Molecular aspects of bio-interactions
Article 1
PR: pathogenesis-related protein, key ingredient of SAR
AMPs: Antimicrobial peptides
SAR: System acquired resistance
PTI: Pathogen-associated molecular pattern-triggered immunity
ETI: Effector-triggered immunity
PAMPs: Pathogen-associated molecular patterns (flagellines, lipopolysaccharides, chitins and glucans)
PRRs: Pattern recognition receptors, recognizes PAMPs activate PTI
HR: Hypersensitive response
Plants use preformed (structural and biochemical e.g. waxes) as well as inducible defense responses
to combat various biotic stresses( e.g. phytoanticipins).
If a pathogen crosses the first layer of defense HR generation of ROS, cell wall cross-linking,
synthesis of antimicrobial molecules like phytoalexins PR protein production.
Jasmonic acid (JA) and Salicylic acid (SA) further activates accumulation of PR proteins.
PR proteins largely differ from each other. They are generally low-molecular weight proteins (6-43
kDa), thermos stable, resistant to proteases and remain soluble at low pH (<3). PR proteins have 2
subgroups, 1) acidic PR protein usually secreted extracellular. 2) basic PR protein transported
to the vacuole by signal sequence located at the c-terminal end.
PR proteins are so called antimicrobial peptides (AMPs) cysteine rich molecules posses potential
and broad range of antimicrobial activity.
, Property/function
PR-protein
PR1 Antifungal, inhibit programme cell dead.
PR2 β-1,3-glucanase
PR3 Class I, II, IV, V, VI, VII chitinases
PR4 Class I, II chitinases
PR5 Thaumatin-like proteins
PR6 Proteinase inhibitor
PR7 Endoproteinase
PR8 Class III chitinase
PR9 Peroxidase
PR10 Ribonuclease-like proteins
PR11 Class I chitinase
PR12 Defensin
PR13 β-1,3-glucanase
PR14 Lipid-transfer protein
PR15 Ocalate oxidase
PR16 Oxidase-like
PR17 Antifungal and antiviral
SA, JA & ET are produced in response to pathogen attack. SA pathway provides resistance to
biotrophic pathogens, jasmonic/ethylene pathways mediate resistance to necrotrophic pathogens as
well as herbivorous pest. Increased expression of PR1, PR2 and PR5 genes respresents the activation
ofSA signalling pathway. Increased expression of PR3, PR4 and PR12 represent the activation of JA
pathway in Arabidopsis.
,Overexpressing PR1 and PR3 in tabacco plants leads to enhanced tolerance to salt and heavy metals.
Overexpression of PR5 also showed enhanced tolerance to abiotic stress. PR10 shows to play a role in
biotic stress tolerance when over expressed.
Lecture 1 repertoire of plant defense mechanisms
Pathogen: organism causing disease (virus or MO; bacterium, fungus, oomycete)
Pest: organism causing damage (animals; insects and nematodes)
Parasite: organism that feeds or grows on other organism
Attackers: all organisms that have negative influence on plant growth and/or physiology
(pest+pathogens)
Symbiont: organism that has an interaction with plants, may cause benefit or harm
Mutualist: symbiotic organism that has mutualistic interaction with plants, to the benefit of both
organisms
Endophyte: microorganism growing inside plant without causing visible damage or disease
symptoms
Compatible interaction: interaction is able to occur, plant and attacker match. In case of pathogen
attach, plant is diseased, pathogen is virulent. In case of mutualist interaction, symbiosis is successful
Incompatible interaction: interaction cannot occur, the plant and its interactor do not match. In case
of a pathogen attack, the plant is healthy (‘resistant’), and the pathogen is ‘avirulent’. Symbiosis fails
Plants must sense attackers and respond: problem recognition signal processing and
transmission gene activation/enzyme activation synthesis of ‘defense products’
Attackers of plants aim to obtain nutrition from plants in order to reproduce, an efficient defense
system blocks nutrient availability and or the reproduction of an attacker. Plants possess broad-
spectrum responses to group of attackers recognition of the problem is the key to deciding
whether defense activation is needed
Plant defense machinery:
- Pre-formed physical and chemical barriers
o Plant surface: cuticle, wax
o cell walls, vascular tissue: pectin, cellulose, lignin
, o Metabolites that are toxic for attackers
o Phytoanticipins: antimicrobial metabolites
o Volatile insect deterrants
- Induced defense mechanisms
o Cell wall reinforcement: callose + lignin deposition
o Production of novel toxic metabolites, Phenolics
o Production of (antimicrobial) enzymes
o Host cell death: Hyper sensitive response
o Oxidative burst: reactive oxygen species (ROS)
o Protease inhibitors: anti-feedant to insects
o Phytoalexins: antimicrobial metabolites
o PR-proteins: chitinase, glucanases, protease, lysozyme
o dsRNA formation RNA interference
Phytoanticipins pre-fromed defense. Always present
e.g. avenacin: phytoanticipin of oat, localised in root cortical cells just below epidermal cell layer.
Protects oat against a number of soil pathogens pathogens that penetrate the cuticle and invade
the cortex are rapidly killed. Degradation of avenacin is important of oat pathogens.
Insect deterrants
Volatile deterrants, smalls bad to chases the insect
Protease inhibitor, induced by wounding (mimics insect feeding)
Plant proteins that inhibit insect gut protease, prevent leaf tissue digestion in the insect gut,
insect is saturated and stops feeding damage is reduced
Phenolics, bad taste, poor digestibility. E.g. alfalone, pistatin (pea), resveratrol (grape,
peanut) and sakuranetin (rice). All formed out phenylalanine flavonoids, isoflavonoids
&stilbenes
Phytoalexins: compounds produced by plants in response to attack by pathogens; they act to poison
or repel the attacking organism
Pathogenesis-related (PR) proteins
-plant proteins induced by pathogens
- at least 17 different classes
- some have hydrolytic activity towards cell wall components of bacteria and fungi, some have true
antifungal or antibacterial activity in vivo, often acting synergistically
- several PR proteins have multiple isoforms that are located either extracellular or in the vacuole
- the later class is only supposed to act when plants cells are damaged by the pathogen (direct of
indirect)
Efficacy of defense mechanisms
Defense against virus:
- Interfere with viral disassembly &replication, or virus particle assembly &transport
- RNA interference
Defense against insect feeding on tissue
- Chase the insects by deterrant volatiles
- Make the tissue poorly digestible (protease inhibitor)
- Avoid flow of nutritious phloem sap
