Transcript Plant Responses to Internal and External Signals

Resistance
Inherent capacity of a host plant to prevent or retard the
development of an infectious disease
Complete resistance
Partial Resistance
vertical resistance
Highly specific (race specific)
Involves evolutionary genetic
interaction (arms race)
between host and one species
of pathogen
QUALITATIVE
horizontal resistance
Not specific- confers resistance to a range
of pathogens
QUANTITATIVE
Gene-for-Gene theory of
Complete Resistance
Pathogen has
virulence (a)
and avirulence
(A) genes
A
a
Plant has resistance gene
RR
rr
If the pathogen has an Avirulence gene and the host a Resistance gene,
then there is no infection
Gene-for-Gene theory of Complete Resistance
 The Avirulence gene codes for an Elicitor molecule or
protein controlling the synthesis of an elicitor
 The Resistance gene codes for a receptor molecule
which ‘recognises’ the Elicitor
 A plant with the Resistance gene can detect the
pathogen with the Avirulence gene
 Once the pathogen has been detected, the plant
responds to destroy the pathogen.
 Once the pathogen has been detected, the plant
responds to destroy the pathogen.
.
Gene-for-Gene theory of
Complete Resistance
What is an elicitor?
It is a molecule which induces any plant defence response.
It can be a polypeptide coded for by the pathogen avirulence gene, a
cell wall breakdown product or low-molecular weight metabolites.
Not all elicitors are associated with gene-for-gene interactions.
What do the Avirulence genes (avr genes) code for?
They are very diverse!
In bacteria, they seem to code for cytoplasmic enzymes involved in
the synthesis of secreted elicitor. In fungi, some code for secreted
proteins, some for fungal toxins.
Gene-for-Gene theory
Specific resistance to a plant disease is based on what
is called gene-for-gene recognition, because it
depends on a precise match-up between a genetic
allele in the plant and an allele in the pathogen.
 This occurs when a plant with a specific dominant
resistance alleles (R) recognizes those pathogens that
possess complementary avirulence (Avr) alleles.
 Specific recognition induces expression of certain plant
genes, products of which defend against the pathogen.
 If the plant host does not contain the appropriate R
gene, the pathogen can invade and kill the plant.
 There are many pathogens and plants have many R genes.
Gene-for-Gene theory
Resistance occurs if the plant has a particular
dominant R allele that corresponds to a specific
dominant Avr allele in the pathogen.
 The product of an R gene is probably a specific
receptor protein inside a plant cell or at its surface.
 The Avr gene probably leads to production of some
“signal” molecule from the pathogen, a ligand capable
of binding specifically to the plant cell’s receptor.
 The plant is able to “key” on this molecule as an
announcement of the pathogen’s presence.
 This triggers a signal-transduction pathway leading to a
defense response in the infected plant tissue.
Gene-for-Gene theory
Disease occurs if there
is no gene-for-gene
recognition because (b)
the pathogen has no
Avr allele matching an
R allele of the plant, (c)
the plant R alleles do
not match the Avr
alleles on the pathogen,
or (d) neither have
recognition alleles.
Gene-for-Gene theory
Even if a plant is infected by a virulent strain of a
pathogen - one for which that particular plant has
no genetic resistance - the plant is able to mount a
localized chemical attack in response to molecular
signals released from cells damaged by infection.
– Molecules called elicitors, often cellulose fragments
called oligosaccharins released by cell-wall damage,
induce the production of antimicrobial compounds
called phytoalexins.
ELICITORS
Elicitors are proteins made by the pathogen avirulence genes, or
the products of those proteins
Elicitors of Viruses
Coat proteins, replicases, transport proteins
Elicitors of Bacteria
40 cloned, 18-100 kDa in size
Elicitors of Fungi
Several now cloned- diverse and many unknown function
Elicitors of Nematodes
Unknown number and function
Model for the action of Xa21
(rice blight resistance gene)
Leucine-rich receptor
Transmembrane domain
Elicitor
Cell Wall
Membrane
Kinase
Signal transduction
([Ca2+], gene expression)
Plant Cell
Plant Defense Response
Compatible
interactiondisease
disease
Compatible interaction
Incompatible
interactionresistance
resistance
Incompatible interaction
3 aspects of response:
1. Hypersensitive
2. Local
3. Systemic
4Before they die, infected cells release a
chemical signal, probably salicylic acid.
3 In a hypersensitive
response (HR), plant
cells produce antimicrobial molecules,
seal off infected areas by
modifying their walls, and
then destroy themselves.
This localized response
Signal
produces lesions and
protects other parts of an
infected leaf.
Hypersensitive
response
2 This identification
step triggers a
Signal transduction
signal transduction
pathway
pathway.
1
Specific resistance is
based on the binding of
ligands from the
pathogen to receptors
in
plant cells.
The signal is distributed
to the rest of the plant.
5
6
In cells remote from the
infection site, the chemical
initiates a signal transduction
pathway.
7
Signal
transduction
pathway
Acquired
resistance
Avirulent
pathogen
R-Avr recognition and
hypersensitive response
Systemic acquired
resistance
Systemic acquired
resistance is
activated: the
production of
molecules that help
protect the cell
against a diversity
of pathogens for
several days.
HR (hypersensitive response)
Rapid localized necrosis of invaded tissue that
accompanies containment of pathogen
• Host membrane changes
–
–
–
–
oxygen radicals (H2O2, -OH) and nitrous oxide
excessive oxidation of polyphenols
signal transduction molecules activated
Lipoxygenases
• Rapid accumulation of phytoalexins and pathogenesisrelated proteins at infection site = decreased pathogen
multiplication
• Membrane collapse (releases antimicrobial substances and
denies biotrophs the necessary living substrate)
Hypersensitive Response
The hypersensitive response
– Causes cell and tissue death near the infection site
– Induces production of phytoalexins and PR proteins,
which attack the pathogen
– Stimulates changes in the cell wall that confine the
pathogen
Local responses
 Cessation of cell cycle
 Induction of genes that promote resistance
– Phenylpropanoid pathway induced: products include salicylic
acid (secondary inducer: induces other pathogenesis-related
proteins), lignins (cell wall), and flavonoids
– Pathogenesis-related (PR) proteins
– Phytoalexins increased
 Fortification of cell walls with lignin, hydroxyprolinerich glycoproteins (HRGPs), etc.
Systemic Acquired Resistance
Inducer inoculation
Local acquired
resistance
3 days to months,
then inoculate
SAR- long-term resistance to a range of
pathogens throughout plant caused by
inoculation with inducer inoculum
Systemic
acquired
resistance
Systemic Acquired
Resistance (SAR)
 It is a set of generalized defense responses in organs
distant from the original site of infection
 It is triggered by the signal molecule salicylic acid (which
activates plant defenses throughout the plant before
infection spreads)
Involves gene activation and a transmitted signal.
Genes induced:
chitinases
β 1,3- glucanases
other PR proteins