Plant Immune System
Plant Physiology
Plants are resistant to most pathogens, therefore most pathogens are
specialized for particular hosts.
Example: APS compendium lists approximately
100 pathogens of soybean, of which only 35 are
economically important.
Some concepts regarding plant immune systems
•
Preformed v. induced
•
Gene for gene interaction
•
Systemic acquired resistance
•
Hypersensitive response
Preformed resistance mechanisms
•
Physical barriers (cutin, cell wall….like our skin)
•
Preformed antimicrobial compounds
How do pathogens overcome these physical barriers?
enzymes (cutinases, pectinases, cellulases, etc.)
Mechanical force (appresoria, binds cell wall and hyphae together)
Alternate routes of entry (wounds, stomatas, etc.)
Preformed antimicrobial compounds are called
‘phytoanticipins’
plants produce a diverse array of secondary
metabolites, some with antimicrobial activity
Phytoanticipins are unique as they are preformed,
rather than being synthesized from remote precursors
after pathogen infection (phytoalexins)
Phytoanticipin
Phytoanticipins are synthesised by the plant at a constant rate and
therefore always present in the tissues of the plant, whereas
phytoalexins are only produced in response to a stimulus such as a
pathogenic invasion.
Constitutive: saponins (glycosylated antimicrobials)
• Saponins bind to sterols to disrupt fungal membranes
• Oats: Reduced saponin levels led to reduced resistance against oat pathogens
inactive precursors processed after tissue damage
or pathogen attack (cyanogenic glycosides and
glucosinolates)
Induced resistance mechanisms
physical barriers (cell wall thickening, callose
deposition, lignification….)
induced antimicrobials (phytoalexins…)
antimicrobial proteins (PR proteins, defensins…)
Hypersensitive response (PCD)
Host defense
peptides
Induced antimicrobials - Phytoalexins
low molecular weight, accumulate after
pathogen infection
chemically diverse (ie. not all the same!)
Camalexin production in response to Botrytis cinerea is a good example
Lignification during the invasion of Phytophthora
PAMP-induced MAPK cascades in the plant defense
(Adapted from Pitzschke et al., 2009)
Pathogen-associated molecular patterns, or PAMPs, are molecules associated
with groups of pathogens, that are recognized by cells of the innate immune
system. These molecules can be referred to as small molecular motifs
conserved within a class of microbes. They are recognized by Toll-like
receptors (TLRs) and other pattern recognition receptors (PRRs) in both plants
and animals.
An effector can also be a protein that is secreted from a pathogen, which
alters the host organism to enable infection, e.g. by suppressing the host's
immune system capabilities.
Hypersensitive response: Cells surrounding the infection site die
immediately depriving the pathogen of nutrients and preventing the spread.
Results in ROS production (Superoxide anion, hydrogen peroxide, hydroxyl
radicals.)
In phase 1, plants detect microbial/pathogen-associated molecular patterns (MAMPs/PAMPs, red
diamonds) via PRRs to trigger PAMP-triggered immunity (PTI). In phase 2, successful pathogens
deliver effectors that interfere with PTI, or otherwise enable pathogen nutrition and dispersal,
resulting in effector-triggered susceptibility (ETS). In phase 3, one effector (indicated in red) is
recognized by an NB-LRR protein, activating effector-triggered immunity (ETI), an amplified
version of PTI that often passes a threshold for induction of hypersensitive cell death (HR). In
phase 4, pathogen isolates are selected that have lost the red effector, and perhaps gained new
effectors through horizontal gene flow (in blue)—these can help pathogens to suppress ETI.
Selection favours new plant NB-LRR alleles that can recognize one of the newly acquired effectors,
resulting again in ETI.
Tomato cell
surface
receptor
C. fulvum
PAMP
A modified Zigzag Model for Cladosporium fulvum and Tomato
interaction
(Adapted from Thomma et al., 2011)
How Cladosporium fulvum and Tomato interaction works?
The C. fulvum PAMP chitin activates PTI in tomato plants, presumably upon perception by
the tomato homolog of the rice cell surface receptor CEBiP. Thus far, a chitin-triggered HR
has not been observed in tomato. To overcome PTI, C. fulvum employs the abundantly
secreted LysM effector Ecp6 that binds chitin, thereby preventing activation of Sl-CEBiP.
Since LysM effectors are widely conserved in the fungal kingdom, they qualify as PAMPs,
and Ecp6-mediated PTI suppression therefore should be referred to as PAMP-triggered
susceptibility (PTS). Tomato genotypes that have evolved to recognize Ecp6 develop an HR
upon Ecp6 infiltration and presumably carry a cell surface receptor for this molecule,
tentatively called C. fulvum resistance to Ecp6 (Cf-Ecp6), again resulting in PTI (PTI2). The
question mark indicates that subsequent susceptibility can again be provoked by C.
fulvum, either through mutation of the Ecp6 protein such that it still sequesters chitin
fragments but is no longer recognized by Cf-Ecp6 or by producing an effector that
suppresses Sl-CEBiP signaling in an alternative manner.
Gene-for-Gene Hypothesis by H.H. Flor
Disease resistance in plants requires two
complementary genes: an avirulence (Avr)
gene in the pathogen and a matching,
resistance (R) gene in the host.
Suggests a receptor-ligand model in which
R-protein-mediated recognition of the
pathogen-derived Avr products leads to
hypersensitive response (HR) in plant.
Flor showed that the inheritance of both
resistance in the host and parasite ability
to cause disease is controlled by pairs of
matching genes. One is a plant gene called
the resistance (R) gene. The other is a
parasite gene called the avirulence (Avr)
gene. Plants producing a specific R gene
product are resistant towards a pathogen
that produces the corresponding Avr gene
product.
http://www.youtube.com/watc
h?v=pDwhr1mTO5s
Model of innate immune signalling activated by LRR receptors in Arabidopsis,
mammals and Drosophila. A putative repressor (R) could control WRKY22 and WRKY29
activity because their overexpression bypasses the requirement of elicitors. The
conserved signalling pathways for innate immune responses in animals are summarized
on the basis of recent reviews on mammals and Drosophila