Acquired Immunity Flashcards
Acquired immunity
Plant resistance induced by stimulus
Enables plants to acquire long lasting and broad spectrum resistance
Develops distal from sites where innate immunity expressed
Happens upon recoveru of previous stress exposure
Augments basal resistance
Controlled by many genes
Different disease phenotypes - some plants more resistance than others
Makes basal resistance more efficient so more plants becomming efficient
Not as effective as qualitative resistance and protection rarely complete
Signals
Similar signals to innate immunity
Systemic acquired resistance
Devlops after infection of lower leaves
Upper leaves more resistant over time
Augementation of basal resistance
Use components of innate immunity to increase efficiency
Augment resistance that is dependent on SA after localised attack
Local tissues generate long distance signals
Induce resistance in distal parts
Augment SA dependent resistance
Herbivore induced volatiles
Airborne volatives to so neighbours respond quickly and induce resistance
Augments JA defences
Signals will result in lower caterpillar growth in neighbouring plants
Beneficial Soil microbes
Non pathogenic rhizobacteria and MC colonise root in mutualistic way
Induces resistance to necrotrophs and insects through JA
Help mobilise critical nutrients
Selected chemicals
Mimic biological resistance phenomena
BABA
Non protein amino acid found in stressed plants in low conc
Induces resistance against many pathogens and abiotic stress - effective and long term
Based on priming of SA dependent and independent defence mechanisms - enhances basal defence
Recognised by specific plant receptor
Faster induction of SA defences
Effectiveness of BABA
No trade offs w growth - tradeoffs when innate immunity but not acquired
Defences aren’t upregulated
Acquired immunity uses same infrastructure as innate but not prolonged upregulation
Plants are primed so can allocate more energy to growth when happy - costly defences not expressed so don’t drain energy
Primed plants
Higher defence activity than unprimed plants as exposed to previous stimulus
Downregulated in distal parts and over time
Mount faster and stronger defence later in life cycle
No major trade offs
Primed plants are fitter and grow more when under disease pressure - slightly reduced growth when no disease pressure but benefits of priming outweigh this
BABA
Promote earlier and stronger defence reactions when pathogens attack
Augment induction of SA dependent defence genes
Wrong conc of BABA causes reduced growth and yield
IBI mutants
Hyper sensitive to BABA induced stress
IBI1 is a receptor of BABA - forces enzyme to lead to defence priming and resistance
IBI1 controls defence priming
Plants become more tolerant to IBI1 and more sensitive to BABA induced resistance
IBI signalling
No priming: IBI1 confined to endoplasmic reticulum
Primed w BABA and no pathogen: IBI1 confined still - treating w BABA along doesn’t change localisation of IBI1
No priming and pathogen present: Some movement of IBI1 to cytoplasm - basal defence
Priming and pathogen: All of IBI1 moved to cytoplasm - augmented defence
VOZ
Regulate SA independent priming of cell wall defence
Tf activate early acting defence against pathogens
Inhibit ABA induced tolerance genes - protection against abiotic stress
Downy mildew
Activates ABA signalling - decoy
Plant invests in tolerance to abiotic stress to plant more susceptible to pathogen
Treating w BABA results in energy into defence instead so pathogen doesn’t succeed
Seedlings treated w BABA
Induced resistance passed onto new cells forming new tissues
JA priming
Defence against herbivores
Seedlings exposed to JA or caterpillar feeding remain immune over logn timer period
JA works w BABA:
Increases resistance to herbivores due to loss of water from damaged tissues
MYC dependent pathway
JA works w ET:
Resistance to necrotrophs to accelerate senescence and cell death
Memory induced in some cells passed on through cell division to new ones
Epigenetic trait
Heritable trait that can’t be explained by variation in DNA sequence
Progenies partially primed to stress suffered by parent
Reduced growth but some resistance
Passed on through meiosis to next gen
DNA methylation
Methylation of cytosons passed on
3 diff sequence contexts
Diff pathways to ensure sufficient DNA methylation
Transposable elements
Hostile DNA that can become active and jump into other genes
Don’t want them expressed
Silence them by methylating DNA at all sequence contexts - tightly packs DNA to TE can’t be expressed
DNA demethylases
Removes methylation at all 3 sequence contexts
Something about mutations?
Too many mutations damages plant
Transposons become active and expressed
Deregulation of other genes
Find mutations that reduce expression of genes
DNA methylation
More methylation = impaired to transgeneration resistance so more vulnerable to disease
Less methylation = plant susceptibility
DDM1 mutation???
Removing this reduced DNA methylation - sick plant but survives
