1. Plant cells detect pathogenic bacteria through recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors, triggering PAMP-triggered immunity (PTI) and stopping bacterial growth. 2. Bacteria have effectors that can suppress PTI, allowing disease development if not recognized. 3. Plants have resistance proteins that recognize specific effectors, activating effector-triggered immunity (ETI) and a hypersensitive response to stop bacterial growth.

1. SHER-E-KASHMIR UNIVERSITY OF AGRICULTURAL SCIENCE
AND TECHNOLOGY, JAMMU
Topic: PTI To ETI: An Overview Of Plant defense Response

2. What is plant immunity?
 It is a state of defense against infectious pathogens
 Pathogens are like Bacteria, Fungi, Virus, Nematode, Oomycetes etc.
 Mode of entry of pathogen depend on type of pathogen
* Bacteria – stomata, hydathodes and wounds
* Nematode – Stylet
* Fungi – Haustoria
Phases of Plant Immunity
PAMPs Triggered Immunity (PTI)
Effector triggered susceptibility (ETS)
Effector Triggered immunity (ETI)

3. PAMP (Pathogen Associated Molecular Pattern)
 The molecules of pathogens, conserved across larger group of
pathogens
 Highly indispensable to the pathogens, required for their survivality
 These molecules do not exist in host
 Ex. Flagellin, EF-Tu, lipid, chitin, protein molecules of pathogens
PRR (Pattern recognition receptor)
 Plasma membrane-localized receptors that recognize the presence of
PAMP’s in the extracellular environment.
 Located in plasma membrane Ex. FLS2, ERF, CEBiP, etc

4. ETS (Effector Triggered Susceptibility)
 Effector are any regulatory molecules secreted by pathogens
 Modifies host protein to establish their growth
 Effector perform three main functions
 Structural role: Ex. Fungi, secret extra haustorial molecule
 Nutrient leakage: Ex. P. syringae HopM effector protein
 Pathogenicity: Ex. HopA1 dephosphorylates MAP kinase results
in inhibition of PTI

5. Effector triggered immunity (ETI)
 The plant defense response elicited by effector recognition.
 The effector molecules are recognized by R protein
 Four major classes of R genes
1. NB-LRR (nucleotide binding leucine rich repeat)genes
2. Ser/Thr kinases
3. Receptor-like kinases (RLKs)
4. Receptor-like proteins (RLPs)

6. From PTI To ETI: An Overview Of Plant
defense Response
 All plant cells are naturally exposed to bacteria and microbe
colonization. These can become pathogens when they invade the
host cell to proliferate. Damaging plant cell is a process which is
crucial to pathogens to access the host nutrients, which are essential
for them to proliferate.
 The main pathogen nutrient is sugar, located within the Apoplastic
space but more copious within the cellular matrix. Thus, the
successful pathogen willing to enter the plant cell has firstly to
degrade the cellular materials but its not an easy process.
 In fact, pathogens approaching to enter the cellular cytosol must
initially overcome the first layer of plant immune system – the
PAMP-triggered immunity (PTI).

7.  Plants defense mechanism depends on immune receptors found on
the plasma membrane which sense the Pathogen Associated
Molecular Patterns (PAMPs) and the Microbial Associated
Molecular Patterns (MAMPs), i.e. conserved pathogens molecules
essential for their reproduction.
 Detection of PAMPs trigger a physiological change in the cell
activated by the Pattern Recognition Receptors (PRRs). These
commence a cascade response which via the recognition of the
conserved microbial molecules PAMPs and MAMPs lead to plant
resistance.
 If this first defense system is defeated, then plant resistance initiates
a second mechanism of defense known as the Effector-Triggered
Immunity (ETI).

8. The Effector-Triggered Immunity
 When PTI results unsuccessful, cells become truly exposed to
pathogenic threats.
 At this stage Type III system proteins inject effectors into the host
cell cytosol via a needle-like structure, whilst other pathogens use
external appendages called haustoria. These are connected to the
host cell PM and function as a bridge to transfer effectors from the
pathogen.
 These pathogenic proteins, when recognized in the cytoplasm by
the nucleotide binding leucine rich repeats (NB-LRR) proteins,
trigger the second layer of plant defense –the Effector-Triggered
Immunity (ETI).

9.  NB-LRRs are proteins coded by R genes and present a leucine-rich
repeats (LRR) giving them specificity for binding interactions.
 ETI is a system which is more amplified and faster than PTI and
which usually develops onto the hypersensitive response (HR)
leading the infected host cell to apoptosis.
 HR does not terminates pathogen incursion but it solely slows it
down.

10. 1. When bacteria get in contact with plant cells.
2. Plant cells detect bacterial molecules (PAMPs) by receptors called
PRR
3. A signaling pathway named PTI (PAMP-Triggered-Immunity) is
activated
PAMPs Recognition
PRR
PRR
PLANT CELL
Signaling Pathway
Principles steps in plant immunity

11. 4. Molecular events occur and
stop bacterial growth: this is
called PTI (or Basal Defense)
BASAL DEFENSE
Phytoalexins :
 Phytoalexins as low mol. Wt. antimicrobial compounds which are
synthesized by and accumulates in plant cells after microbial
infection.
 Should be fungistatic & bacteristatic and active at very low conc.
 Produced by the host in response to infection or metabolic bye
products of micro-organisms and stimuli.
 Many phytoalexins have been isolated from plants (>20 ) families.
E.g. leguminosae, solanaceae, malvaceae, graminae, compositae,
umbelliferae, chenopodiaceae.

12.  Produced in large quantity in response to weak pathogen or non
pathogen than virulent one.
 Produced relatively quickly in cells after infection
Phytoalexin molecules

13. 1. Bacteria often have a Type III
Secretion System allowing them to
inject proteins (called “effectors”)
directly into plant cells.
2. Some effectors can suppress the host
basal defense
3. If basal defense is suppressed, then
bacterial growth is not inhibited, and
disease develops.
BASAL DEFENSE
BASAL DEFENSE
DISEASE
ETI RESPONSE:

14. R
ETI
4. Plant cells have proteins that can recognize effectors, they are called
Resistance proteins (R) and are specific to one effector.
5. A signaling pathway named ETI (Effector-Triggered-Immunity) is
activated.
6. If ETI is activated, the Hypersensitive Response occurs (HR) and
stops bacterial growth: The plant is resistant to the bacterium.
RESISTANCE

16. References:
 Faulkner, C. and Robatzek, S. (2012). Plants and pathogens:
putting infection strategies and defense mechanisms on the map.
Current Opinion in Plant Biology 15 (6), 699-707.
 Giraldo, M. C. and Valent, B. (2013). Box 1: Apoplastic and
symplastic compartments in plants. Nature Reviews Microbiology
11 (3), 800-814.
 Segonzac, C. and Zipfel, C. (2011). Activation of plant pattern-
recognition receptors by bacteria. Current Opinion in Microbiology
14 (1), 54-61.
 Cunnac, S., Lindeberg, M. and Collmer, A. (2009). Pseudomonas
syringae type III secretion system
 Greenberg, J. T. and Yao, N. (2004). The role and regulation of
programmed cell death in plant–pathogen interactions. Cellular
Microbiology 6 (3), 201-211.