Innate Immunity Flashcards
Innate system
Regulatory system controlling activation of defence mechanisms
Defence system controls genetically innate defence reactions
MAMPs and DAMPs
Chemical signatures that indicate the plant is under attack
MAMPs: Microbe derived molecules recognised as they are foreign signatures so recognise attack
DAMPs: degradation products of tissue damage recognised as found floating in intercellular space so recognise attack
Spatiotemporal model
Infection of tissue via fungal spore leads to defence:
- Preinvasive - recognition before pathogen enters causing ABA induced stomata closure, but some can produce chemicals to reopen them
- Early post invasive - intense early acting defence expressed locally; accumulation of ROS and signal cascade for defences to reinforce cell wall
- Late post invasive - SA and JA activated for defence to produce long lasting defence signals; costly defences
SA
Against biotrophic pathogens
PRRs recognise pathogens by binding to molecular signatures
Activate rapid signal transduction pathway and tf
Activate downstream genes that encode for enzymes that produce SA
Slow reponse so reliant on early defences
Accumulation of SA
Induces rapid fluctuations of redox state of cell
NPR1 protein reduced
Move to nucleus and recruit other tf
Activate defence genes
JA
Against necrotrophs and insect herbivores
PRRs recognise DAMPs from plants
Pathway1 (slow): activation of tf which activate genes that encode for biosynthesis of enzymes of JA
Pathway2 (fast): enzymes that produce JA may be in cell so activated faster
Accumulation of JA:
Becomes active when linked to thingy
Facilitates interaction between protein and JAZ
Labels JAZ for degradation so no longer bound to tf
Tf liberated and move to promotor region of defence genes to mount defence
ET
Against biotrophs and necrotrophs
Amplifies SA against biotrophs through sensitising neighbouring tissues
Helps JA defence response against necrotrophs
ABA
Against insects and abiotic stress
Accumulates w JA after attack by caterpillers
Hormones can be slow
Faster to build up preexisting quantities of inactive defence chemicals
Glucosinolates (brassicas) and benzoxazinoids (poaceae) - inactivated by binding to sugar group
Glucosinolates from amino acids; bound to sugar
Benzoxazinoids bound by simple ester bond
When attacked: cells lose integrity and hydrolytic enzymes contact w defence compound
Chemical reactions w toxic breakdown products
Evolutionary zig zag model
Specific for biotrophic pathogens which rely on living tissue
Quantitative disease resistance
Based on lots of genes so hard to select for
Effective against lots of unrelated pathogens and very durable
Non host: Very effective and efficient
Basal: Weaker (notr strong enough to prevent infection) but slows biotrophs; spectrum of resistance
Qualitative disease resistance
Controlled by resistance genes and very effective - almost completely protects plant from pathogen
Narrow range of effective - specific biotrophs
Easy to select for - varieties either very susceptible or very resistance
Not durable
Hypersensitive defence in cluster of cells - programmed cell death to deprive pathogen from food
R genes
Encode for proteins which sit inside cell (cytoplasmic)
Receptor domain interacts w other proteins
Binds to ATP so energy consuming
Variable N terminus
Signal transduction pathway that leads to cell death
Zig zag diagram
PRRs recognises DAMPs/MAMPS
Quick reaction increases defence intensity and provides non-host resistance
Specialised pathogens evolve ways to interfere w signal transcription pathways
Reduces defence intensity and weakens host
Plant evolved to recognise this - race specific resistance
Basal resistance to recognise effectors
Rapid localised cell death to kill attackers
Microbes evolve again - 2nd gen effectors deregulate pathways to reduce plant back to basal resistance
Plants evolve 2nd gen NLR proteins
