Natural Disease-Resistance Pathways

Natural disease-resistance pathways: overlap between pests and diseases

 Table 7.1
 No immune system that produce specific cells to attack invading microbes; rather
 Adopted more general defence systems and show many similarities with the innate defence systems of mammals.
 E.g. cellular damage caused by plant’s response to pathogen and plant pests trigger general defence systems
 Model plants such as tobacco and Arabidopsis in which the most recent molecular work has been done.

Four different levels of defence will be considered
(1) Anatomical defences;
(2) Pre-existing protein and chemical protection;
(3) Inducible systems;
(4) Systemic responses

Levels 1 and 2 were the basis general defences.
Inducible also contribute to these but also show more-specific defence responses.

(1) Anatomical defences
 Pathogen invade plants through wound due to plants have developed morphological and structural systems that preclude pathogen access to living cells.
 This can be thick layers of protective material, e.g. cuticle, bark, or waxes.
 If this defence breached, cascades of defence systems come into play.

(2) Pre-existing protein and chemical protection
 made up of antimicrobial proteins produced by the plant in defence against infectious agents
 structure : conserved 3-d folding pattern, a superfamily of peptides that pre-dates the divergence of plants and animals
 frequently associated with seeds at germination period

(3) Inducible System
Third level defence - a switch to counterattack that relies on protein systhesis de novo.
Normally switch off, but when some mechanisms of plant detect infection, this level of defence will be switch on. Why?
Costly for plant to permanently switched on its defence system.

Elicitor response
 The inducers, or elicitors (pathogen) that gain entry or arrives into a living cell, it may induce resistance to infection.
 The elicitors are of a number of different types, and the responses are complex.
 Local response involves interaction with molecules released by pathogen (exogenous elicitor). OR
 Host itself response to pathogen attack (endogenous elicitor) by the receptor molecules on the host .
 This will stimulate general defense systems in both host and non-host plants OR race-specific interactions inducing defense responses to specific cultivars.
 Both interaction may lead to cascade of reaction that include hypersensitive response (HR).
 Or, induction of systemic resistance & even passage of signals to other plants
 Fig 7.1, table 7.2

General response
 Damage of plant cell wall in first stage of infection.
 Fungi or bacteria (invaders) release proteolytic enzymes (e.g. oligogalacturonides) cause release wall fragments pectic-oligomers – general signals of endogenous elicitors, bind to specific receptor & induces cascade of reactions of specific defense genes.
 Specific defense genes involve in coding :
(1) Enzymes – synthesize structural components for cell wall thickening (to repair damage)
(2) Enzymes for 20 metabolism,
(3) Lectins (multimeric sugar-binding pt that agglutinate cells)
(4) And many pathogenesis-related (PR) proteins.
• Fig 7.3
• PR protein include chitinases & β-1,3-glucanases, protease inhibitors, non-specific lipid-transfer proteins, ribosomal inhibitor proteins & various antimicrobial protein (eg, defensins eg SN1 - active against bacterial & fungal pathogens in potato
• A number of PR gene products have been identified as latex allergens
• Function of the defence proteins depends on the pathogens.
• E.g. chitinases and glucanases may cause degradation of fungal hyphae cell wall. Causing production of chitin and β-1,3-glucan oligomers which act as signal molecules (exogenous elicitor), which bind to membrane receptor & re-enforce the induction of defence systems.
• The cell may also produce phytoalexins (phenolic compound or terpenes) that kill any pathogen & cell in the vicinity of the infection, therefore limiting the spread

Race-specific response
 Pathogens carried the avirulence gene (Avr) codes protein recognized by a specific receptor proteins in plant cell, encoded by resistance gene (R).
 Most important!!! Either of the proteins is absent on this gene-gene system will cause disease in the plant.
 Fig 7.2
 This interaction induces
 (a) the HR, which is manifested as a local necrosis that develops through a NADPH-dependent oxidative burst and/or the release of phenolics & nitric oxide
 (b) many pathogenesis-related (PR) proteins
 The gene-gene system is one of the most important ways plants have of switching on resistance systems eg for the interaction between plants & aphids, nematodes, fungi, viruses & bacteria
 Many of the bacterial avirulence protein fall into a class of proteins transported into the plant cell by the type III protein-secretion system (TTSS)
 They might function as virulence factors, subverting cellular functions through interactions with plant-encoded pathogenicity targets
 Ex, a type III efector from Pseudomonas syringae (pv.) phaseolicoli, VirPphA, blocks other masked Avr proteins from inducing the HR response
 Different type effectors able to suppress PAMP-induced defences. (PAMP – pathogen-associated molecular patterns)
 AvrPto has been shown to suppress the expression of a set of genes that encode cell wall & defence proteins

Elicitor receptors (R proteins)
 Fit into five basic structural groups.
 Biggest group having a nucleotide-binding site and a leucine-rich repeat region (NB-LRR proteins).
 Other four groups are structurally diverse but the R protein also contain an LRR region or R protein interacts with anther protein that contains he LRR domains.
 Fig 7.3
 Plant use receptors of similar structure comparison for the sensing of different types of elicitor that have evolved from a limited number of ancient receptors.
 Many elicitor proteins are key factors in the biology of the pathogen, favour plant defence mechanisms.
 Some plant R proteins come from mutation of LRR domain.

(4) Systemic responses
 The induction of local defense pathways may lead to the induction of intercellular signals that produce a systemic response –systemic acquired resistance (SAR)
 Both avirulent & virulent pathogens may result in the induction of SAR
 SAR has two phases :
(1) the initiation phase
(2) the maintenance phase
Initiation and Maintenance phase
 Initiation phase
cells at the foci of the infection release signal molecules (typically salicylic acid)  phloem  transported to target cells where SAR genes (eg, certain PR protein) are expressed
 Maintenance phase
quasi-steady-state resistance against virulent pathogens
 Fig 7.4

Induced systemic resistance
 independent of salicyclic acid
 induced by avirulent pathogens through pathway which induce ethylene or jasmonic acid (JA) as messengers
 result in induction of different classes of defence proteins
 Evidence : signals carried by volatile chemicals, such as methyl jasomenate, can travel between plants to warn of an attack
 Fig 7.5 (pg 171)

Development from transcriptomics study
 Significant levels of crosstalk between biotic (pathogen wounding, mechanical wounding by insects) and abiotic (drought, high salinity, cold) stress signaling networks.
 Same gene are expressed in response to different stresses & same hormone regulate these processes
 Reactive oxygen species (ROS) regulate these phenomena
 ROS + nitric oxide  establishment of HR
 ROS – a common signal that trigger downstream processes in many stress responses

Host Resistance
 Different plants defence systems have significant levels of overlap – plant innate immune system
 Host resistance is dependent upon the interaction of an R gene with a TTSS protein  HR reaction
 TTSS – type III protein-secretion system

Non-host Resistance
 Non-host resistance is more complex and composed of various defence genes including R proteins
 2 types
(1) Does not induce an HR reaction and involves general defence mechanism eg the physical barriers of the cell wall, antimicrobial compounds, 2⁰ matabolites followed by the response to PAMPs à pathogen cannot get further in its attack
(PAMP – pathogen-associated molecular patterns)
(2) Produce a non-host HR reaction
 Pathogen enters the cell
(a) Response to cell surface elicitors, (fungi or oomycetes), or
(b) TTSS-R-gene interaction (bacteria)