistance is assumed to be dominant and RR
can be replaced by Rr.
• Virulence is assumed to be recessive.
However, recessive resistance and dominant
virulence are also known. R= resistant S=
suscep
11. • Vander Plank (1978) elaborated protein for
proteins hypothesis as a biochemical
explanation of gene for gene interaction.
• The protein for protein hypothesis states that
in gene -for -gene diseases the mutual
recognition of host and pathogen is not by the
genes themselves but by their coded proteins.
12. • Vander Plank (1978) hypothesized that in susceptibility the
pathogen excretes a protein (virulence for product) into the host
cell which copolymerizes with a complementary host protein
(resistance gene product).
• This co-polymerization interferes with one auto regulation of the
host gene that codes for the protein used by pathogen as a food
and by so doing turns the gene on to produce more protein.
• In resistance, the protein specified by the gene for avirulence in the
pathogen and excreted into the host does not polymerize with the
protein coded for by the gene for resistance.
• It is not recognized by the host at all.
13. Antigenic relation b/w host and
pathogen
• Compatible reaction = susceptibilty , in such situations
protein/ antigen pd by Path is similar to antigen pd by host
• Boubly et al 1960 conducted expt. on Flax – Melamspora
lini system.(rust causing path)
4 var of flax and 4 isolates if M.lini
• From serological studies –titers of rust anti sera & Flax
antigen / protein are similar (1:60)
• Resistant reaction -1:20 less common antigens
14. • De vay et al 1972 - that tolerance of parasite by host
increases with increasing protein / antigenic similarity ,
Resistance is chara by increasing disparity
• antigen common to host and pathogen implies –
genetic similarity & vice versa
• More the matching of host genes by pathogen more
susceptibilty
• Eg:- Ustilago maidis shares similar antigen with oat
seedlings, so that it can penetrate