Identification of host factors recruited by plant pathogens

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IDENTIFICATION OF HOST
FACTORS RECRUITED BY
PLANT PATHOGENS
Ester Buiate
Physiology of Plant Health and Disease
Instructor - Dr. Aardra Kachroo
What are host factors?

Gene-for-gene hypothesis
 For
every avirulence (Avr) gene in the
pathogen there is a resistance (R) gene in the
host
 The interaction between those proteins leads
to activation of host defense system, that
stops the pathogen growth
Host factor
Effector protein
The effector proteins


Avirulence genes encoded by pathogens that cause
infection
Effector proteins can suppress host defense
responses (Nomura et al.,2006)
PAMPs and MAMPs

Provides a basal resistance

Pathogen-Associated Molecular Patterns
 Chitin:
fungal cell walls
 Flagellin: bacteria

PAMP Recognition Receptors (PRRs)
 Plant
receptors that recognize PAMPs
Resistance pathway
Jones & Dangl, 2006 Nature
How does effectors work?

Sctructural roles
 Haustorial
matrix

Promote nutrient leakage to the pathogen

Supress resistance response:
 Inhibit
PAMPs signaling pathway
 Cell traffcking
Fungi
Fungi
Ustilago maydis
 Infects
mayze and teosinte
 Model organism
Picture: The American Phytopathological Society
Type II Secretory System
Can be ATP-dependent
Talbot, Nature 2007
Ustilago maydis and Pep1

Gene clusters upregulated during biotrophic
development were mutated
 None

was essential for the initial development
Search for an effector gene that
 Carry
a secretion signal
 Produced a novel protein
Protein essential during prenetration 1
Ustilago maydis and Pep1
GFP
RFP
Ustilago maydis and Pep1
SG200
Fungal hyphae inside plant
SG200 pep1
Mutant was arrested
Ustilago maydis and Pep1
Insertion of RFP on citoplasm and GFP on Pep1
A- media culture B – penetration of maize epidermis C,D,E – intracellularly growth
Ustilago maydis and Pep1


Pep1 does not affect saprophytic growth neither
appressoria formation
Pep1 is essential for successful invasion of maize
 Plant
defense responses are downregulated after
penetration

Pep1 is a pathogen effector absolutely required for
the transition from saprophytic to biotrophic growth
Ustilago maydis and Pep1

How Pep1 works?
 Pep1
could active other effector proteins
 Pep1 could interfere with plant signalling
Virus
Tobacco Mosaic Virus
 Infects
tobacco, tomato and other solanaceous
 First virus discovered
Picture: The American Phytopathological Society
Tobacco Mosaic Virus


Are host dependent
Virus RNA are recognized and induce RNA
interference defense pathways in the host
Study focused on TMV replicase protein
and NAC domain protein ATAF2, which is
associated with host defense responses
and changes in virus accumulation
Tobacco Mosaic Virus degradation of ATAF2
GFP
expression
with TMV
Tobacco Mosaic Virus degradation of ATAF2
Reduction of
ATAF2 levels
Tobacco Mosaic Virus degradation of ATAF2
ATAF2 mRNA
levels are high
Tobacco Mosaic Virus degradation of ATAF2
Proteasome
inhibitor
increased
ATAF2 level
Tobacco Mosaic Virus

Interaction between pathogen replicase and host
NAC protein ATAF2
 Low

GFP in infected tissues
Virus-directed protein degradation
Disrupt host defenses
Bacteria
Bacteria
Pseudomonas syringae
 Infects
a wide range of plants and crops
 Model organism
 Tomato bacterial speck
Picture: K. Loeffler and A. Collmer, Cornell University
Type III secretion system

Protein of bacteria that
injects effector proteins
from the pathogen into
the host cell
Picture: University of Kansas, Dr. Tang
Pseudomonas syringae

Mutation in an effector gene (HopM1)
 No
symptoms, low bacterial population

Plants with hopM1 complemented the virulence defect

They found A. thaliana HopM interactors (AtMIN)
 AtMIN
encondes a protein that is crucial for vesicle
trafficking system
Pseudomonas syringae
DC3000 – wild type
∆CEL – lacks HopM
hrcC – secretion defective
Pseudomonas syringae
Inoculation with
a trafficking
inhibitor
DC3000 – wild type
∆CEL – lacks HopM
hrcC – secretion defective
Bacteria


AtMIN encodes ARF GEF protein, that are crucial for
vesicle trafficking system in eukaryotic cells
HopM1 probably adapts to that protein, and
targets it to the host proteasome system
Eliminating a component of vesicle traffic pathway
is an effective strategy of avoiding the
extracellular cell wall–associated host defense
Conclusions

Understand effector proteins and their coevolution with resistance genes
 How
immune system works
 New disease management

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