L8- Plant innate immunity

Question 1

how long does it take for plants to adapt to biotic stress

Answer 1

they can respond from seconds to multiple generations

Question 3

what is the internal defence strategy of planty

Answer 3

innate plant strategies they are born with
often molecular chemical signals, operate on timescale from seconds to days, involves acitvation of toxic metabolites

Question 4

how does innate immunity pass to genetic adaptation

Answer 4

Question 5

do plants have epigenetic immunity mechansims

Answer 5

they do, found diseases aradopsis seedlings from diseased plants had slightly more resistance

Question 6

define plant innate immunity

Answer 6

defence system that controls genetically innate defence reactions of plants to non-self and damaged-self pattens MAMPS and DAMPS

Question 7

what are the 2 models of plant innate immunity

Answer 7

spatiotemporal model
evolutionary zig-zag model

Question 8

what is the spatiotemporal model

Answer 8

induced defence, as these take energy and have ecological costs, they are only induced under attakc

• shows that defence take place in different places over time
  first step is pre invasive- such as stomatal closure, this tries to prevent entry point for pathogen

second step- is early acting post invasive pathogen, timescale of seconds to mins, often includes reactive oxygen species such as peroxides (toxic to pathogen), but also substrate to peroxides that help build jelly matrix called callus, and also secondary lignin cell walls

lastly, for dangerous pathogens, they supress early defence and progress further into plant this acitvates later acting post-invasive defence, these are hormone-controlled defence, this reprogrammes plant into defence mode

Question 9

what are the plant defence hormones

Answer 9

Question 10

what is biotrophic v necrotrophic

Answer 10

biotrophic lives within cells parastically
necrotrophic kills cells and feeds off remains

Question 11

what is the salicylic acid dependent immune response

Answer 11

• biotrophic pathogen triggers microbe (pathogen)-associated molecular patten (PAMPS)
  -Triggers PRR (pattern recognition receptors)
  -recognise a protein in flagella of pathogen
• this activates transcription factors that acitvate genes for salicylic acid
• once hormone reaches certain threshold, cause rapid fluctuations in the redox state
• this effects NPR1proteins, in healthy state they live in oxidised state, but they become reduced through SA response this breaks down sulphate bridges that allow it to enter nucleus to activate defence genes, happens over few hours, as against biotrophic which dont kill cell but more stealthy

Question 12

what is plant JA dependent immune response

Answer 12

necrotrophic pathogens trigger damage associated molecular patterns (DAMPS)
-trigger PRR (pattern recognition receptors), this causes transcription factors to trigger expression of JA biosynthesis (these enzymes are usually already present just need to be turned on, faster for necrotrophic attack)
- JA conjugates with amino acid isoleucine, this then causes complex downstream pathway
- COI1 protein labels JAZ proteins with ubiquitin, this will break them down in proteasome, once this is down it releases MYC2 that used to be attached to JAZ, liberated MYC2 activates defence genes in promoter regions

Question 13

how do plants have rapid chemical defence by phytoanticipins

Answer 13

glucosinolates in brassicaceae and benzoxazinoids in poaceae

these are present in pre existing quantities, these are attached to sugars in vacuole so not toxic, when plant is under attack it releases myrosinase enzyme (glucosinolates) or glucoside hydrolase (benzoxazinoides) , this will break down complex to release sugar group of toxic compounds

Question 14

what is the evolutionary model of innate immunity

Answer 14

mostly replies to biotrophic pathogens

two types
qualitative disease resistence
this is race specific resistance, this relies on single genes that are effective against certain genes, this means a narrow range of effectiveness

quantitative disease
-non-host resistence- most common and efficient immune response (pattern-triggered immunity), broad range of effectiveness and very effective
-basal resistence, similar to above but less effective, manifest itself in plant under attack by virulent pathogen, contributes to slowing down disease

Question 15

discuss quantitative v qualitative resistance

Answer 15

quantitative
- broad range of effectiveness, and durable based on lots of genes and mechanisms, this is good as it is hard for pathogen to respond and break down lots of different genes
-difficult to select by crop breeders and basal resistance is weak and not completely effective

qualitative
- easy to select for by crop breeders, and very strong specific resistance
- not durable, based on single R gene that can cause defence wars, narrow range of effectiveness

Question 16

hwo does qualitative resistance work

Answer 16

based on R genes, these encode NLR proteins or NBS-NLR proteins
NLR proteins are intracellular receptor proteins that control the hyper sensitive defence response (response that kills cell if they are infected, stops parasite)
these enclude the
TIR-NBS-LRR and LZ-NBS-LRR proteins that increase SA concentrations

Question 17

so what is the evolutionary zigzag model

Answer 17

from start
MAMP triggers PRR
this triggers non-host resistance (pattern triggered immunity), very intense

but pathogens evolve effectors (virulence factors), plants evolve to recognise these factors and trigger hypersensitive cell death (race-specific resistance) ETI

pathogen will evolve 2nd gen effectors that supress ETI, and so plants have to respond again to these ectect

Question 18

what types of resistence are specific to different pathogens

Answer 18